Login Register Cart 0
Generic placeholder image

Current Pharmaceutical Design

Editor-in-Chief

ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

Back
Journal Home About Journal Editorial Board Journal Insight Current Issue Volumes/Issues
Subscribe
Mini-Review Article

Nitric Oxide Donors as Potential Drugs for the Treatment of Vascular Diseases Due to Endothelium Dysfunction

Author(s): Michele Paulo, Daniela E. F. R. Costa, Daniella Bonaventura, Claure N. Lunardi and Lusiane M. Bendhack*

Volume 26, Issue 30, 2020

Page: [3748 - 3759] Pages: 12

DOI: 10.2174/1381612826666200519114442

Price: $65

Abstract

Endothelial dysfunction and consequent vasoconstriction are a common condition in patients with hypertension and other cardiovascular diseases. Endothelial cells produce and release vasodilator substances that play a pivotal role in normal vascular tone. The mechanisms underlying endothelial dysfunction are multifactorial. However, enhanced reactive oxygen species (ROS) production and consequent vasoconstriction instead of endothelium-derived relaxant generation and consequent vasodilatation contribute to this dysfunction considerably. The main targets of the drugs that are currently used to treat vascular diseases concerning enzyme activities and protein functions that are impaired by endothelial nitric oxide synthase (eNOS) uncoupling and ROS production. Nitric oxide (NO) bioavailability can decrease due to deficient NO production by eNOS and/or NO release to vascular smooth muscle cells, which impairs endothelial function. Considering the NO cellular mechanisms, tackling the issue of eNOS uncoupling could avoid endothelial dysfunction: provision of the enzyme cofactor tetrahydrobiopterin (BH4) should elicit NO release from NO donors, to activate soluble guanylyl cyclase. This should increase cyclic guanosine-monophosphate (cGMP) generation and inhibit phosphodiesterases (especially PDE5) that selectively degrade cGMP. Consequently, protein kinase-G should be activated, and K+ channels should be phosphorylated and activated, which is crucial for cell membrane hyperpolarization and vasodilation and/or inhibition of ROS production. The present review summarizes the current concepts about the vascular cellular mechanisms that underlie endothelial dysfunction and which could be the target of drugs for the treatment of patients with cardiovascular disease.

Keywords: NO donors, endothelial dysfunction, vascular diseases, NO production, tolerance to nitrovadilators, cGMP.

« Previous Next »
[1]
Triggle CR, Samuel SM, Ravishankar S, Marei I, Arunachalam G, Ding H. The endothelium: influencing vascular smooth muscle in many ways. Can J Physiol Pharmacol 2012; 90(6): 713-38.
[http://dx.doi.org/10.1139/y2012-073] [PMID: 22625870]
[2]
Furchgott RF, Zawadzki JV. The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine. Nature 1980; 288(5789): 373-6.
[http://dx.doi.org/10.1038/288373a0] [PMID: 6253831]
[3]
Knowles RG, Moncada S. Nitric oxide synthases in mammals. Biochem J 1994; 298(Pt 2): 249-58.
[http://dx.doi.org/10.1042/bj2980249] [PMID: 7510950]
[4]
Alderton WK, Cooper CE, Knowles RG. Nitric oxide synthases: structure, function and inhibition. Biochem J 2001; 357(Pt 3): 593-615.
[http://dx.doi.org/10.1042/bj3570593] [PMID: 11463332]
[5]
Förstermann U, Sessa WC. Nitric oxide synthases: regulation and function. Eur Heart J 2012; 33(7): 829-37.
[http://dx.doi.org/10.1093/eurheartj/ehr304] [PMID: 21890489]
[6]
Fleming I, Bauersachs J, Busse R. Calcium-dependent and calcium-independent activation of the endothelial NO synthase. J Vasc Res 1997; 34(3): 165-74.
[http://dx.doi.org/10.1159/000159220] [PMID: 9226298]
[7]
Chang FJ, Lemme S, Sun Q, Sunahara RK, Beuve A. Nitric oxide-dependent allosteric inhibitory role of a second nucleotide binding site in soluble guanylyl cyclase. J Biol Chem 2005; 280(12): 11513-9.
[http://dx.doi.org/10.1074/jbc.M412203200] [PMID: 15649897]
[8]
Lucas KA, Pitari GM, Kazerounian S, et al. Guanylyl cyclases and signaling by cyclic GMP. Pharmacol Rev 2000; 52(3): 375-414.
[PMID: 10977868]
[9]
Korhonen R, Lahti A, Kankaanranta H, Moilanen E. Nitric oxide production and signaling in inflammation. Curr Drugs Targets- Inflammation Allergy 2005; 4: 471-9.
[http://dx.doi.org/10.2174/1568010054526359]
[10]
Montfort WR, Wales JA, Weichsel A. Structure and activation of soluble guanylyl cyclase, the nitric oxide sensor. Antioxid Redox Signal 2017; 26(3): 107-21.
[http://dx.doi.org/10.1089/ars.2016.6693] [PMID: 26979942]
[11]
Bian K, Murad F. What is next in nitric oxide research? From cardiovascular system to cancer biology. Nitric Oxide 2014; 43: 3-7.
[http://dx.doi.org/10.1016/j.niox.2014.08.006] [PMID: 25153032]
[12]
Buys ES, Zimmer DP, Chickering J, et al. Discovery and development of next generation sGC stimulators with diverse multidimensional pharmacology and broad therapeutic potential. Nitric Oxide 2018; 78: 72-80.
[http://dx.doi.org/10.1016/j.niox.2018.05.009] [PMID: 29859918]
[13]
Derbyshire ER, Marletta MA. Structure and regulation of soluble guanylate cyclase. Annu Rev Biochem 2012; 81: 533-59.
[http://dx.doi.org/10.1146/annurev-biochem-050410-100030] [PMID: 22404633]
[14]
Kots AY, Bian K, Murad F. Nitric oxide and cyclic GMP signaling pathway as a focus for drug development. Curr Med Chem 2011; 18(22): 3299-305.
[http://dx.doi.org/10.2174/092986711796504646] [PMID: 21728973]
[15]
Underbakke ES, Iavarone AT, Marletta MA. Higher-order interactions bridge the nitric oxide receptor and catalytic domains of soluble guanylate cyclase. Proc Natl Acad Sci USA 2013; 110(17): 6777-82.
[http://dx.doi.org/10.1073/pnas.1301934110] [PMID: 23572573]
[16]
Evora PR, Evora PM, Celotto AC, Rodrigues AJ, Joviliano EE. Cardiovascular therapeutics targets on the NO-sGC-cGMP signaling pathway: a critical overview. Curr Drug Targets 2012; 13(9): 1207-14.
[http://dx.doi.org/10.2174/138945012802002348] [PMID: 22716077]
[17]
Pereira AC, Paulo M, Araújo AV, Rodrigues GJ, Bendhack LM. Nitric oxide synthesis and biological functions of nitric oxide released from ruthenium compounds. Braz J Med Biol Res 2011; 44(9): 947-57.
[http://dx.doi.org/10.1590/S0100-879X2011007500084] [PMID: 21755266]
[18]
Shimizu T, Huang D, Yan F, et al. Gaseous O2, NO, and CO in signal transduction: structure and function relationships of heme-based gas sensors and heme-redox sensors. Chem Rev 2015; 115(13): 6491-533.
[http://dx.doi.org/10.1021/acs.chemrev.5b00018] [PMID: 26021768]
[19]
Lunardi CN, da Silva RS, Bendhack LM. New nitric oxide donors based on ruthenium complexes. Braz J Med Biol Res 2009; 42(1): 87-93.
[http://dx.doi.org/10.1590/S0100-879X2009000100013] [PMID: 19219301]
[20]
Kraehling JR, Sessa WC. Contemporary approaches to modulating the nitric oxide-cGMP pathway in cardiovascular disease. Circ Res 2017; 120(7): 1174-82.
[http://dx.doi.org/10.1161/CIRCRESAHA.117.303776] [PMID: 28360348]
[21]
Beuve A. Thiol-based redox modulation of soluble guanylyl cyclase, the NO Receptor. Antioxid Redox Signal 2017; 26(3): 137-49.
[http://dx.doi.org/10.1089/ars.2015.6591] [PMID: 26906466]
[22]
Tsai AL, Berka V, Sharina I, Martin E. Dynamic ligand exchange in soluble guanylyl cyclase (sGC): implications for sGC regulation and desensitization. J Biol Chem 2011; 286(50): 43182-92.
[http://dx.doi.org/10.1074/jbc.M111.290304] [PMID: 22009742]
[23]
Priviero FB, Webb RC. Heme-dependent and independent soluble guanylate cyclase activators and vasodilation. J Cardiovasc Pharmacol 2010; 56(3): 229-33.
[http://dx.doi.org/10.1097/FJC.0b013e3181eb4e75] [PMID: 20571429]
[24]
Baskaran P, Heckler EJ, van den Akker F, Beuve A. Aspartate 102 in the heme domain of soluble guanylyl cyclase has a key role in NO activation. Biochemistry 2011; 50(20): 4291-7.
[http://dx.doi.org/10.1021/bi2004087] [PMID: 21491881]
[25]
Heinecke JL, Khin C, Pereira JC, et al. Nitrite reduction mediated by heme models. Routes to NO and HNO? J Am Chem Soc 2013; 135(10): 4007-17.
[http://dx.doi.org/10.1021/ja312092x] [PMID: 23421316]
[26]
Frey R, Becker C, Saleh S, Unger S, van der Mey D, Mück W. Clinical pharmacokinetic and pharmacodynamic profile of riociguat. Clin Pharmacokinet 2018; 57(6): 647-61.
[http://dx.doi.org/10.1007/s40262-017-0604-7] [PMID: 29086344]
[27]
Nakayama T. Genetic polymorphisms of prostacyclin synthase gene and cardiovascular disease. Int Angiol 2010; 29(2)(Suppl.): 33-42.
[PMID: 20357747]
[28]
Yokoyama C, Yabuki T, Shimonishi M, et al. Prostacyclin-deficient mice develop ischemic renal disorders, including nephrosclerosis and renal infarction. Circulation 2002; 106(18): 2397-403.
[http://dx.doi.org/10.1161/01.CIR.0000034733.93020.BC] [PMID: 12403673]
[29]
Mitchell JA, Ahmetaj-Shala B, Kirkby NS, et al. Role of prostacyclin in pulmonary hypertension. Glob Cardiol Sci Pract 2014; 2014(4): 382-93.
[http://dx.doi.org/10.5339/gcsp.2014.53] [PMID: 25780793]
[30]
Cuíñas A, García-Morales V, Viña D, Gil-Longo J, Campos-Toimil M. Activation of PKA and Epac proteins by cyclic AMP depletes intracellular calcium stores and reduces calcium availability for vasoconstriction. Life Sci 2016; 155: 102-9.
[http://dx.doi.org/10.1016/j.lfs.2016.03.059] [PMID: 27142830]
[31]
Shabb JB. Physiological substrates of cAMP-dependent protein kinase. Chem Rev 2001; 101(8): 2381-411.
[http://dx.doi.org/10.1021/cr000236l] [PMID: 11749379]
[32]
Vanhoutte PM. Endothelium-dependent contractions in hypertension: when prostacyclin becomes ugly. Hypertension 2011; 57(3): 526-31.
[http://dx.doi.org/10.1161/HYPERTENSIONAHA.110.165100] [PMID: 21220708]
[33]
Mitchell JA, Evans TW. Cyclooxygenase-2 as a therapeutic target. Inflamm Res 1998; 47(Suppl. 2): S88-92.
[http://dx.doi.org/10.1007/s000110050287] [PMID: 9831329]
[34]
Catella-Lawson F, McAdam B, Morrison BW, et al. Effects of specific inhibition of cyclooxygenase-2 on sodium balance, hemodynamics, and vasoactive eicosanoids. J Pharmacol Exp Ther 1999; 289(2): 735-41.
[PMID: 10215647]
[35]
Bombardier C, Laine L, Reicin A, et al. VIGOR Study Group. Comparison of upper gastrointestinal toxicity of rofecoxib and naproxen in patients with rheumatoid arthritis. N Engl J Med 2000; 343(21): 1520-8.
[http://dx.doi.org/10.1056/NEJM200011233432103] [PMID: 11087881]
[36]
Chen G, Suzuki H, Weston AH. Acetylcholine releases endothelium-derived hyperpolarizing factor and EDRF from rat blood vessels. Br J Pharmacol 1988; 95(4): 1165-74.
[http://dx.doi.org/10.1111/j.1476-5381.1988.tb11752.x] [PMID: 2851359]
[37]
Michelakis ED, Reeve HL, Huang JM, et al. Potassium channel diversity in vascular smooth muscle cells. Can J Physiol Pharmacol 1997; 75(7): 889-97.
[http://dx.doi.org/10.1139/y97-111] [PMID: 9315358]
[38]
Araújo AV, Grando MD, da Silva RS, Bendhack LM. Function and expression of potassium channels in mesenteric resistance arteries isolated from 2K-1C hypertensive rats. J Hypertens 2014; 3: 1-7.
[39]
Araújo AV, Pereira AC, Grando MD, da Silva RS, Bendhack LM. The new NO donor Terpy induces similar relaxation in mesenteric resistance arteries of renal hypertensive and normotensive rats. Nitric Oxide 2013; 35: 47-53.
[http://dx.doi.org/10.1016/j.niox.2013.08.001] [PMID: 23968803]
[40]
Bonaventura D, Oliveira FS, da Silva RS, Bendhack LM. Decreased vasodilation induced by a new nitric oxide donor in two kidney, one clip hypertensive rats is due to impaired k channel activation. Clin Exp Pharmacol Physiol 2005; 32(5-6): 478-81.
[http://dx.doi.org/10.1111/j.1440-1681.2005.04215.x] [PMID: 15854162]
[41]
Pomposiello S, Rhaleb NE, Alva M, Carretero OA. Reactive oxygen species: role in the relaxation induced by bradykinin or arachidonic acid via EDHF in isolated porcine coronary arteries. J Cardiovasc Pharmacol 1999; 34(4): 567-74.
[http://dx.doi.org/10.1097/00005344-199910000-00014] [PMID: 10511133]
[42]
Matoba T, Shimokawa H, Nakashima M, et al. Hydrogen peroxide is an endothelium-derived hyperpolarizing factor in mice. J Clin Invest 2000; 106(12): 1521-30.
[http://dx.doi.org/10.1172/JCI10506] [PMID: 11120759]
[43]
Chidgey J, Fraser PA, Aaronson PI. Reactive oxygen species facilitate the EDH response in arterioles by potentiating intracellular endothelial Ca(2+) release. Free Radic Biol Med 2016; 97: 274-84.
[http://dx.doi.org/10.1016/j.freeradbiomed.2016.06.010] [PMID: 27320188]
[44]
Barlow RS, White RE. Hydrogen peroxide relaxes porcine coronary arteries by stimulating BKCa channel activity. Am J Physiol 1998; 275(4): H1283-9.
[PMID: 9746477]
[45]
Bény JL, von der Weid PY. Hydrogen peroxide: an endogenous smooth muscle cell hyperpolarizing factor. Biochem Biophys Res Commun 1991; 176(1): 378-84.
[http://dx.doi.org/10.1016/0006-291X(91)90935-Z] [PMID: 1708249]
[46]
Sobey CG, Heistad DD, Faraci FM. Mechanisms of bradykinin-induced cerebral vasodilatation in rats. Evidence that reactive oxygen species activate K+ channels. Stroke 1997; 28(11): 2290-4.
[http://dx.doi.org/10.1161/01.STR.28.11.2290] [PMID: 9368578]
[47]
Miura H, Bosnjak JJ, Ning G, Saito T, Miura M, Gutterman DD. Role for hydrogen peroxide in flow-induced dilation of human coronary arterioles. Circ Res 2003; 92(2): e31-40.
[http://dx.doi.org/10.1161/01.RES.0000054200.44505.AB] [PMID: 12574154]
[48]
Silva BR, Pernomian L, Grando MD, Amaral JH, Tanus-Santos JE, Bendhack LM. Hydrogen peroxide modulates phenylephrine-induced contractile response in renal hypertensive rat aorta. Eur J Pharmacol 2013; 721(1-3): 193-200.
[http://dx.doi.org/10.1016/j.ejphar.2013.09.036] [PMID: 24091168]
[49]
Olas B. Gasomediators (•NO, CO, and H2S) and their role in hemostasis and thrombosis. Clin Chim Acta 2015; 445: 115-21.
[http://dx.doi.org/10.1016/j.cca.2015.03.027] [PMID: 25818241]
[50]
Altaany Z, Moccia F, Munaron L, Mancardi D, Wang R. Hydrogen sulfide and endothelial dysfunction: relationship with nitric oxide. Curr Med Chem 2014; 21(32): 3646-61.
[http://dx.doi.org/10.2174/0929867321666140706142930] [PMID: 25005182]
[51]
Sánchez-Ferrer CF, Marín J. Endothelium-derived contractile factors. Gen Pharmacol 1990; 21(5): 589-603.
[http://dx.doi.org/10.1016/0306-3623(90)91003-A] [PMID: 2276580]
[52]
Shepherd TJ, Katusić ZS. Endothelium-derived vasoactive factors: I. Endothelium-dependent Relaxation 1991; 8: 53-5.
[53]
Félétou M, Huang Y, Vanhoutte PM. Vasoconstrictor prostanoids. Pflugers Arch 2010; 459(6): 941-50.
[http://dx.doi.org/10.1007/s00424-010-0812-6] [PMID: 20333529]
[54]
Hall JE, Granger JP, do Carmo JM, et al. Hypertension: physiology and pathophysiology. Compr Physiol 2012; 2(4): 2393-442.
[PMID: 23720252]
[55]
Crimi E, Ignarro LJ, Napoli C. Microcirculation and oxidative stress. Free Radic Res 2007; 41(12): 1364-75.
[http://dx.doi.org/10.1080/10715760701732830] [PMID: 18075839]
[56]
Radomski MW, Palmer RMJ, Moncada S. Comparative pharmacology of endothelium-derived relaxing factor, nitric oxide and prostacyclin in platelets. Br J Pharmacol 1987; 92(1): 181-7.
[http://dx.doi.org/10.1111/j.1476-5381.1987.tb11310.x] [PMID: 3311265]
[57]
Morris SM Jr. Recent advances in arginine metabolism: roles and regulation of the arginases. Br J Pharmacol 2009; 157(6): 922-30.
[http://dx.doi.org/10.1111/j.1476-5381.2009.00278.x] [PMID: 19508396]
[58]
Michel JB, Feron O, Sacks D, Michel T. Reciprocal regulation of endothelial nitric-oxide synthase by Ca2+-calmodulin and caveolin. J Biol Chem 1997; 272(25): 15583-6.
[http://dx.doi.org/10.1074/jbc.272.25.15583] [PMID: 9188442]
[59]
Potje SR, Grando MD, Chignalia AZ, Antoniali C, Bendhack LM. Reduced caveolae density in arteries of SHR contributes to endothelial dysfunction and ROS production. Sci Rep 2019; 9(1): 6696.
[http://dx.doi.org/10.1038/s41598-019-43193-8] [PMID: 31040342]
[60]
Rodrigues GJ, Restini CB, Lunardi CN, et al. Caveolae dysfunction contributes to impaired relaxation induced by nitric oxide donor in aorta from renal hypertensive rats. J Pharmacol Exp Ther 2007; 323(3): 831-7.
[http://dx.doi.org/10.1124/jpet.107.127241] [PMID: 17785608]
[61]
Rodrigues GJ, Restini CB, Lunardi CN, Neto Mdos A, Moreira JE, Bendhack LM. Decreased number of caveolae in endothelial cells impairs the relaxation induced by acetylcholine in hypertensive rat aortas. Eur J Pharmacol 2010; 627(1-3): 251-7.
[http://dx.doi.org/10.1016/j.ejphar.2009.11.010] [PMID: 19903465]
[62]
Schulz E, Gori T, Münzel T. Oxidative stress and endothelial dysfunction in hypertension. Hypertens Res 2011; 34(6): 665-73.
[http://dx.doi.org/10.1038/hr.2011.39] [PMID: 21512515]
[63]
Virdis A, Bacca A, Colucci R, et al. Endothelial dysfunction in small arteries of essential hypertensive patients: role of cyclooxygenase-2 in oxidative stress generation. Hypertension 2013; 62(2): 337-44.
[http://dx.doi.org/10.1161/HYPERTENSIONAHA.111.00995] [PMID: 23734008]
[64]
Manrique C, Lastra G, Gardner M, Sowers JR. The renin angiotensin aldosterone system in hypertension: roles of insulin resistance and oxidative stress. Med Clin North Am 2009; 93(3): 569-82.
[http://dx.doi.org/10.1016/j.mcna.2009.02.014] [PMID: 19427492]
[65]
Paulo M, Banin TM, de Andrade FA, Bendhack LM. Enhancing vascular relaxing effects of nitric oxide-donor ruthenium complexes. Future Med Chem 2014; 6(7): 825-38.
[http://dx.doi.org/10.4155/fmc.14.26] [PMID: 24941875]
[66]
Liu H, Ledingham JM, Mullaney I, Laverty R. Endothelial function in mesenteric resistance arteries from the genetically hypertensive rat. Clin Exp Pharmacol Physiol 2002; 29(5-6): 405-11.
[http://dx.doi.org/10.1046/j.1440-1681.2002.03676.x] [PMID: 12010184]
[67]
White RM, Rivera CO, Davison CB. Differential contribution of endothelial function to vascular reactivity in conduit and resistance arteries from deoxycorticosterone-salt hypertensive rats. Hypertension 1996; 27(6): 1245-53.
[http://dx.doi.org/10.1161/01.HYP.27.6.1245] [PMID: 8641731]
[68]
Christensen FH, Stankevicius E, Hansen T, et al. Flow- and acetylcholine-induced dilatation in small arteries from rats with renovascular hypertension--effect of tempol treatment. Eur J Pharmacol 2007; 566(1-3): 160-6.
[http://dx.doi.org/10.1016/j.ejphar.2007.03.058] [PMID: 17482591]
[69]
Vanhoutte PM, Shimokawa H, Tang EH, Feletou M. Endothelial dysfunction and vascular disease. Acta Physiol (Oxf) 2009; 196(2): 193-222.
[http://dx.doi.org/10.1111/j.1748-1716.2009.01964.x] [PMID: 19220204]
[70]
Risbano MG, Gladwin MT. Therapeutics targeting of dysregulated redox equilibrium and endothelial dysfunction. Handb Exp Pharmacol 2013; 218: 315-49.
[http://dx.doi.org/10.1007/978-3-662-45805-1_13] [PMID: 24092346]
[71]
Silva BR, Pernomian L, Bendhack LM. Contribution of oxidative stress to endothelial dysfunction in hypertension. Front Physiol 2012; 3: 441.
[http://dx.doi.org/10.3389/fphys.2012.00441] [PMID: 23227009]
[72]
Araújo AV, Andrade FA, Paulo M, et al. NO donors induce vascular relaxation by different cellular mechanisms in hypertensive and normotensive rats. Nitric Oxide 2019; 86: 12-20.
[http://dx.doi.org/10.1016/j.niox.2019.02.004] [PMID: 30772501]
[73]
Flaherty JT. Role of nitrates in acute myocardial infarction. Am J Cardiol 1992; 70(8): 73B-81.
[http://dx.doi.org/10.1016/0002-9149(92)90597-R] [PMID: 1529929]
[74]
Brunton L. On the use of nitrite of amyl in angina pectoris. Lancet 1867; ii: 97-8.
[http://dx.doi.org/10.1016/S0140-6736(02)51392-1]
[75]
Bonaventura D, de Lima RG, da Silva RS, Bendhack LM. NO donors-relaxation is impaired in aorta from hypertensive rats due to a reduced involvement of K(+) channels and sarcoplasmic reticulum Ca(2+)-ATPase. Life Sci 2011; 89(17-18): 595-602.
[http://dx.doi.org/10.1016/j.lfs.2011.07.022] [PMID: 21839096]
[76]
Paulo M, Araujo AV, Bendhack LM. Sodium nitroprusside activates potassium channels in the vena cava in normotensive but not in hypertensive rats. Hypertens Res 2013; 36(9): 765-9.
[http://dx.doi.org/10.1038/hr.2013.49] [PMID: 23784507]
[77]
Tocchetti CG, Wang W, Froehlich JP, et al. Nitroxyl improves cellular heart function by directly enhancing cardiac sarcoplasmic reticulum Ca2+ cycling. Circ Res 2007; 100(1): 96-104.
[http://dx.doi.org/10.1161/01.RES.0000253904.53601.c9] [PMID: 17138943]
[78]
Rodrigues GJ, Lunardi CN, Lima RG, et al. Vitamin C improves the effect of a new nitric oxide donor on the vascular smooth muscle from renal hypertensive rats. Nitric Oxide 2008; 18(3): 176-83.
[http://dx.doi.org/10.1016/j.niox.2007.12.002] [PMID: 18194676]
[79]
Rodrigues GJ, Pereira AC, Vercesi JA, Lima RG, Silva RS, Bendhack LM. Long-lasting hypotensive effect in renal hypertensive rats induced by nitric oxide released from a ruthenium complex. J Cardiovasc Pharmacol 2012; 60(2): 193-8.
[http://dx.doi.org/10.1097/FJC.0b013e31825bacc4] [PMID: 22635073]
[80]
Potje SR, Troiano JA, Grando MD, et al. Endothelial modulation of a nitric oxide donor complex-induced relaxation in normotensive and spontaneously hypertensive rats. Life Sci 2018; 201: 130-40.
[http://dx.doi.org/10.1016/j.lfs.2018.03.055] [PMID: 29604271]
[81]
Potje SR, Hildebrand MC, Munhoz FC, et al. The hypotensive effect of the ruthenium complex [Ru(terpy)(bdq)NO]3+ is higher in male than in female spontaneously hypertensive rats (SHR). Naunyn Schmiedebergs Arch Pharmacol 2014; 387(11): 1045-51.
[http://dx.doi.org/10.1007/s00210-014-1020-2] [PMID: 25066265]
[82]
Pereira AC, Araújo AV, Paulo M, et al. Hypotensive effect and vascular relaxation in different arteries induced by the nitric oxide donor RuBPY. Nitric Oxide 2017; 62: 11-6.
[http://dx.doi.org/10.1016/j.niox.2016.11.001] [PMID: 27845191]
[83]
Silva BR, Pernomian L, Grando MD, Bendhack LM. Phenylephrine activates eNOS Ser 1177 phosphorylation and nitric oxide signaling in renal hypertensive rat aorta. Eur J Pharmacol 2014; 738: 192-9.
[http://dx.doi.org/10.1016/j.ejphar.2014.05.040] [PMID: 24886887]
[84]
Tomoda T, Kato H, Ueki T, et al. Combination of diclofenac and sublingual nitrates is superior to diclofenac alone in preventing pancreatitis after endoscopic retrograde cholangiopancreatography. Gastroenterology 2019; 156(6): 1753-60.e1.
[http://dx.doi.org/10.1053/j.gastro.2019.01.267] [PMID: 30772342]
[85]
Redfield MM, Anstrom KJ, Levine JA, et al. NHLBI Heart Failure Clinical Research Network. Isosorbide mononitrate in heart failure with preserved ejection fraction. N Engl J Med 2015; 373(24): 2314-24.
[http://dx.doi.org/10.1056/NEJMoa1510774] [PMID: 26549714]
[86]
Nyolczas N, Dékány M, Muk B, Szabó B. Combination of hydralazine and isosorbide-dinitrate in the treatment of patients with heart failure with reduced ejection fraction. Adv Exp Med Biol 2018; 1067: 31-45.
[http://dx.doi.org/10.1007/5584_2017_112] [PMID: 29086392]
[87]
Bath PM, Scutt P, Anderson CS, et al. RIGHT-2 Investigators. Prehospital transdermal glyceryl trinitrate in patients with ultra-acute presumed stroke (RIGHT-2): an ambulance-based, randomised, sham-controlled, blinded, phase 3 trial. Lancet 2019; 393(10175): 1009-20.
[http://dx.doi.org/10.1016/S0140-6736(19)30194-1] [PMID: 30738649]
[88]
Rosenbaek JB, Al Therwani S, Jensen JM, et al. Effect of sodium nitrite on renal function and sodium and water excretion and brachial and central blood pressure in healthy subjects: a dose-response study. Am J Physiol Renal Physiol 2017; 313(2): F378-87.
[http://dx.doi.org/10.1152/ajprenal.00400.2016] [PMID: 28490529]
[89]
Bock JM, Treichler DP, Norton SL, Ueda K, Hughes WE, Casey DP. Inorganic nitrate supplementation enhances functional capacity and lower-limb microvascular reactivity in patients with peripheral artery disease. Nitric Oxide 2018; 80: 45-51.
[http://dx.doi.org/10.1016/j.niox.2018.08.007] [PMID: 30118808]
[90]
Menezes EF, Peixoto LG, Teixeira RR, Justino AB, Puga GM, Espindola FS. Potential benefits of nitrate supplementation on antioxidant defense system and blood pressure responses after exercice performance. Oxid Med Cell Longev 2019; 2019: 7218936
[http://dx.doi.org/10.1155/2019/7218936] [PMID: 31049136]
[91]
McCarthy O, Moser O, Eckstein ML, Bain SC, Pitt J, Bracken R. Supplementary nitric oxide donors and exercise as potential means to improve vascular health in people with type 1 diabetes: Yes to NO? Nutrients 2019; 11(7): 11-7.
[http://dx.doi.org/10.3390/nu11071571] [PMID: 31336832]
[92]
Sabbah HN, Tocchetti CG, Wang M, et al. Nitroxyl (HNO): A novel approach for the acute treatment of heart failure. Circ Heart Fail 2013; 6(6): 1250-8.
[http://dx.doi.org/10.1161/CIRCHEARTFAILURE.113.000632] [PMID: 24107588]
[93]
Cowart D, Venuti R, Guptill J, Noveck R, Foo S. A phase 1 study of the safety and pharmacokinetics of the intravenous nitroxyl prodrug, CXL-1427. J Am Coll Cardiol 2015; 65: A876.
[http://dx.doi.org/10.1016/S0735-1097(15)60876-2]
[94]
Tita C, Gilbert EM, Van Bakel AB, et al. A Phase 2a dose-escalation study of the safety, tolerability, pharmacokinetics and haemodynamic effects of BMS-986231 in hospitalized patients with heart failure with reduced ejection fraction. Eur J Heart Fail 2017; 19(10): 1321-32.
[http://dx.doi.org/10.1002/ejhf.897] [PMID: 28677877]
[95]
Fry NL, Mascharak PK. Photoactive ruthenium nitrosyls as NO donors: how to sensitize them toward visible light. Acc Chem Res 2011; 44(4): 289-98.
[http://dx.doi.org/10.1021/ar100155t] [PMID: 21361269]
[96]
Gori T, Parker JD. Nitrate-induced toxicity and preconditioning: a rationale for reconsidering the use of these drugs. J Am Coll Cardiol 2008; 52(4): 251-4.
[http://dx.doi.org/10.1016/j.jacc.2008.04.019] [PMID: 18634978]
[97]
Münzel T, Daiber A, Mülsch A. Explaining the phenomenon of nitrate tolerance. Circ Res 2005; 97(7): 618-28.
[http://dx.doi.org/10.1161/01.RES.0000184694.03262.6d] [PMID: 16195486]
[98]
Elkayam U, Kulick D, McIntosh N, Roth A, Hsueh W, Rahimtoola SH. Incidence of early tolerance to hemodynamic effects of continuous infusion of nitroglycerin in patients with coronary artery disease and heart failure. Circulation 1987; 76(3): 577-84.
[http://dx.doi.org/10.1161/01.CIR.76.3.577] [PMID: 3113764]
[99]
Zimrin D, Reichek N, Bogin KT, et al. Antianginal effects of intravenous nitroglycerin over 24 hours. Circulation 1988; 77(6): 1376-84.
[http://dx.doi.org/10.1161/01.CIR.77.6.1376] [PMID: 3131041]
[100]
Parker JD, Farrell B, Fenton T, Cohanim M, Parker JO. Counter-regulatory responses to continuous and intermittent therapy with nitroglycerin. Circulation 1991; 84(6): 2336-45.
[http://dx.doi.org/10.1161/01.CIR.84.6.2336] [PMID: 1835676]
[101]
Münzel T, Heitzer T, Kurz S, et al. Dissociation of coronary vascular tolerance and neurohormonal adjustments during long-term nitroglycerin therapy in patients with stable coronary artery disease. J Am Coll Cardiol 1996; 27(2): 297-303.
[http://dx.doi.org/10.1016/0735-1097(95)00475-0] [PMID: 8557897]
[102]
Thadani U. Challenges with nitrate therapy and nitrate tolerance: prevalence, prevention, and clinical relevance. Am J Cardiovasc Drugs 2014; 14(4): 287-301.
[http://dx.doi.org/10.1007/s40256-014-0072-5] [PMID: 24664980]
[103]
Knorr M, Hausding M, Kröller-Schuhmacher S, et al. Nitroglycerin-induced endothelial dysfunction and tolerance involve adverse phosphorylation and S-Glutathionylation of endothelial nitric oxide synthase: beneficial effects of therapy with the AT1 receptor blocker telmisartan. Arterioscler Thromb Vasc Biol 2011; 31(10): 2223-31.
[http://dx.doi.org/10.1161/ATVBAHA.111.232058] [PMID: 21757654]
[104]
Schulz E, Jansen T, Wenzel P, Daiber A, Münzel T. Nitric oxide, tetrahydrobiopterin, oxidative stress, and endothelial dysfunction in hypertension. Antioxid Redox Signal 2008; 10(6): 1115-26.
[http://dx.doi.org/10.1089/ars.2007.1989] [PMID: 18321209]
[105]
Channon KM, Guzik TJ. Mechanisms of superoxide production in human blood vessels: relationship to endothelial dysfunction, clinical and genetic risk factors. J Physiol Pharmacol 2002; 53(4 Pt 1): 515-24.
[PMID: 12512689]
[106]
Landmesser U, Dikalov S, Price SR, et al. Oxidation of tetrahydrobiopterin leads to uncoupling of endothelial cell nitric oxide synthase in hypertension. J Clin Invest 2003; 111(8): 1201-9.
[http://dx.doi.org/10.1172/JCI200314172] [PMID: 12697739]
[107]
Michell BJ, Chen Zp, Tiganis T, et al. Coordinated control of endothelial nitric-oxide synthase phosphorylation by protein kinase C and the cAMP-dependent protein kinase. J Biol Chem 2001; 276(21): 17625-8.
[http://dx.doi.org/10.1074/jbc.C100122200] [PMID: 11292821]
[108]
Daiber A, Oelze M, Wenzel P, et al. Nitrate tolerance as a model of vascular dysfunction: roles for mitochondrial aldehyde dehydrogenase and mitochondrial oxidative stress. Pharmacol Rep 2009; 61(1): 33-48.
[http://dx.doi.org/10.1016/S1734-1140(09)70005-2] [PMID: 19307691]
[109]
Münzel T, Gori T, Bruno RM, Taddei S. Is oxidative stress a therapeutic target in cardiovascular disease? Eur Heart J 2010; 31(22): 2741-8.
[http://dx.doi.org/10.1093/eurheartj/ehq396] [PMID: 20974801]
[110]
Münzel T, Sayegh H, Freeman BA, Tarpey MM, Harrison DG. Evidence for enhanced vascular superoxide anion production in nitrate tolerance. A novel mechanism underlying tolerance and cross-tolerance. J Clin Invest 1995; 95(1): 187-94.
[http://dx.doi.org/10.1172/JCI117637] [PMID: 7814613]
[111]
Esplugues JV, Rocha M, Nuñez C, et al. Complex I dysfunction and tolerance to nitroglycerin: an approach based on mitochondrial-targeted antioxidants. Circ Res 2006; 99(10): 1067-75.
[http://dx.doi.org/10.1161/01.RES.0000250430.62775.99] [PMID: 17053193]
[112]
Wenzel P, Mollnau H, Oelze M, et al. First evidence for a crosstalk between mitochondrial and NADPH oxidase-derived reactive oxygen species in nitroglycerin-triggered vascular dysfunction. Antioxid Redox Signal 2008; 10(8): 1435-47.
[http://dx.doi.org/10.1089/ars.2007.1969] [PMID: 18522491]
[113]
Chen Z, Zhang J, Stamler JS. Identification of the enzymatic mechanism of nitroglycerin bioactivation. Proc Natl Acad Sci USA 2002; 99(12): 8306-11.
[http://dx.doi.org/10.1073/pnas.122225199] [PMID: 12048254]
[114]
Diniz MC, Olivon VC, Tavares LD, et al. Mechanisms underlying sodium nitroprusside-induced tolerance in the mouse aorta: Role of ROS and cyclooxygenase-derived prostanoids. Life Sci 2017; 176: 26-34.
[http://dx.doi.org/10.1016/j.lfs.2017.03.016] [PMID: 28341178]
[115]
Paulo M, Grando MD, da Silva RS, Minshall RD, Bendhack LM. The nitric oxide donor RuBPY does not induce in vitro cross-tolerance with acetylcholine. Nitric Oxide 2017; 69: 69-77.
[http://dx.doi.org/10.1016/j.niox.2017.05.004] [PMID: 28559108]
[116]
Playfair L. On the nitroprusside: A new class of salts. Philos Trans R Soc Lond 1849; 139: 141.
[117]
Tinker JH, Michenfelder JD. Sodium nitroprusside: pharmacology, toxicology and therapeutics. Anesthesiology 1976; 45(3): 340-54.
[http://dx.doi.org/10.1097/00000542-197609000-00016] [PMID: 962181]
[118]
Page IH, Corcoran AC, Dustan HP, Koppanyi T. Cardiovascular actions of sodium nitroprusside in animals and hypertensive patients. Circulation 1955; 11(2): 188-98.
[http://dx.doi.org/10.1161/01.CIR.11.2.188] [PMID: 13231256]
[119]
Nightingale SL. From the food and drug administration. JAMA 1991; 265(7): 847-51.
[http://dx.doi.org/10.1001/jama.1991.03460070029012] [PMID: 1899454]
[120]
Vesey CJ, Cole PV, Simpson PJ. Cyanide and thiocyanate concentrations following sodium nitroprusside infusion in man. Br J Anaesth 1976; 48(7): 651-60.
[http://dx.doi.org/10.1093/bja/48.7.651] [PMID: 797397]
[121]
Arnold WP, Longnecker DE, Epstein RM. Photodegradation of sodium nitroprusside: biologic activity and cyanide release. Anesthesiology 1984; 61(3): 254-60.
[http://dx.doi.org/10.1097/00000542-198409000-00004] [PMID: 6089613]
[122]
Opasich C, Cioffi G, Gualco A. Nitroprusside in decompensated heart failure: what should a clinician really know? Curr Heart Fail Rep 2009; 6(3): 182-90.
[http://dx.doi.org/10.1007/s11897-009-0026-4] [PMID: 19723460]
[123]
Belani KG, Singh H, Beebe DS, et al. Cyanide toxicity in juvenile pigs and its reversal by a new prodrug, sulfanegen sodium. Anesth Analg 2012; 114(5): 956-61.
[http://dx.doi.org/10.1213/ANE.0b013e31824c4eb5] [PMID: 22392971]

Rights & Permissions Print Cite
Article Metrics
32
5
1
© 2024 Bentham Science Publishers | Privacy Policy