[1]
Meng L, Chen D, Yang Y, Zheng Y, Hui R. Depression increases the risk of hypertension incidence: A meta-analysis of prospective cohort studies. J Hypertens 2012; 30(5): 842-51.
[2]
Bergantin LB. Hypertension, diabetes and neurodegenerative diseases: Is there a clinical link through the Ca2+/cAMP signalling interaction? Curr Hypertens Rev 2019; 15(1): 32-9.
[3]
Bergantin LB, Caricati-Neto A. Challenges for the pharmacological treatment of neurological and psychiatric disorders: Implications of the Ca2+/cAMP intracellular signalling interaction. Eur J Pharmacol 2016; 788: 255-60.
[4]
Bergantin LB, Caricati-Neto A. Advances for the pharmacotherapy of depression - Presenting the rising star: Ca2+/camp signaling interaction. J Syst Integr Neurosci 2017; 3(3): 1-5.
[5]
Miranda-Ferreira R, de Pascual R, Smaili SS, et al. Greater cytosolic and mitochondrial calcium transients in adrenal medullary slices of hypertensive, compared with normotensive rats. Eur J Pharmacol 2010; 636(1-3): 126-36.
[6]
Tully PJ, Peters R, Pérès K, Anstey KJ, Tzourio C. Effect of SSRI and calcium channel blockers on depression symptoms and cognitive function in elderly persons treated for hypertension: Three city cohort study. Int Psychogeriatr 2018; 21: 1-10.
[7]
Bergantin LB, Souza CF, Ferreira RM, et al. Novel model for “calcium paradox” in sympathetic transmission of smooth muscles: Role of cyclic AMP pathway. Cell Calcium 2013; 54(3): 202-12.
[8]
Devilliers AS, Russell VA, Carsters ME, et al. Noradrenergic function and hypothalamic-pituitary-adrenal axis activity in primary major depressive disorder. Psychiatry Res 1987; 22(2): 127-39.
[9]
Lake CR, Pickar D, Zeigler MG, Lipper S, Slater S, Murphy DL. High plasma norepinephrine levels in patients with major affective disorder. Am J Psychiatry 1982; 139(10): 1315-8.
[10]
Roy A, Pickar D, Linnoila M, Potter WZ. Plasma norepinephrine levels in affective disorders. Relationship to melancholia. Arch Gen Psychiatry 1985; 42(12): 1181-5.
[11]
Cooper SJ, Kelly JG, King DJ. Adrenergic receptors in depression. Effects of electroconvulsive therapy. Br J Psychiatry 1985; 147: 23-9.
[12]
Maes M, Meltzer HY, Suy E, Minner B, Calabrese J, Cosyns P. Sleep disorders and anxiety as symptom profiles of sympathoadrenal system hyperactivity in major depression. J Affect Disord 1993; 27(3): 197-207.
[13]
Sommer N, Loschmann PA, Northoff GH, et al. The antidepressant rolipram suppresses cytokine production and prevents autoimmune encephalomyelitis. Nat Med 1995; 1: 244-8.
[14]
Xiao L, O’Callaghan JP, O’Donnell JM. Effects of repeated treatment with phosphodiesterase-4 inhibitors on cAMP signaling, hippocampal cell proliferation, and behavior in the forced-swim test. J Pharmacol Exp Ther 2011; 338: 641-7.
[15]
Douglas WW, Rubin RP. The role of calcium in the secretory response of the adrenal medulla to acetylcholine. J Physiol 1961; 159: 40-57.
[16]
Baker PF, Knight DE. Calcium-dependent exocytosis in bovine adrenal medullary cells with leaky plasma membranes. Nature 1978; 276(5688): 620-2.
[17]
Kreye VA, Luth JB. Proceedings: Verapamil-induced phasic contractions of the isolated rat vas deferens. Naunyn Schmiedebergs Arch Pharmacol 1975; 287(Suppl.): R43.
[18]
French AM, Scott NC. A comparison of the effects of nifedipine and verapamil on rat vas deferens. Br J Pharmacol 1981; 73(2): 321-3.
[19]
Moritoki H, Iwamoto T, Kanaya J, Maeshiba Y, Ishida Y, Fukuda H. Verapamil enhances the non-adrenergic twitch response of rat vas deferens. Eur J Pharmacol 1987; 140(1): 75-83.
[20]
Caricati-Neto A, Garcia AG, Bergantin LB. Pharmacological implications of the Ca2+/cAMP signaling interaction: From risk for antihypertensive therapy to potential beneficial for neurological and psychiatric disorders. Pharmacol Res Perspect 2015; 3(5): e00181
[21]
Larkman AU, Jack JJ. Synaptic plasticity: Hippocampal LTP. Curr Opin Neurobiol 1995; 5(3): 324-34.
[22]
Nicoll RA, Malenka RC. Contrasting properties of two forms of long-term potentiation in the hippocampus. Nature 1995; 377(6545): 115-8.
[23]
Duman RS. Depression: A case of neuronal life and death? Biol Psychiatry 2004; 56(3): 140-5.
[24]
Miranda-Ferreira R, de Pascual R, de Diego AM, et al. Single-vesicle catecholamine release has greater quantal content and faster kinetics in chromaffin cells from hypertensive, as compared with normotensive, rats. J Pharmacol Exp Ther 2008; 324(2): 685-93.
[25]
Miranda-Ferreira R, de Pascual R, Caricati-Neto A, Gandia L, Jurkiewicz A, Garcia AG. Role of the endoplasmic reticulum and mitochondria on quantal catecholamine release from chromaffin cells of control and hypertensive rats. J Pharmacol Exp Ther 2009; 329(1): 231-40.
[26]
Davison K, Jonas BS, Dixon KE, Markovitz JH. Do depression symptoms predict early hypertension incidence in young adults in the CARDIA study. Arch Intern Med 2000; 160: 1495-500.
[27]
Bergantin LB, Caricati-Neto A. Emerging concepts for neuroscience field from Ca2+/cAMP signalling interaction. J Neurol Exp Neurosci 2017; 3(1): 29-32.
[28]
Caricati-Neto A, Bergantin LB. Pharmacological modulation of neural Ca2+/camp signaling interaction as therapeutic goal for treatment of Alzheimer’s disease. J Syst Integr Neurosci 2017; 3: 185.
[29]
Caricati-Neto A, Bergantin LB. The passion of a scientific discovery: the “calcium paradox” due to Ca2+/camp interaction. J Syst Integr Neurosci 2017; 3: 186.
[30]
Caricati-Neto A, Bergantin LB. From a “eureka insight” to a novel potential therapeutic target to treat Parkinson’s disease: The Ca2+/camp signalling interaction. J Syst Integr Neurosci 2017; 4: 187.
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