Chronic resveratrol consumption prevents hypertension development altering electrophysiological currents and Ca2+ signaling in chromaffin cells from SHR rats

Author(s)

Bomfim, Guilherme Henrique Souza ^{[1, 2]} ; Musial, Diego Castro ^[3] ; Mendez-Lopez, Iago ^[1] ; Jurkiewicz, Aron ^[3] ; Jurkiewicz, Neide Hyppolito ^[3] ; Padin, Juan Fernando ^[4] ; Garcia, Antonio G. ^{[1, 5]}

Affiliation

^[1] Univ Autonoma Madrid ITH UAM, Inst Teofilo Hernando, Fac Med, Dept Farmacol & Terapeut, Madrid - Spain

^[2] NYU, Coll Dent, Dept Mol Pathobiol, New York, NY 10010 - USA

^[3] Univ Fed Sao Paulo UNIFESP, Escola Paulista Med, Dept Farmacol, Sao Paulo - Brazil

^[4] Univ Castilla La Mancha UCLM, Fac Med, Dept Ciencias Med, Ciudad Real - Spain

^[5] Univ Autonoma Madrid UAM, Hosp Univ Princesa, Inst Invest Sanitaria, Madrid - Spain

• Document type: Journal article
• Source: CELLULAR SIGNALLING; v. 76, DEC 2020.
• Web of Science Citations: 0

Abstract

Resveratrol (RESV) is one of the most abundant polyphenol-stilbene compounds found in red wine with well-established cardioprotective and antihypertensive effects. Hyperactivity of the sympathoadrenal axis seems to be one of the major contributing factors in the pathogenesis of human essential hypertension. Alterations in outward voltage-dependent potassium currents (I-K) and inward voltage-dependent sodium (I-Na), calcium (I-Ca) and nicotinic (I-ACh) currents, CCs excitability, Ca2+ homeostasis, and catecholamine exocytosis were previously related to the hypertensive state. This raised the issue of whether in vivo long-term RESV treatment can directly act as a modulator of Ca2+ influx or a regulator of ion channel permeability in CCs. We monitored outward and inward currents, and cytosolic Ca2+ concentrations ({[}Ca-+(2)](c)) using different pharmacological approaches in CCs from normotensive (WKY) and hypertensive (SHR) animals chronically exposed to trans-RESV (50 mg/L/v.o, 28 days). The long-term RESV treatment prevented the increase of the systolic blood pressure (SBP) in SHR, without reversion of cardiac hypertrophy. We also found an increase of the outward I-K, reduction in inward I-Na, I-Ca, and I-ACh, and the mitigation of {[}Ca2+](c) overload in CCs from SHR at the end of RESV treatment. Our data revealed that electrophysiological alterations of the CCs and in its Ca2+ homeostasis are potential new targets related to the antihypertensive effects of long-term RESV treatment. (AU)

• FAPESP's process: 14/01569-0 - Interference of drugs producing disturbances in the drug-receptor interactions in hypertension, hyperglycemia and neurotransmission emphasizing the modulator role of histamine
• Grantee: Neide Hyppolito Jurkiewicz
• Support Opportunities: Regular Research Grants