Electrophysiological properties and augmented catecholamine release from chromaffin cells of WKY and SHR rats contributing to the hypertension development elicited by chronic EtOH consumption

• Published in: European journal of pharmacology Vol. 803; pp. 65 - 77
• Main Authors: Bomfim, Guilherme Henrique Souza, Méndez-López, Iago, Fernández-Morales, José Carlos, Padín, Juan Fernando, Jurkiewicz, Aron, Jurkiewicz, Neide Hyppolito, García, Antonio García
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 15-05-2017
• Subjects: Action Potentials - drug effects; Alcohol Drinking - adverse effects; Animals; Augmented catecholamine release; Calcium - metabolism; Catecholamines - secretion; Chromaffin Cells - drug effects; Chromaffin Cells - metabolism; Chromaffin Cells - pathology; Chromaffin Cells - secretion; Chromaffin cells electrophysiological properties; Chronic EtOH consumption; Cytosol - drug effects; Cytosol - metabolism; Electrophysiological Phenomena - drug effects; Ethanol - pharmacology; Hypertension - chemically induced; Hypertension - metabolism; Hypertension - pathology; Hypertension - physiopathology; Hypertension development; Male; Potassium - metabolism; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Time Factors; Hypertension development; Chronic EtOH consumption; Chromaffin cells electrophysiological properties; Augmented catecholamine release
• ISSN: 0014-2999; 1879-0712
• DOI: 10.1016/j.ejphar.2017.03.017

It is known that chronic ethanol (EtOH) consumption leads to hypertension development and has been associated with deleterious effects on the cardiovascular system. Whether this condition alters calcium (Ca2+) signaling and exocytosis in adrenal chromaffin cells (CCs) as the case is for genetic hypertension, is unknown. We explored this question in four randomized experimental groups, male Wistar Kyoto (WKY/EtOH) and Spontaneously Hypertensive (SHR/EtOH) rats were subjected to the intake of increasing EtOH concentrations (5–20%, for 30 days) and their respective controls (WKY/Control and SHR/Control) received water. WKY/EtOH developed hypertension and cardiac hypertrophy; blood aldehyde dehydrogenase (ALDH) and H2O2 were also augmented. In comparison with WKY/Control, CCs from WKY/EtOH had the following features: (i) depolarization and higher frequency of spontaneous action potentials; (ii) decreased Ca2+ currents with slower inactivation; (iii) decreased K+ currents; (iv) augmented K+-elicited cytosolic Ca2+ transients ([Ca2+]c); (v) enhanced K+-elicited catecholamine release. These cardiovascular, blood and CCs changes were qualitatively similar to those undergone by SHR/Control and SHR/EtOH. The results suggest that the hypertension elicited by chronic EtOH has pathogenic features common to genetic hypertension namely, augmented [Ca2+]c transients and catecholamine release from their CCs.
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