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

Abstract

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 (Ca) 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 HO 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 Ca currents with slower inactivation; (iii) decreased K currents; (iv) augmented K-elicited cytosolic Ca transients ([Ca]); (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 [Ca] transients and catecholamine release from their CCs.

Is the Wistar Rat a more Suitable Normotensive Control for SHR to Test Blood Pressure and Cardiac Structure and Function?

“…16,17 Such differences have been confirmed by several studies that classified WKY as both normotensive 8,13 and hypertensive. 6,7,11,20,37 It is noteworthy that no previous work was found when assessing the biological variability of WIS. Thus, the long-term behavior of blood pressure observed in the WKY group allows for its use, though it draws attention and requires caution in the use of these animals as an SHR control.…”

Adaptation of the adrenal medulla to stress: Pathophysiological implications

“…Merecen destacarse la disminución de las corrientes a través de los canales ca v y K v , lo que unido a una mayor acumulación y liberación de ca 2+ inducida por ca 2+ desde el retículo endoplásmico favorecería elevaciones de la concentración intracelular de ca 2+ de mayor amplitud y duración, con la consiguiente potenciación de la respuesta secretora (81, 90, 91, 92) (Figura 1). Es de destacar que estas alteraciones se producirían también en otros modelos experimentales de HtA como los que consisten en la administración de alcohol, de deoxicorticosterona y sal o de estreptozotocina (induce también diabetes), lo que reforzaría el vínculo entre la médula adrenal y la HtA (83,92,93). Además, el hecho de que en ratas SHR prehipertensas se observen también algunas de estas alteraciones, apoyaría una relación causal con la HtA (84).…”

Participação da interleucina-6 no aumento da pressão arterial e dano oxidativo vascular induzidos pelo consumo crônico de etanol

“…No que concerne à ativação do SNS, diversos estudos demonstraram a capacidade do etanol de promover a hiperatividade desse sistema, caracterizada pelo aumento das concentrações plasmáticas de adrenalina e noradrenalina (Silva et al, 2015;Bomfim et al, 2017). O aumento na atividade do SNS está associado à liberação de renina pelas células justaglomerulares localizadas na artéria aferente renal, promovendo assim a maior atividade do sistema renina angiotensina (SRA) (Kim et al, 2007).…”