Influence of hypertension on acetaldehyde-induced vasorelaxation in rat thoracic aorta

Ethanol causes vasoconstriction and contributes to the development of hypertension. Acetaldehyde (ACA), the primary metabolite of ethanol, elevates blood pressure by releasing endogenous catecholamines. In vitro, ACA leads to vasorelaxation, although the response may vary among various vascular beds. This study examined the influence of hypertensive state on the ACA-induced vasorelaxant responsiveness. Ring segments of thoracic aorta were isolated from Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) and isometric tension development was measured. In aorta with or without intact endothelium, the contractile responses to KCl and norepinephrine were greatly attenuated, whereas vasoconstrictive response to 5-HT was enhanced, by hypertension. Vasorelaxant response to histamine was similar between WKY and SHR groups. ACA (1-30 mM) elicited endothelium-intact as well as -denuded vasorelaxation in a dose-dependent manner in aorta from both WKY and SHR groups. Interestingly, the ACA-induced endothelium-intact vasorelaxation was significantly diminished, whereas the ACA-induced endothelium-denuded vasorelaxation was significantly augmented, by hypertension. These data indicated that the ACA-induced vasorelaxant response, either endothelium-intact or-denuded, is altered by the hypertensive state.