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Clarification of the effect of chronic ethanol consumption upon cardiovascular reactivity in rats.Spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) normotensive rats were randomly allocated in groups of 10 to ethanol in tap water [20% (v:v) after the first week or tap water for 7–12 weeks].Intra-arterial blood pressure and heart rate were measured at rest and in response to vibration and noise stress. Vascular reactivity was assessed in isolated paired perfused hindquarters and in mesenteric arterioles in a Mulvany-Halpern myograph.Resting intra-arterial blood pressure but not heart rate was lower in both ethanol-treated groups. The ethanol treatment increased the SHR heart rate response to sudden noise but the WKY response did not increase. Pressor responses to noise were initially greater in the ethanol-treated SHR. The ethanol had no effect upon isolated perfused hindquarter resistance at maximal dilation, dose-response curves in response to noradrenaline or vasopressin, or maximal contractile strength. Isolated mesenteric arterioles showed that ethanol had no effect upon responses to nerve stimulation or upon the 50% effective dose required for a response to noradrenaline or vasopressin.Ethanol treatment heightened the heart rate reactivity to stress without substantially affecting vascular neuro-effector characteristics in SHR. This is likely to be a central effect, caused by suppression of the central nervous inhibitory systems that influence the heart rate and baroreflex activity in a strain of rat already showing evidence of an impaired ability to modulate the heart rate and blood pressure in response to stress. The small reduction in resting blood pressure may be a consequence of the lower weight in the ethanol-treated rats, and/or may reflect a direct depressing action by the alcohol on vascular and cardiac muscle. These findings are discussed in the context of ethanol-induced hypertension in humans and possible genetic variations in central nervous, cardiac and vascular effects.