Adrenergic and nonadrenergic regulation of hindlimb blood flow during stress in rats.

A conditioned emotional response paradigm was established to determine the roles of adrenergic and nonadrenergic neurotransmitters in the hemodynamic responses during stress in conscious rats. The alpha adrenoceptor antagonists, prazosin (alpha-1-selective) or phentolamine (nonselective), blocked the stress-induced increase in mean arterial pressure (MAP), but not the increase in iliac blood flow or the decrease in iliac vascular resistance. Stress-induced iliac dilation was eliminated by the nonselective beta-adrenoceptor antagonist sotalol. In rats treated with prazosin plus sotalol, stress increased MAP but did not alter iliac vascular resistance. In contrast, stress did not increase MAP after complete adrenergic blockade with phentolamine plus sotalol yet did decrease iliac vascular resistance. Bilateral adrenal demedullation (ADM) did not affect the hemodynamic responses during stress, but ganglionic blockade eliminated them in both intact rats and in rats subjected to ADM. The stress-induced vasodilation in rats with ADM was not altered by sotalol, in direct contrast to intact rats. Finally, in rats with ADM, neither atropine nor sotalol (individually or when combined) altered any of the hemodynamic responses elicited by stress. The data suggest that during a conditioned emotional response: 1) adrenal catecholamines are not critical to the hemodynamic responses; 2) the increase in MAP is mediated by alpha-1 and alpha-2 adrenoceptor activation and 3) most critically, the hindquarter vasodilation is mediated by the release of neural adrenergic and nonadrenergic, noncholinergic factors.