Effects of Prazosin and Phenoxybenzamine on α- and β-Receptor-Mediated Responses in Intestinal Resistance and Capacitance Vessels

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Abstract
Previous studies have suggested that prazosin is a selective post-synaptic alpha-receptor blocker. It has also been suggested that it may have greater blocking actions on arterioles than on venous beds. These aspects have been investigated in cats anesthetized with pentobarbital. Prazosin had no effect on conductance in the acutely denervated hindlimb bed but caused a slowly developing vasoconstriction in the acutely denervated intestinal bed. The vasoconstrictor responses to sympathetic nerve stimulation were reduced to a similar extent in both vascular beds. Since maximal doses of prazosin produce only partial block of the alpha-receptor responses, there may be more than one type of postsynaptic alpha-receptor, and it is suggested that the postsynaptic receptors are of both alpha 1- and alpha 2-types. In the intestinal bed, prazosin produced similar reductions in both resistance and capacitance responses to sympathetic nerve stimulation. In isolated guinea pig aorta and portal vein, prazosin blocked the responses to noradrenaline competitively, and the pA3 values for the aorta and portal vein were similar. Thus, no selectivity for resistance vessels compared to capacitance vessels could be demonstrated in the intestine, and this result is compared to our previous observations in the liver. Although prazosin only reduced the vasoconstrictor responses to sympathetic nerve stimulation in the intestine, phenoxybenzamine reversed the response to a beta-receptor-mediated vasodilatation, as reported some years ago. These observations support our earlier hypothesis that nerve stimulation does not normally activate beta-receptors, but after phenoxybenzamine, the increased release of noradrenaline combined with alpha-receptor blockade results in a beta-receptor-mediated vasodilatation in the intestinal bed.