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  • Title: Comparison of effects of urapidil and prazosin on vascular influence of circulating and neuronally released catecholamines in canine muscle vascular bed.
    Author: Zeigler DW, Zimmerman BG.
    Journal: J Cardiovasc Pharmacol; 1985; 7(6):1020-6. PubMed ID: 2418283.
    Abstract:
    Two series of experiments were conducted in anesthetized dogs to compare the vascular effects of the alpha 1-adrenoceptor antagonists urapidil and prazosin. In the first series of experiments vasoconstrictor responses to sympathetic nerve stimulation and phenylephrine injected intraarterially were elicited in the pump-perfused hindlimb. Urapidil and prazosin administered intravenously in the doses of 2 and 0.25 mg/kg, respectively, were equivalent in their ability to block these responses. Yohimbine, an alpha 2-adrenoceptor antagonist, in the dose of 0.05 mg/kg, had no additional effect on the responses, but did decrease the vascular resistance after prazosin infusion. This suggested that urapidil, but not prazosin, exerted an alpha 2-blocking effect which decreased vascular resistance. In the second series of experiments the effect of urapidil administered intravenously was determined on the innervated and denervated gracilis muscle, after maximal alpha 1-adrenoceptor blockade with prazosin. The purpose of these experiments was to confirm whether or not urapidil had an additional effect on vascular resistance attributable to alpha 2-antagonism. Prazosin, 0.25 mg/kg followed by 0.50 mg/kg i.v., decreased vascular resistance in both the innervated and denervated gracilis muscles, and maximal alpha 1-blockade was achieved based on the blockade of the pressor responses to phenylephrine. A further reduction in vascular resistance was found after urapidil infusion, 2 mg/kg, which appears to be due to blockade of the effect of circulating catecholamines on alpha 2-adrenoceptors. The difference between the vascular resistance seen immediately following acute sympathetic denervation and the level achieved 15 min afterward appears to be due to the influence of circulating catecholamines.
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