Characterization of α-adrenoreceptor mediated reduction of flow in a saline-perfused constant pressure model of rat perfused hindquarters

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Abstract
An analysis of vasopressor responses elicited by .alpha.-adrenoreceptor agonists and KCl in a constant pressure saline perfused model of rat perfused hindquarters is presented. Using methoxamine (.alpha.1), cirazoline (.alpha.1), B-HT 920 (.alpha.2) and St 587 (.alpha.1) as .alpha.-adrenoreceptor agonists, and rauwolscine and prazosin as selective .alpha.2-and .alpha.1-adrenoreceptor agonists, respectively, it is concluded that .alpha.-adrenoreceptor mediated vasoconstriction in this model is mediated by the .alpha.1-subtype. Pretreatment of the animals with reserpine (i.p., at various doses and dose-regimens) or addition of angiotensin II (10-9-10-6M), PGF2.alpha. (10-8 and 5 .times. 10-7M) or KCl (2 and 4 .times. 10-3M), or changing [Mg2+] did not significantly affect the potency or intrinsic activity of the .alpha.-adrenoreceptor agonists studied. Experiments with the calcium entry blocking drugs gallopamil and nifedipine, or deletion of CaCl2 from the perfusion solution, did not reveal a contribution from the influx of extracellular calcium towards .alpha.1-adrenoreceptor-mediated reduction of flow in RPH. KCl-induced vasoconstriction in RPH was found to be sensitive to the blockade of calcium entry by calcium entry blocking drugs, but not to .alpha.-adrenoreceptor-blocking drugs and calmodulin antagonists. It is concluded that the model described here is of potential value in the characterization of .alpha.-adrenoreceptor antagonists and calcium entry blocking drugs under in vitro conditions in resistance vessels of the rat.

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