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 antagonists, 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(-6) M), PGF2 alpha(10(-8) & 5 X 10(-7) M) or KCl (2 & 4 X 10(-3) M), 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 antagonist. 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.