Vascular alpha adrenoceptors were functionally characterized in two sequential intrarenal arteries of rabbits: renal artery first order branch (IRBA) and interlobar artery (ILA). The larger diameter IRBA exhibited greater contractile sensitivity to exogenous norepinephrine (NE) and to phenylephrine than the smaller ILA. Maximum active smooth muscle cell stress to NE and phenylephrine was greater than 3 x 105 N/m2 for both types of vessel. The alpha-1 adrenoceptor antagonists prazosin and WB4101 shifted concentration-response curves to NE rightward, whereas the alpha-2 adrenoceptor antagonist yohimbine had no significant effect. High concentrations of clonidine and UK14304 elicited only weak contractile responses in both types of artery. Pretreatment of arteries with chloroethylclonidine significantly attenuated NE-induced contraction in the IRBA, but not in the ILA. Chloroethylclonidine and also prazosin pretreatment eliminated the difference in contractile sensitivity to NE in the two types of vessels. The combined results suggested that: 1) NE-induced vasoconstriction in rabbit intrarenal arteries (IRBA and ILA) is mediated predominantly via alpha-1 adrenoceptors; 2) a subtype (or subtypes) of alpha- 1 adrenoceptor mediating vasoconstriction in the IRBA is either absent or nonfunctional in the ILA; and 3) regional differences in subtypes of alpha-1 adrenoceptor populations account for the differing functional responsiveness to NE observed in the IRBA and ILA.
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