Evidence for an a r Adrenoceptor Subtype Mediating Adrenergic Vasoconstriction in Wistar Normotensive and StrokeProne Spontaneously Hypertensive Rat Kidney

We wished to characterise the α1-adrenoceptor subtypes mediating renal vasoconstrictor responses in pentobarbital anaesthetised normotensive rats and stroke-prone spontaneously hypertensive rats (SPSHR). Renal nerve stimulation, close renal arterial administration of phenylephrine (PE, a mixed α1a- and α1b-adrenoceptor agonist) and methoxamine (a putative α1a-adrenoceptor agonist) resulted in frequency and dose-dependent renal vasoconstrictor responses. Both dihy-dropyridine calcium channel antagonist amlodipine (200 μg kg-1plus 50 μg kg-1h-1and twice this dose) and the α1a-adrenoceptor antagonist 5-methylurapidil (5 μg kg-1plus 1.25 μg kg-1h-1and twice this dose) suppressed renal nerve-, PE-, and methoxamine-induced vasoconstrictions by between 21 and 59 (p < 0.05–0.001) in normotensive rats and SPSHR. The α1b-adrenoceptor alkylating agonist chloroethylclonidine (5μg kg-1plus 1.25 4mUg kg-1h-1and twice this dose) attenuated renal nerve-mediated vasoconstrictions by 20 (p < 0.01), but not those induced by PE and methoxamine. This pattern of agonist and blocking drug interaction suggests that the renal postjunctional α1-adrenoceptors require extracellular calcium and are sensitive to 5-methylurapidil, characteristics of the α1a-adrenoceptor subtype. Moreover, a similar situation exists at the renal resistance vessels of SPSHR.