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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.

We characterised the functional α1-adrenoceptors involved in mediating adrenergic vasoconstrictor responses in kidney of two-kidney one-clip (2K1C) Goldblatt and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. In sodium pentobarbital-anaesthetised rats, frequency- and dose-dependent renal vasoconstrictor responses were obtained by direct electrical renal nerve stimulation, close renal arterial administration of phenylephrine (PE), and methoxamine. Administration of amlodipine, a dihydropyridine calcium channel antagonist (bolus dose of 200 and 400 μg/kg and an infusion of 50 and 100 μg/kg/h, respectively) and the α1-adrenoceptor antagonist 5-methylurapidil (5 μg/kg plus 1.25 μg/kg/h and twice this dose) suppressed renal nerve-, PE-, and methoxamine-induced vasoconstrictions 14–70 (p < 0.05–0.001) in 2K1C Goldblatt and DOCA-salt hypertensive rats. The α1-adrenoceptor alkylating agent, chloroethylclonidine (5 (μg/kg plus 1.25 μg/kg/h and twice this dose) caused significant attenuation (p < 0.001) of renal nerve-induced vasoconstriction by 19–23 in DOCA-salt hypertensive rats but did not affect PE- and methoxamine-induced vasoconstriction in either 2K1C Goldblatt or DOCA-salt hypertensive rats. In contrast, in 2K1C Goldblatt rats vasoconstrictor responses were potentiated by renal nerve stimulation and methoxamine. The data show that the functional renal postjunctional α1-adrenoceptors on the vasculature of both hypertensive models are primarily of the α1A-subtype, as reflected by their sensitivity to amlodipine and 5-methylurapidil. Moreover, an interaction appears to occur between the α1-adrenoceptor subtypes at renal vessels in 2K1C Goldblatt hypertensive rats.

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 dihydropyridine 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 (5 μg kg-1plus 1.25 μg 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.