α 1b‐Adrenoceptors mediate renal tubular sodium and water reabsorption in the rat

Abstract

It is known that activation of α1‐adrenoceptors causes renal vasoconstriction and increased tubular Na+ and water reabsorption, with the α1a‐subtype mediating the constrictor effect. This study examines which subtype of α1‐adrenoceptors mediates tubular Na+ and water reabsorption in pentobarbitone‐anaesthetized rats. In order to avoid systemic effects, phenylephrine (0.3 to 30 μg kg−1), methoxamine (0.1–10 μg kg−1) and vehicle were infused into the right renal artery (via the suprarenal artery) of three groups of rats. Two other groups of rats were continuously infused with the irreversible selective α1b‐adrenoceptor antagonist, chloroethylclonidine (3 mg kg−1 h−1) for 1 h, prior to the construction of dose‐response curves to phenylephrine or methoxamine. Another group was continuously infused with the irreversible selective α1a‐adrenoceptor antagonist, SZL‐49 (10 μg kg−1 h−1) for 1 h, prior to the construction of dose‐response curves to phenylephrine. Mean arterial pressure (MAP), heart rate (HR), urine flow, Na+ and K+ excretion, and urine osmolality were monitored. Phenylephrine and methoxamine did not affect MAP or HR but dose‐dependently and significantly decreased urine flow, urine osmolality as well as Na+ excretion and, slightly increased K+ excretion, although this was significant only for phenylephrine. The antidiuretic, antinatriuretic and kaliuretic effects of phenylephrine were abolished by pretreatment with chloroethylclonidine, but were not inhibited by SZL‐49. The inhibitory effects of methoxamine on urine flow and Na+ excretion were also almost totally abolished by chloroethylclonidine. Our results show that α1b‐adrenoceptors mediate renal tubular Na+ and water reabsorption. 1994 British Pharmacological Society