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

1 It is known that activation of α 1 ‐adrenoceptors causes renal vasoconstriction and increased tubular Na + and water reabsorption, with the α 1a ‐subtype mediating the constrictor effect. 2 This study examines which subtype of α 1 ‐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 α 1b ‐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 α 1a ‐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. 3 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. 4 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. 5 Our results show that α 1b ‐adrenoceptors mediate renal tubular Na + and water reabsorption.