ALPHA-1B-ADRENOCEPTORS MEDIATE RENAL TUBULAR SODIUM AND WATER REABSORPTION IN THE RAT

1 It is known that activation of alpha(1)-adrenoceptors causes renal v asoconstriction and increased tubular Na+ and water reabsorption, with the alpha 1a-subtype mediating the constrictor effect. 2 This study e xamines which subtype of alpha(1)-adrenoceptors mediates tubular Na+ a nd water reabsorption in pentobarbitone-anaesthetized rats. In order t o avoid systemic effects, phenylephrine (0.3 to 30 mu g kg(-1)), metho xamine (0.1-10 mu g kg(-1)) and vehicle were infused into the right re nal artery (via the suprarenal artery) of three groups of rats. Two ot her groups of rats were continuously infused with the irreversible sel ective alpha 1a-adrenoceptor antagonist, chloroethyldonidine (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 infuse d with the irreversible selective alpha(1a)-adrenoceptor antagonist, S ZL-49 (10 mu g kg(-1) h(-1)) for 1 h, prior to the construction of dos e-response curves to phenylephrine. Mean arterial pressure (MAP), hear t rate (HR), urine flow, Na+ and K+ excretion, and urine osmolality we re monitored. 3 Phenylephrine and methoxamine did not affect MAP or HR but dose-dependently and significantly decreased urine flow, urine os molality as well as Naf excretion and, slightly increased K+ excretion , although this was significant only for phenylephrine. 4 The antidiur etic, antinatriuretic and kaliuretic effects of phenylephrine were abo lished by pretreatment with chloroethylclonidine, but were not inhibit ed by SZL-49. The inhibitory effects of methoxamine on urine flow and Na+ excretion were also almost totally abolished by chloroethylclonidi ne. 5 Our results show that alpha(1a)-adrenoceptors mediate renal tubu lar Na+ and water reabsorption.