Abstract
We investigated effects of β-adrenoceptor agonists (β1-selective: T-1583 and dobutamine, β2-selective: fenoterol, non-selective: isoproterenol) on urine outflow rate, blood pressure, heart rate, respiratory rate and rectal temperature. The drugs were applied into the paraventricular nuclei (PVN) of spontaneously hypertensive (SHR), Wistar-Kyoto (WKY) and Wistar rats. Fenoterol and isoproterenol markedly decreased the urine outflow rate, compared with T-1583 and dobutamine in the rats. There was no marked difference among the three strains in responsiveness to fenoterol and isoproterenol. The antidiuretic effects of fenoterol were inhibited by a β2-selective antagonist, butoxamine, more markedly than β1-selective antagonist, atenolol, in SHR; and the inhibitory effects of these drugs were partial in WKY. In Wistar rats, the effect of fenoterol was inhibited by a non-selective β-antagonist, timolol, but not by atenolol or butoxamine. A vasopressin antagonist (i.v.) did not diminish the antidiuretic effect of fenoterol. Fenoterol reduced the blood pressure in SHR and WKY, but not in Wistar rats. It was suggested that there were predominantly β2-adrenoceptors mediating antidiuresis in SHR. In WKY and Wistar rats, however, the β-adrenoceptor subtypes mediating antidiuresis have yet to be determined. The ability of β-adrenoceptor agonists to decrease urine outflow rates in SHR was not altered as compared to that in the control rats. β-Adrenoceptor-mediated antidiuresis was not due to vasopressin release.
