Vasodilation by medroxalol mediated by beta 2-adrenergic receptor stimulation.

A contribution by active vasodilation to the hypotensive effect of medroxalol was investigated in anesthetized dogs and reserpinized pithed rats. In anesthetized dogs, intravenous doses of medroxalol, which decreased blood pressure and heart rate, also produced a dose-related vasodilation in the isolated perfused gracilis muscle in situ. This vasodilator effect of medroxalol was completely blocked by propranolol; the hypotensive effect of medroxalol was inhibited 50% by propranolol but not at all by practolol. In reserpinized pithed rats with angiotensin-supported blood pressure, intravenous doses of medroxalol also produced propranolol-sensitive decreases in diastolic blood pressure and did not alter heart rate. Labetalol produced similar effects but was significantly less potent. Comparatively, equivalent amounts of isoproterenol and pindolol decreased diastolic blood pressure but increased heart rate. In the isolated guinea pig trachea, medroxalol produced a propranolol-sensitive relaxation at concentrations that antagonized the relaxant effects of salbutamol. Identical concentrations of medroxalol did not increase rate of isolated guinea pig atria. It is concluded that a substantial portion of the hypotensive effect of medroxalol is due to a beta 2-adrenergic-receptor-mediated vasodilation.