Effects of Several β-Blockers On Blood Pressure in the Rat

Abstract

Abstract-Effects of practolol, alprenolol and pindolol on blood pressure in the rat were studied. Also effects of these three (3-blocking agents on blood pressure and heart rate in spinal rats during adrenaline infusion were studied and compared with those of propranolol.The 33-blocking agents produced a sustained pressor action in the rat, and in the spinal rat infused with adrenaline.The magnitude of the pressor action induced by the 3-blockers was in the following order: pindolol>propranolol~ alprenolol>practolol.Minimum doses of these j3-blockers required to cause a pres sor action in the spinal rat infused with adrenaline were in the following order; prac tolol>alprenolol>propranolol>pindolol.The magnitude of the pressor action produced by the same dose of these 5-blockers and minimum doses of these ;3-blockers required to cause a pressor action in the spinal rat infused with adrenaline seemed to be roughly proportional to their l3-receptor blocking activities. It was concluded that the minimum doses of these 5-blockers required to cause a pressor action and the magnitude of the pressor action induced by the 1s-blockers in the spinal rat in fused with adrenaline could be used to compare their ,5-blocking activities and that practolol, a cardioselective ,5-blocker, seems to block not only cardiac 15-receptor but to some extent also peripheral vascular receptors.Propranolol has been shown to produce little change or a fall in blood pressure in various species of experimental animals (1-3). Clinically, hypotensive effects of this agent after prolonged oral administration were reported in patients with several types of hyper tension (4-7).On the other hand, it was shown in our previous papers (8-10) that propranolol pro duces a sustained rise in blood pressure in the rat, and in the spinal rat during the infusion of i3-adrenergic stimulating agents. This pressor action in the rat may be due to the block ade of the i3-adrenoceptive vasodilator tone in the peripheral vascular beds which was probably mediated by direct sympathetic discharges from the central nervous system and the catecholamines released from the adrenal glands. Also the pressor response to pro pranolol in the spinal rat is considered to be due to the blockade of the (3-adrenoceptive vasodilator tone which was induced artificially by the infusion of 13-adrenergic stimulating agents.If this view were correct, other j3-blocking agents would produce a sustained pressor action in the rat, and in the spinal rat in which the 3-receptor vascular tone was induced by infusions of '3-adrenergic stimulating agents as well as propranolol . The present study was undertaken to examine this assumption, and further to investigate the mechanism of