Effects of β1 and β2-Adrenoceptor Stimulation on Hemodynamics in the Anesthetized Rat

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Abstract
The role of .beta.1-adrenoceptors in mediation of vasodilation is not clear. The microsphere technique was used to compare the effects of mixed .beta.-, .beta.1-, and .beta.2-stimulation on blood flow and conductance changes in five groups of pentobarbital-anesthetized rats: I, vehicle; II, mixed .beta.-stimulation; III, .beta.1-stimulation; IV, .beta.2-stimulation; and V, mixed .beta.-blockade. Isoproterenol (32 ng/kg/min) was infused into rats either without (group II) or with ICI 118,551 (.beta.2-blocker, 30 .mu.g/kg, group III), atenolol (.beta.1-blocker, 100 .mu.g/kg, group IV), or both blockers (group V), respectively. At the doses selected, ICI 118,551 shifted the dose-vasodepressor response curve of salbutamol (.beta.2-agonist) to the right but had no effect on the dose-chronotropic response curve of dobutamine (.beta.1-agonist), whereas atenolol shifted the dosechronotropic response curve of dobutamine to the right and had no effect on the dose-vasodepressor response curve of salbutamol. The results show that isoproterenol increased heart rate (HR) and arterial conductances in the coronary and skeletal muscle beds but had no effects in other beds. Combined with ICI 118,551, isoproterenol caused similar increases in HR and coronary arterial conductance but markedly less increase in skeletal muscle conductance. Atenolol abolished the increase in HR by isoproterenol but did not affect the increases in coronary and muscular arterial conductances. With both blockers, isoproterenol produced no increase in coronary and skeletal muscle conductance. Therefore, both .beta.1- aand .beta.2-adrenoceptors play a role in coronary and skeletal muscle vasodilatation. Whether coronary vasodilatation subsequent to .beta.1-stimulation is entirely due to metabolic factors or is additionally contributed to by direct effects is not clear.