Effect of d- and l-propranolol on the discharge of cardiac vagal C fibers

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Abstract
Dl-Propranolol has both .beta.-adrenergic-receptor-blocking and nonspecific membrane-stabilizing (local anesthetic) effects. The purpose of this study was to determine if the discharge of left atrial and left ventricular mechanoreceptors with nonmyelinated vagal afferents (mean conduction velocity 1.4 ml/s) is altered by the .beta.-adrenergic-receptor-blocking effect of l-propranolol or the membrane stabilizing effect of d- and l-propranolol in 12 open-chest pentobarbital-anesthetized cats. The location of the receptors was established by probing the open heart. Graded occlusion of the ascending aorta resulted in increases in the firing of atrial endings that were linearly related to left atrial pressure (1.5 impulses/s mmHg) and in the firing of ventricular endings that correlated best with left ventricular diastolic pressure (0.69 impulses/s mmHg). d-Propranolol (0.3-0.6 mg/kg), which has membrane-stabilizing but not .beta.-adrenergic-receptor-blocking properties, did not alter the response of atrial or ventricular endings to aortic occlusion. l-Propranolol (0.3-0.6 mg/kg), which has both membrane-stabilizing and .beta.-adrenergic-receptor-blocking effects, markedly decreased the sensitivity of ventricular (0.25 impulses/s mmHg) but not atrial endings. This effect was the result of l-propranolol induced changes in contraction mechanics due to .beta.-adrenergic-receptor blockade. The response of atrial endings to aortic occlusion was not changed following isoproterenol (6 .mu.g bolus). Atrial endings are not influenced by the .beta.-adrenergic-receptor-blocking or membrane-stabilizing effects of d- and l-propranolol, nor are they influenced by .beta.-receptor stimulation, whereas .beta.-adrenergic blockade, but not membrane stabilization, reduced the firing of ventricular endings.