In the heart and in the blood vessel walls, complex adrenergic-cholinergic interactions occur both prejunctionally, at the level of the autonomic nerve terminals, and postjunctionally, at the level of the responding cells themselves. The principal prejunctional interaction appears to be an inhibition of the release of norepinephrine from adrenergic nerve terminals by the acetylcholine liberated from nearby cholinergic nerve endings. This inhibitory effect is mediated by muscarinic receptors located on the postganglionic sympathetic nerve terminals. The inhibitory effect of acetylcholine on cardiac and vascular tissues are therefore achieved in part by a direct influence of the cholinergic neurotransmitter on the cardiac and vascular muscle cells, and in part by an indirect influence on sympathetic neurotransmission.
We applied trains of stimuli to the vagosympathetic trunks of anesthetized dogs and studied the time courses of the resultant chronotropic and inotropic responses. These responses were maximum soon after the onset of the test stimulus train but then declined over the next 1-5 min despite continued stimulation. The fade ratio was defined as the magnitude of this decline divided by the magnitude of the maximum response. For both inotropic and chronotropic responses, maximum increased with stimulation frequency, but the fade ratio did not change. In some experiments, conditioning stimulus trains of variable duration were applied before a standard rest period, after which the test stimulus train was applied. The longer the conditioning period, the lower was the subsequent fade ratio of the inotropic responses to the test stimulation train. In other experiments, a conditioning train of 2 min was applied, and then variable rest periods were interposed before the test train was applied. The longer the rest period, the greater were the subsequent maximum and fade ratios of the inotropic responses to the test stimulus train. These results indicate that some factor persists well after the cardiac responses to a given stimulus, and this factor affects the next response to an identical vagal stimulation. The chronotropic responses faded about three times faster than the inotropic responses. Thus different mechanisms may account for the fade of the inotropic and chronotropic responses.
The effects of autonomic neural stimulation and changes in atrial pacing frequency on atrioventricular (AV) conduction were determined in anesthetized open-chest dogs. Increases in vagal stimulation frequency and in pacing rate significantly increased the AV interval, whereas increases in sympathetic stimulation frequency reduced the AV interval. Vagal stimulation (1.4 Hz) prolonged the AV interval by 17 ms when the atrial pacing rate was 2 Hz. On the other hand, the same vagal stimulation increased the AV interval by 29 ms when the pacing rate was 2.73 Hz. In addition, sympathetic stimulation (1.2 Hz) reduced the AV interval by 29 ms when the pacing rate was 2 Hz. In contrast, the same sympathetic stimulation reduced the AV interval 54 ms when the pacing rate was 2.73 Hz. However, the increase in vagal stimulation did not significantly alter the positive dromotropic response of the AV node to sympathetic stimulation. Therefore, the response of AV conduction to combined sympathetic and vagal stimulation was essentially the algebraic sum of the responses to the individual stimulations. Furthermore, the level of activity in one autonomic division did not alter appreciably the interaction between the pacing rate and the activity in the other autonomic division; i.e., the interaction between pacing rate, sympathetic stimulation, and vagal stimulation was not significant.
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