Sympathetic nerve discharge

When stimulated electrically, the sympathetic nerve discharges the contents of part of its vesicles, including norepinephrine, into the extracellular space. Liberated norepinephrine reacts with adrenoceptors located postjunctionally on the membrane of effector cells or prejunctionally on the membrane of varicosities. Activation of pre-syn-aptic a2-receptors inhibits norepinephrine release. Through this negative feedback, release can be regulated. 

Z. S. Huang, G. L. Gebber, S. Zhong, and S. Barman, Forced oscillations in sympathetic nerve discharge. Am. J. Physiol. 263 R564-571 (1992). 

Sympathetic nerves going to the arterioles are tonically active. In other words, these nerves discharge continuously, causing vasomotor tone. As a result, under resting conditions, arterioles are partially constricted. This vasomotor tone is important because it helps to maintain MAP in the range... 

The rate of pacemaker discharge within these specialized myocytes is influenced by the activity of both divisions of the autonomic nervous system. Increased sympathetic nerve activity to the heart, the release of catecholamines from the adrenal medulla, or the exogenous administration of adrenomimetic amines will cause an increase in the rate of pacemaker activity through stimulation of -adrenoceptors on the pacemaker cells (Figure 16.3). 

The antihypertensive activity of clonidine can be ascribed solely to a decrease in the sympathetic activity transmitted from the brain to the peripheral vasculature. After clonidine administration, direct measurements of sympathetic nerve activity show that electrical discharge is reduced in a number of sympathetic nerves, including the cardiac, splanchnic, and cervical nerves. 

Some compensatory responses that occur during congestive heart failure. In addition to the effects shown, sympathetic discharge facilitates renin release, and angiotensin II increases norepinephrine release by sympathetic nerve endings (dashed arrows). 

The sinoatrial (SA) node is innervated by both the sympathetic (beta and parasympathetic (vagus) nervous systems. Sympathetic activation increases the discharge rate of the SA pacemaker cells, and thereby increases heart rate (a positive chronotropic effect). Sympathetic nerves also innervate adrenergic receptors (betaj) on cardiac ventricular cells leading to an increase in stroke volume (a positive inotropic effect). Vagal activation, on the other hand, has the opposite effect and decreases heart rate and conduction velocity. In normal adults, cardiac vagal innervation is functionally predominant, so abolition of vagal activity results in a pronounced tachycardia (increased heart rate). 

In general, the cardiovascular responses to nicotine are due to stimulation of sympathetic ganglia and the adrenal medulla, together with the discharge of catecholamines from sympathetic nerve endings. Also contributing to the sympathomimetic response to nicotine is the activation of chemoreceptors of the aortic and carotid bodies, which reflexly results in vasoconstriction, tachycardia, and elevated blood pressure. 

At the same time it promotes a discharge of epinephrine from the adrenal medulla, as well as discharge of catecholamines from sympathetic nerve endings, resulting in activation of spinal cord and brain descending inhibitory pain pathways. 

The direct slowing of sinoatrial rate and atrioventricular conduction that is produced by muscarinic agonists is often opposed by reflex sympathetic discharge, elicited by the decrease in blood pressure (see Figure 6-7). The resultant sympathetic-parasympathetic interaction is complex because muscarinic modulation of sympathetic influences occurs by inhibition of norepinephrine release and by postjunctional cellular effects. Muscarinic receptors that are present on postganglionic parasympathetic nerve terminals allow neurally released acetylcholine to inhibit its own secretion. The neuronal muscarinic receptors need not be the same subtype as found on effector cells. Therefore, the net effect on heart rate depends on local concentrations of the agonist in the heart and in the vessels and on the level of reflex responsiveness. 

E) A condition that reduces the sensitivity of the sensory baroreceptor nerve endings might cause an increase in sympathetic discharge... 

Sympathetic discharge causes constriction of the renal resistance vessels and a fall in renal blood flow. This is the typical response in severe exercise or hypotension. The answer is (C). Each of these agents has a different mechanism of action, yet all but one act on the sympathetic postganglionic nerve terminal (site 5). Site 3 is a cholinergic nerve ending. The answer is (A). 

Electrical stimulation of the afferent carotid sinus nerve mimicing baroreceptor activation, results in vagal bradycardia and peripheral vasodilation by inhibition of sympathetic discharge. When carotid sinus nerve stimulation is employed in a preparation with the ventricles paced at a constant rate reflex parasympathetic coronary vasodilation is observed in anesthetized (Hackett et ai, 1972 Religa et al., 1972) and unanesthetized preparations (Vatner et al., 1970). However, it is difficult to equate a given nerve stimulation frequency with the carotid sinus pressure that physiologically activates baroreceptors. 

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