Heart parasympathetic innervation

Peripheral mAChRs are known to mediate the well-documented actions of ACh at parasympathetically innervated effector tissues (organs) including heart, endocrine and exocrine glands, and smooth muscle tissues [2, 4]. The most prominent peripheral actions mediated by activation of these receptors are reduced heart rate and cardiac contractility, contraction of... 

The heart is innervated by both sympathetic and parasympathetic neurons however, their distribution in the heart is quite different. Postganglionic noradrenergic fibers from the stellate and inferior cervical ganglia innervate the sinoatrial (S-A) node and myocardial tissues of the atria and ventricles. Activation of the sympathetic outflow to the heart results in an increase in rate (positive chronotropic effect), in force of contraction (positive inotropic effect), conduction tissue (positive dro-motropic effect). 

In a normal resting subject who is receiving no drugs, there is a moderate parasympathetic tone to the heart, and sympathetic activity is relatively low. The ventricular muscle receives little, if any, parasympathetic innervation. As the blood pressure rises in response to norepinephrine, the baroreceptor reflex is activated, parasympathetic impulses (which are inhibitory) to the heart increase in frequency, and what little sympathetic outflow there is may be reduced. Heart rate is slowed so much that the direct effect of norepinephrine to increase the rate is masked and there is a net decrease in rate. Under the conditions described, however, the impact of the reflex on the ventricles is very slight because there is no parasympathetic innervation and the preexisting level of sympathetic activity is already low. A further decrease in sympathetic activity therefore would have little further effect on contractility in this subject. Thus, a decrease in heart rate and an increase in stroke volume will occur, and cardiac output will change very little. 

Except for skeletal muscle, virtually all tissues in the body are innervated in some way by the ANS.9 Table 18-1 summarizes the innervation and effects of the sympathetic and parasympathetic divisions on some of the major organs and tissues in the body. As indicated in Table 18-1, some organs, such as the heart, are innervated by both sympathetic and parasympathetic neurons. Other tissues, however, may only be supplied by the sympathetic division. The peripheral arterioles, for instance, are innervated by the sympathetic division but receive no parasympathetic innervation. 

The heart responds constantly to hormonal and nervous system signals. Sympathetic nervous system terminals releasing norepinephrine are found in cardiac cells of the atria and ventricles. This allows for reflex regulation of heart muscle contractility. Sympathetic innervation is also present to the SA node and AV junction, where norepinephrine release acts to increase heart rate (enhanced phase 4 depolarization) and also to increase conduction velocity by reducing the AV junction impedance to conduction. Parasympathetic innervation is provided by cranial nerve 10, the vagus nerve, to the SA node and the AV junction. These fibers release acetylcholine, which slows SA node activity (decreasing the rate of phase 4 depolarization) and decreases conduction throughout the AV junction. 

ACh (used as a drug) decreases blood pressure and heart rate, but the latter effect is overcome and reversed by a sympathetic reflex. Because Drug X abolishes only the reflex tachycardia, it must be the ganglion blocker, hexametho-nium (choice A). Remember, AChE inhibitors do not vasodilate because there is no parasympathetic innervation of the vasculature ... 

The heart is innervated by both sympathetic and parasympathetic nerve fibers of the autonomic nervous system. Although the heart can generate its own heartbeat independently of nervous control, stress, exercise, and physical trauma make it advantageous to adjust cardiac contraction to meet the needs at the time. Thus, the cardiovascular control system (Figure 6.20.5), which is located in the brain, controls the contractility of the myocardium (the muscle of the heart), and produces both inotrophic (force of contraction) and chronotrophic (rate of contraction) effects. 

The autonomic nervous system guides the electrical and mechanical functions of the heart. The heart is innervated by both the sympathehc and parasympathetic systems, which have opposite effects and are activated reciprocally. They play important roles in arrhythmia susceptibility. Sympathetic shmulation originates from the intermediolateral column of the thoracic spinal cord. Its neurotransmitter, norepinephrine, is released from neurons of postganglionic fibers of stellate ganglia and epinephrine is released from the adrenal medulla. Both of these act on cardiac p-adrenergic receptors. Sympathetic nerves are predominantly on... 

The mechanism of these blood pressure and other cardiovascular effects has been the subject for much study. Reduction in blood pressure in anesthesized dogs caused by administration of 2.5 mg/kg i.v. of A -THC is accompanied by a decrease in cardiac output and an increase in local vascular resistance. The fractional blood flow to the vital coronary, cerebral and renal beds was unchanged The reduction in cardiac output appears to result from the action of A -THC on the heart rate (bradycardia) as well as venous return. A maximal degree of bradycardia is produced only when both sympathetic and parasympathetic innervation of the heart is intact. A -THC appears to be devoid of any ganglionic or 8-... 

Dmgs that mimic or inhibit the actions of neurotransmitters released from parasympathetic or sympathetic nerves innervating the heart may also be used to treat supraventricular bradyarrhythmias, heart block, and supraventricular tachyarrhythmias. Those used in the treatment of arrhythmias may be found in Table 1. 

Because cardiac muscle is myogenic, nervous stimulation is not necessary to elicit the heart beat. However, the heart rate is modulated by input from the autonomic nervous system. The sympathetic and parasympathetic systems innervate the SA node. Sympathetic stimulation causes an increase in heart rate or an increased number of beats/min. Norepinephrine, which stimulates ( -adrenergic receptors, increases the rate of pacemaker depolarization by increasing the permeability to Na+ and Ca++ ions. If the heart beat is generated more rapidly, then the result is more beats per minute. 

The autonomic nervous system exerts the primary control on heart rate. Because the sympathetic and parasympathetic systems have antagonistic effects on the heart, heart rate at any given moment results from the balance or sum of their inputs. The SA node, which is the pacemaker of the heart that determines the rate of spontaneous depolarization, and the AV node are innervated by the sympathetic and parasympathetic systems. The specialized ventricular conduction pathway and ventricular muscle are innervated by the sympathetic system only. 

The effects of the autonomic nervous system on MAP are summarized in Figure 15.4. The parasympathetic system innervates the SA node and the AV node of the heart. The major cardiovascular effect of parasympathetic stimulation, by way of the vagus nerves, is to decrease HR, which decreases CO and MAP. 

Figure 15.5 Effects of sympathetic and parasympathetic nervous activity on mean arterial pressure. The parasympathetic nervous system innervates the heart and therefore influences heart rate and cardiac output. The sympathetic nervous system innervates the heart and veins and thus influences cardiac output. This system also innervates the arterioles and therefore influences total peripheral resistance. The resulting changes in cardiac output and total peripheral resistance regulate mean arterial pressure.

Acetylcholine is the primary neurotransmitter in the parasympathetic division of the autonomic nervous system, which mainly innervates the gastrointestinal tract, eyes, heart, respiratory tract, and secretory glands. Although its receptors are crucial for maintaining all normal functions of the body, an extremely small number of illnesses can be explained by the dysfunction of cholinergic regions of the peripheral autonomic system. 

Many neurons of both divisions of the autonomic nervous system are tonicaUy active that is, they are continually carrying some impulse traffic. The moment-to-moment activity of an organ such as the heart, which receives a dual innervation by sympathetic (noradrenergic) and parasympathetic (cholinergic) neurons, is controlled by the level of tonic activity of the two systems. 

The cholinesterase inhibitors can increase activity in both sympathetic and parasympathetic ganglia supplying the heart and at the acetylcholine receptors on neuroeffector cells (cardiac and vascular smooth muscles) that receive cholinergic innervation. 

If an organ is innervated by both the sympathetic and parasympathetic divisions, a physiologic antagonism typically exists between these divisions. That is, if both divisions innervate the tissue, one division usually increases function, whereas the other decreases activity. For instance, the sympathetics increase heart rate and stimulate cardiac output, whereas the parasympathetics cause bradycardia. However, it is incorrect to state that the sympathetics are always excitatory in nature and that the parasympathetics are always inhibitory. In tissues such as the gastrointestinal tract, the parasympathetics tend to increase intestinal motility and secretion, whereas the sympathetics slow down intestinal motility. The effect of each division on any tissue must be considered according to the particular organ or gland. 

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). 

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