Parasympathetic nerves, heart rate

Parasympathetic stimulation decreases heart rate. Acetylcholine, the neurotransmitter released from the vagus nerve (the parasympathetic nerve to the heart), binds to muscarinic receptors and causes the following effects ... 

Figure 14.1 Effect of autonomic nervous system stimulation on action potentials of the sinoatrial (SA) node. A normal action potential generated by the SA node under resting conditions is represented by the solid line the positive chronotropic effect (increased heart rate) of norepinephrine released from sympathetic nerve fibers is illustrated by the short dashed line and the negative chronotropic effect (decreased heart rate) of acetylcholine released from parasympathetic nerve fibers is illustrated by the long dashed line.

Perhaps the most prominent and well-studied class of synthetic poisons are so-called cholinesterase inhibitors. Cholinesterases are important enzymes that act on compounds involved in nerve impulse transmission - the neurotransmitters (see the later section on neurotoxicity for more details). A compound called acetylcholine is one such neurotransmitter, and its concentration at certain junctions in the nervous system, and between the nervous system and the muscles, is controlled by the enzyme acetylcholinesterase the enzyme causes its conversion, by hydrolysis, to inactive products. Any chemical that can interact with acetylcholinesterase and inhibit its enzymatic activity can cause the level of acetylcholine at these critical junctions to increase, and lead to excessive neurological stimulation at these cholinergic junctions. Typical early symptoms of cholinergic poisoning are bradycardia (slowing of heart rate), diarrhea, excessive urination, lacrimation, and salivation (all symptoms of an effect on the parasympathetic nervous system). When overstimulation occurs at the so-called neuromuscular junctions the results are tremors and, at sufficiently high doses, paralysis and death. 

Stimulation of the parasympathetic system releases acetylcholine at the neuromuscular junction in the sinoatrial node. The binding of acetylcholine to its receptor inhibits adenylate cyclase activity and hence decreases the cyclic AMP level. This reduces the heart rate and hence reduces cardiac output. This explains why jumping into very cold water can sometimes stop the heart for a short period of time intense stimulation of the vagus nerve (a parasympathetic nerve) markedly increases the level of... 

Although stimulation of parasympathetic cardioinhibitory neurons would tend to lower heart rate, this response is overridden by the simultaneous stimulation of sympathetic cardio-accelerant neurons and the adrenal medulla. Stimulation of sympathetic nerves resulting in release of norepinephrine gives rise to vasoconstriction peripheral resistance rises. 

The injection of a vasoconstrictor, which causes an increase in mean arterial blood pressure, results in activation of the baroreceptors and increased neural input to the cardiovascular centers in the medulla oblongata. The reflex compensation for the drug-induced hypertension includes an increase in parasympathetic nerve activity and a decrease in sympathetic nerve activity. This combined alteration in neural firing reduces cardiac rate and force and the tone of vascular smooth muscle. As a consequence of the altered neural control of both the heart and the blood vessels, the rise in blood pressure induced by the drug is opposed and blunted. 

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. 

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). 

The baroreflex system consists of mechanosensitive receptors in the aorta and carotid sinus that detect changes in blood pressure. The receptors give rise to afferent nerve fibers that relay impulses to the CNS. Within the CNS, the afferent signals are processed and ultimately transmitted to efferent sympathetic and parasympathetic fibers to the vasculature and heart. Increases in blood pressure will increase baro-receptors activity leading to an inhibition of sympathetic impulses to the blood vessels (thereby relaxing them) and to the heart (decreasing heart rate and contractility). In addition, parasympathetic activity to the heart is increased leading to a reduction in heart rate and possibly contractility. 

The prolonged action of acetylcholine at the parasympathetic nerve ending would greatly slow the rate of the heart (bradycardia) and also slow conduction of the cardiac impulse over the atria and the atrioventricular (AV) node. 

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. 

In the peripheral nervous system, norepinephrine is an important neurotransmitter in the sympathetic branch of the autonomic system. Sympathetic nerve transmission operates below the level of consciousness in controlling physiological function of many organs and tissues of the body. The sympathetic system plays a particularly important role in regulating cardiovascular function in response to postural, exertional, thermal, and mental stress. With sympathetic activation, the heart rate is increased, peripheral arterioles are constricted, skeletal arterioles are dilated, and the blood pressure is elevated. In addition, sympathetic nerve stimulation dilates pupils inhibits smooth muscles of the intestines, bronchi, and bladder and closes the sphincters. Sympathetic signals work in balance with the parasympathetic portion of the autonomic nervous system to maintain a stable internal environment. 

Acetylcholine is the transmitter at parasympathetic nerve endings innervating the sinus node (the vagus nerve). When blood pressure increases, the vasomotor center tries to return it to normal by slowing the heart rate. The answer is (A),... 

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. 

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