Heart rate autonomic nervous system effects

Carbon dioxide is a rapid, potent stimulus to ventilation. Inhalation of 10% CO can produce minute volumes of 75 L/min in normal individuals. Carbon dioxide acts at multiple sites to stimulate ventilation. Elevated Pco causes bronchodilation, whereas hypocarbia causes constriction of airway smooth muscle these responses may play a role in matching pulmonary ventilation and perfusion. Circulatory effects of CO result from the combination of direct local effects and centrally mediated effects on the autonomic nervous system. The direct effects are diminished contractility of the heart and vascular smooth muscle (vasodilation). The indirect effects result from the capacity of CO to activate the sympathetic nervous system these indirect effects generally oppose the local effects ofCO. Thus, the balance of opposing local and sympathetic effects determines the total circulatory response to CO. The net effect of CO inhalation is an increase in cardiac output, heart rate, and blood pressure. In blood vessels, however, the direct vasodilating actions of carbon dioxide appear more important, and total peripheral resistance decreases when the Pco is increased CO also is a potent coronary vasodilator. Cardiac arrhythmias associated with increased Pco are due to the release of catecholamines. 

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. 

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.

Their efficacy in many illnesses is explained by the competitive binding of )3-adrenore-ceptors in the autonomic nervous system by basically any of the employed drags of the l-aryloxy-3-aminopropanol-2 class, which result in reduction of heart rate and strength of cardiac beats, slowing of atrioventricular conductivity, reduction of the level of renin in the plasma, and reduction of blood pressure. The main effects of 8-adrenoblockers are expressed at the level of the vasomotor center in the hypothalamus, which result in a slowing of the release of sympathetic, tonic impulses. Included in the main group of... 

The autonomic nervous system is divided into the sympathetic and parasympathetic components, which typically exert opposing effects. The sympathetic system is involved in the fight or flight reaction (increased blood pressure and heart rate, and accommodation for increased vision, for example) that prepares the organism for stressful situations. The parasympathetic system conversely establishes a more relaxed situation, for instance, the rest period after a meal. The autonomic nervous system that is responsible for the independent control of the mechanical and secretory functions of the gastrointestinal tract is sometimes called the enteric system. 

Autonomic and hormonal control of cardiovascular function. Note that two feedback loops are present the autonomic nervous system loop and the hormonal loop. The sympathetic nervous system directly influences four major variables peripheral vascular resistance, heart rate, force, and venous tone. It also directly modulates renin production (not shown). The parasympathetic nervous system directly influences heart rate. In addition to its role in stimulating aldosterone secretion, angiotensin II directly increases peripheral vascular resistance and facilitates sympathetic effects (not shown). The net feedback effect of each loop is to compensate for changes in arterial blood pressure. Thus, decreased blood pressure due to blood loss would evoke increased sympathetic outflow and renin release. Conversely, elevated pressure due to the administration of a vasoconstrictor drug would cause reduced sympathetic outflow, reduced renin release, and increased parasympathetic (vagal) outflow. 

Inhaled anesthetics change heart rate either directly by altering the rate of sinus node depolarization or indirectly by shifting the balance of autonomic nervous system activity. Bradycardia can be seen with halothane, probably because of direct vagal stimulation. In contrast, enflurane, and sevoflurane have little effect, and both desflurane and isoflurane increase heart rate. In the case of desflurane, transient sympathetic activation with elevations in catecholamine levels can lead to marked increases in heart rate and blood pressure when high inspired gas concentrations are administered. 

The actions of Salvia divinorum on the physiology of the body have not been studied as of 2002 and are thus unknown. However, other hallucinogenic substances have substantial effects on the autonomic nervous system, the part of the nervous system that governs bodily functions. These effects may include dilation of the pupils, blurred vision, tremors, uncoordination, elevated heart rate, heart palpitations, elevated body temperature, and sweating. 

The other branch of the autonomic nervous system is the parasympathetic branch, which in general balances the actions of the sympathetic branch by exerting opposite effects. Parasympathetic activity reduces heart rate, bkxxl pressure, and so on. In contrast to sympathetic neurons, parasympathetic synapses arc primarily cholinergic. 

Stimulants are classic examples of sympathomimetic drugs that is, they act to stimulate or mimic activity in the sympathetic branch of the autonomic nervous system. Thus, many of their physiological effects arc the same as those seen during emotional arousal heart rate is up, blood pressure is up, respiratory rate is up, and sweating increases meanwhile, blood flow decreases to the internal organs and extremities but increases to the large muscle groups and the brain. Finally, body temperature is elevated and pupils arc dilated. 

Effects of the test substance on the autonomic nervous system should be assessed. For example, binding to receptors relevant for the autonomic nervous system, functional responses to agonists or antagonists in vivo or in vitro, direct stimulation of autonomic nerves and measurement of cardiovascular responses, baroreflex testing, and heart rate variability can be used. 

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. 

Fetotoxicity Cocaine exposure in utero may have a direct effect on autonomic nervous system regulation, cardiac control mechanisms, and cardiovascular functioning in neonates [33 ]. In 21 prenatally cocaine-exposed infants and 23 non-exposed controls, studied within 120 hours of birth, there was a positive interaction between prenatal cocaine exposure and orthostatic stress. Whereas both exposed and non-exposed infants had increased heart rates and heart rate variability, the responses of the exposed... 

Back (Ref 18) discusses proplnt toxicology, including toxicological effects on blood pressure, heart rate, and effects on autonomical central nervous systems caused by N2H4 derivs, penta- decaboranes, F compds. and Be compds... 

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