68 - effects of sympathetic and parasympathetic system on heart and blood vessels

As shown in the following table, activation of sympathetic efferent nerves to the heart increases heart rate (positive chronotropy), contractility (positive ionotrophy), rate of relaxation (increased lusitropy), and conduction velocity (positive dromotropy). Parasympathetic effects are opposite. Parasympathetic effects on inotropy are weak in the ventricle, but relatively strong in the atria. Physiologically, whenever the body activates the sympathetic system, it down regulates parasympathetic activity, and visa versa, so that the activities of these two branches of the autonomic nervous system respond reciprocally.

In blood vessels, sympathetic activation constricts arteries and arterioles (resistance vessels), which increases resistance and decreases distal blood flow. Sympathetic-induced constriction of veins (capacitance vessels) decreases venous compliance and blood volume, and thereby increases venous pressure . Most blood vessels in the body do not have parasympathetic innervation. However, parasympathetic nerves do innervate salivary glands, gastrointestinal glands, and genital erectile tissue where they cause vasodilation.

The overall effect of sympathetic activation is to increase cardiac output, systemic vascular resistance (both arteries and veins), and arterial blood pressure. Enhanced sympathetic activity is particularly important during exercise, emotional stress, and during hemorrhagic shock.

	Sympathetic	Parasympathetic
Heart
Chronotropy (rate)	+ + +	_ _ _
Inotropy (contractility)	+ + +	_ 1
Lusitropy (relaxation)	+ + +	_ 1
Dromotropy (conduction velocity)	+ +	_ _ _
Vessels
Arterial constriction	+ + +	0 2
Venous constriction	+ + +	0

Relative magnitude of responses indicated by number of + or - signs. ¹ More pronounced in atria than ventricles. ² Major vasodilator effects only in specific organs such as genitalia

The actions of autonomic nerves are mediated by the release of neurotransmitters that bind to specific cardiac receptors and vascular receptors . These receptors are coupled to signal transduction pathways which evoke changes in cellular function.

67 - bezold jarisch reflex

The Bezold-Jarisch reflex is an eponym for a triad of responses (apnea, bradycardia, and hypotension) following intravenous injection of veratrum alkaloids in experimental animals. The observation was first reported in 1867 by von Bezold and Hirt, and confirmed in 1938-1940 by Jarisch. The triad depends on intact vagi and is mediated through cranial nervous medullary centers controlling respiration, heart rate, and vasomotor tone. The respiratory effects are mediated through pulmonary vagal afferents and the bradycardia and vasodepression through cardiac vagal afferents. The veratrum alkaloids activate all known receptors in the carotid-aortic and cardiopulmonary areas. The cardiopulmonary receptors (baroreceptors, cough receptors, and parenchymal stretch receptors) also respond to other chemical substances: nicotine, capsaicin, venom, antihistaminics, halogenated anesthetics, diguanides, and serotonin (5-hydroxytryptamine). Derivatives of last-mentioned amine activate Type 1, 2, or 3 receptors and have potential therapeutic use. Since several types of cardiopulmonary receptors participate in the Bezold-Jarisch reflex, it has been difficult to develop a blockade to one type of receptor for therapeutic use (cough, bronchospasm, pulmonary hypertension, or coronary vasospasm). Axon reflexes influence pulmonary blood vessels, bronchial blood vessels, and bronchial smooth muscles. These intrapulmonary reflexes need further study as to how they relate to the Bezold-Jarisch reflex in health and disease. The cardiopulmonary and carotid-aortic reflexes can serve as defense mechanisms against chemical hazards that are likely to be inhaled in the workplace and in the environment.