Neural Activation of the 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 inotropy), 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. When the body activates the sympathetic system, it generally 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 vascular resistance and decreases distal blood flow. When this occurs throught the body, the increased vascular resistance causes arterial pressure to increase. 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.
|Chronotropy (rate)||+ + +||− − −|
|Inotropy (contractility)||+ + +||− 1|
|Lusitropy (relaxation)||+ + +||− 1|
|Dromotropy (conduction velocity)||+ +||− − −|
|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 that evoke changes in cellular function.