The medulla, located in the brainstem above the spinal cord, receives sensory input from different systemic and central receptors (e.g., baroreceptors and chemoreceptors) as well as signals from other brain regions (e.g., hypothalamus). Autonomic outflow from the brainstem is divided principally into sympathetic and parasympathetic (vagal) branches. Efferent fibers of these autonomic nerves travel to the heart and blood vessels where they modulate the activity of these target organs.
The heart is innervated by vagal and sympathetic fibers. The right vagus nerve primarily innervates the SA node, whereas the left vagus innervates the AV node; however, there can be significant overlap in the anatomical distribution. Atrial muscle is also innervated by vagal efferents, whereas the ventricular myocardium is only sparsely innervated by vagal efferents. Sympathetic efferent nerves are present throughout the atria (especially in the SA node) and ventricles, including the conduction system of the heart.
Cardiac function is altered by neural activation. Sympathetic stimulation increases heart rate (positive chronotropy), inotropy and conduction velocity (positive dromotropy), whereas parasympathetic stimulation of the heart has opposite effects.Sympathetic and parasympathetic effects on heart function are mediated by beta-adrenoceptors and muscarinic receptors, respectively.
Sympathetic adrenergic nerves travel along arteries and nerves and are found in the adventitia (outer wall of a blood vessel). Varicosities, which are small enlargements along the nerve fibers, are the site of neurotransmitter release. Capillaries receive no innervation. Activation of vascular sympathetic nerves causes vasoconstriction of arteries and veins mediated by alpha-adrenoceptors.
Parasympathetic fibers are found associated with blood vessels in certain organs such as salivary glands, gastrointestinal glands, and in genital erectile tissue. The release of acetylcholine (ACh) from these parasympathetic nerves has a direct vasodilatory action (coupled to nitric oxide formation and guanylyl cyclase activation). ACh release can stimulate the release of kallikrein from glandular tissue that acts upon kininogen to form kinins (e.g., bradykinin). Kinins cause increased capillary permeability and venous constriction, along with arterial vasodilation in specific organs.
