Smooth muscle neural control

Smooth muscle cell activity is in general under neural control. Thus, the many transmitters of the autonomic nervous system are paired with receptors on the smooth muscle cell membrane. One of the current questions about smooth muscle function is What intracellular processes are the different transmitters modulating in the smooth muscle cells, in addition to their effects on the contractile state ... 

FIG. 5. Ca2+ sparks drive electrical activity in myocytes. In contrast to the traditional concept of electrical activity deriving from descending neural control via postsynaptic responses, spontaneous Ca2+ release results in electrical activity in smooth muscle. The figure shows a Ca2+ spark activating sarcolemmal Ca2+-activated Cl- channels and spontaneous transient inward currents (STICs) (current trace above). Whether Ca2+ sparks activate outward STOCs (Ca2+-activated K+ currents) or STICs will depend on the proportion of channels expressed and the resting potential of the myocyte. 

Anatomically, the nervous system is divided into the central nervous system (CNS) consisting of the brain and the spinal cord and the peripheral nervous system comprised of neural cells forming a network throughout the body. The peripheral system is itself subdivided into two sections the somatic system, where control of skeletal muscles allows movement and breathing, and the autonomic system which controls the actions of smooth muscle, cardiac muscle and glandular tissues. Further subdivision of the autonomic system based on anatomical and biochemical factors creates the sympathetic and parasympathetic nervous systems. 

The primary neural control of total peripheral resistance is through sympathetic nerves. The diameter of blood vessels is controlled by the tonic activity of noradrenergic neurons. There is a continuous outflow of noradrenergic impulses to the vascular smooth muscle, and therefore some degree of constant vascular constriction is maintained. An increase in impulse outflow causes further contraction of the smooth muscle, resulting in greater vasoconstriction. A decrease in impulse outflow permits the smooth muscle to relax, leading to vasodilation. 

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. 

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