Blood vessel innervation

In sympathetically innervated tissues, such as vas deferens or blood vessels, ATP produces fast responses mediated by P2X receptors followed by a slower component mediated by G protein-coupled a-adrenoceptors (Fig. 2) NPY usually acts as a pre-or postjunctional modulator of the release and/or action of NA and ATP. Similarly, for parasympathetic nerves supplying the urinary bladder, ATP provokes a fast, short-lasting twitch response via P2X receptors, whereas the slower component is mediated by G... 

Although skeletal muscle comprises the bulk of muscle tissue in the body, smooth muscle is far more important in terms of homeostasis. Most smooth muscle is found in the walls of tubes and hollow organs. Contraction and relaxation of the smooth muscle in these tissues regulates the movement of substances within them. For example, contraction of the smooth muscle in the wall of a blood vessel narrows the diameter of the vessel and leads to a decrease in the flow of blood through it. Contraction of the smooth muscle in the wall of the stomach exerts pressure on its contents and pushes these substances forward into the small intestine. Smooth muscle functions at a subconscious level and is involuntary. It is innervated by the autonomic nervous system, which regulates its activity. 

Multiunit smooth muscle is located in the large blood vessels, eyes (iris and ciliary muscle of the lens), and piloerector muscles at the base of hair follicles. This type of muscle consists of discrete smooth muscle cells or units that function independently. Each of these units is innervated by the... 

The sympathetic system also innervates vascular smooth muscle and regulates the radius of the blood vessels. All types of blood vessels except capillaries are innervated however, the most densely innervated vessels include arterioles and veins. An increase in sympathetic stimulation of vascular smooth muscle causes vasoconstriction and a decrease in stimulation causes vasodilation. Constriction of arterioles causes an increase in TPR and therefore MAP. Constriction of veins causes an increase in venous return (VR) which increases end-diastolic volume (EDV), SV (Frank-Starling law of the heart), CO, and MAP. 

Sympathetic nerves are distributed to most vascular beds. They are most abundant in the renal, gastrointestinal, splenic, and cutaneous circulations. Recall that these tissues receive an abundant blood flow, more than is necessary simply to maintain metabolism. Therefore, when blood is needed by other parts of the body, such as working skeletal muscles, sympathetic vasoconstrictor activity reduces flow to the tissues receiving excess blood so that it may be redirected to the muscles. Interestingly, there is no sympathetic innervation to cerebral blood vessels. In fact, these vessels do not have a.j-adrenergic receptors, so they cannot be affected by circulating catecholamines. No physiological circumstance exists in which blood should be directed away from the brain. 

The effect of sympathetic stimulation on venous resistance is minimal. As previously stated, it is the larger, less flexible veins that provide resistance to blood flow. However, these blood vessels are sparsely innervated therefore, little change takes place in vessel radius and physiological effect on blood flow is relatively insignificant. 

Adrenoceptors of the /3-subtype are important mediators of the sympathetic activation of the heart, kidney, and bronchi. /3-Adrenoceptors are also found in other organs and tissues such as blood vessels and the central nervous system. Accordingly, /3-adrenoceptor antagonists or jS-blockers inhibit the stimulating influence of the endogenous catecholamines (noradrenaline, adrenaline) on the various organs and tissues which are subject to sympathetic innervation. In cardiovascular medicine the /3-blockers are used in particular to blunt the sympathetic activation of the heart and kidneys. These effects are mediated by the /3i-subtype of the /3-adrenoceptors. The currently used /3-blockers are all competitive antagonists of the /3i-adrenoceptor, which is the basis of their therapeutic application. 

In any blood vessel, the final integrated response to either neuronally released norepinephrine or to circulating epinephrine probably depends on the relative participation of at least four populations of a-adreno-ceptors postjunctional i- and az-adrenoceptors mediate constriction of vascular smooth muscle, while prejunctional and endothelial az-adrenoceptors mediate vasodilation. An understanding of the vessel vascular response to adrenomimetic drugs also must include the effects of drugs on adventitial innervation, smooth muscle, and other vascular factors that may be present. 

Burnstock G and Griffith SG. Nonadrenergic Innervation of Blood Vessels. Boca Raton, FL CRC, 1988. 

External urethral sphincter muscle probably has cholinergic and adrenergic autonomic innervation as well as cholinergic striated muscle innervation (Elbadawi and Schenk, 1974). This rhabdosphincter is unique when compared to other striated muscle in that it has a higher density of neural end-plates as well as blood vessel-independent neural plexuses. Efferent rhabdosphincter innervation is probably via the pudendal nerve while the lissosphincter efferents probably emanate from the pelvic plexus (Elbadawi and Schenk, 1974). 

The endothelium of most blood vessels releases EDRF (endothelium-derived relaxing factor), which causes marked vasodilation, in response to muscarinic stimuli. However, unlike the receptors innervated by sympathetic cholinergic fibers in skeletal muscle blood vessels, these muscarinic receptors are not innervated and respond only to circulating muscarinic agonists. 

Most blood vessels receive no direct innervation from the parasympathetic system. However, parasympathetic nerve stimulation dilates coronary arteries, and sympathetic cholinergic nerves cause vasodilation in the skeletal muscle vascular bed (see Chapter 6). Atropine can block this vasodilation. Furthermore, almost all vessels contain endothelial muscarinic receptors that mediate vasodilation (see Chapter 7). These receptors are readily blocked by antimuscarinic drugs. At toxic doses, and in some individuals at normal doses, antimuscarinic agents cause cutaneous vasodilation, especially in the upper portion of the body. The mechanism is unknown. 

Most blood vessels, the sweat glands, and the spleen are innervated only by one division of the autonomic nervous system. In the salivary glands, the two divisions of the autonomic nervous system supplement one another. In the bladder, bronchi, gastrointestinal tract, heart, pupil, and sex organs, the two divisions of the autonomic nervous system have opposing effects (see Figure 14.5). 

VIP is widely distributed in the central and peripheral nervous systems where it functions as a neurotransmitter or neuromodulator. It is also present in several organs including the gastrointestinal tract, heart, lungs, kidneys, and thyroid gland. Many blood vessels are innervated by VIP neurons. VIP is present in the circulation but does not appear to function as a hormone. 

In contrast, the content of norepinephrine is substantially lower than the content of dopamine (28). Catecholamine-containing neurons do not innervate the parenchymal cells of the bovine parathyroid gland only an occasional norepinephrine-containing neuron terminating upon a blood vessel is demonstrated by fluorescence histochemistry (22). 

A low level of tonic activity of the sympathetic nerves to vascular smooth muscle adrenergic receptors exists so that withdrawal of sympathetic vasomotor tone results in vasodilatation and reduced pressure. Conversely, enhancement of sympathetic vasomotor tone augments the level of vasoconstriction leading to elevated pressure. While the parasympathetic branch of the autonomic nervous system innervates some blood vessels, it does not generally play a role in regulating peripheral resistance. 

Decrease in blood pressure Injection of acetylcholine causes vasodilation and the lowering of blood pressure. Although no innervation of the vasculature by the parasympathetic system exists, there are cholinergic receptors on the blood vessels that respond by causing vasodilation. The vasodilation is due to an acetylcholine-induced rise in intracellular Ca++—caused by the phosphatidylinositol system—that results in the formation of nitric oxide (NO) from arginine in endothelial cells.2 [Note NO is also known as endothelium-derived relaxing factor (EDRF).] (See p. 176 for more detail on nitric oxide.) In the absence of adminis-... 

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