Smooth muscle, autonomic nervous system activity

On the other hand, a decrease in blood pressure causes less than normal distension or stretch of the aorta and carotid arteries and a decrease in baroreceptor stimulation. Therefore, fewer afferent nerve impulses are transmitted to the vasomotor center. The vasomotor center then alters autonomic nervous system activity so that sympathetic stimulation of vascular smooth muscle and the heart is increased and parasympathetic stimulation of the heart is decreased. As a result, venous return, CO, and TPR increase so that MAP is increased back toward its normal value. The effects are summarized in Figure 15.5. 

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 ... 

The autonomic nervous system (ANS), also known as the visceral or involuntary nervous system, functions below the level of consciousness. Because it innervates cardiac muscle, smooth muscle, and various endocrine and exocrine glands, this nervous system influences the activity of most of the organ systems in the body. Therefore, it is evident that the ANS makes an important contribution to the maintenance of homeostasis. Regulation of blood pressure gastrointestinal responses to food contraction of the urinary bladder focusing of the eyes and thermoregulation are just a few of the many... 

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. 

Action potentials are generated in single-unit smooth muscle. Simultaneous depolarization of 30 to 40 smooth muscle cells is required to generate a propagated action potential the presence of gap junctions allows this to occur readily. Because single-unit smooth muscle is self-excitable and capable of generating action potentials without input from the autonomic nervous system, it is referred to as myogenic. In this muscle, the function of the autonomic nervous system is to modify contractile activity only. Input is not needed to elicit contraction. 

The autonomic nervous system (ANS) modifies contractile activity of both types of smooth muscle. As discussed in Chapter 9, the ANS innervates the smooth muscle layer in a very diffuse manner, so neurotransmitter is released over a wide area of muscle. Typically, the effects of sympathetic and parasympathetic stimulation in a given tissue oppose each other one system enhances contractile activity while the other inhibits it. The specific effects (excitatory or inhibitory) that the two divisions of the ANS have on a given smooth muscle depend upon its location. 

The cardiovascular effects of local anesthetics result in part from direct effects of these drugs on the cardiac and smooth muscle membranes and from indirect effects on the autonomic nervous system. As described in Chapter 14, local anesthetics block cardiac sodium channels and thus depress abnormal cardiac pacemaker activity, excitability, and conduction. At extremely high concentrations, local anesthetics can also block calcium channels. With the notable exception of cocaine, local anesthetics also depress myocardial contractility and produce direct arteriolar dilation, leading to systemic hypotension. Cardiovascular collapse is rare, but has been reported after large doses of bupivacaine and ropivacaine have been inadvertently administered into the intravascular space. 

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. 

Previous studies have shown that accommodation mediated via ciliary smooth muscle activity also receives sympathetic innervation. Sympathetic nerves reach the ciliary muscle through the uveal blood vessels in close association with arteries and terminal arterioles. The distribution of the adrenergic fibers in the ciliary muscle appears to vary across species. In primates sympathetic nerve terminals, mainly 3 receptors, can generally be found in the anterior portion of the ciliary muscle. The accommodative amplitude significantly decreased in human subjects after instillation of phenylephrine (an a agonist) or hydroxyamphetamine (an a and (3 agonist). Such observations provide evidence that both sympathetic and parasympathetic divisions of the autonomic nervous system can affect accommodation but not equally. Furthermore, the nature of sympathetic innervation can be summarized as follows ... 

Smooth muscle is unstriated with innervations from 2 both sympathetic (flight or fight) and parasympathetic (more relaxed) nerves of the autonomic nervous system. E. Smooth muscle appears unstriated under a polarized light microscope, because the myofilaments inside are less or-ganized. Smooth muscle fibers contain actin and myosin myofilaments which are more haphazardly arranged than they are in skeletal muscles. The sympathetic neurotransmitter, Ach, and parasympathetic neurotransmitter, norepinephrine, activate this type of muscle tissue. 

There are three distinct types of muscle tissue in vertebrates striated, smooth, and cardiac. Striated, or skeletal, muscle is attached, at least at one end, to the skeleton via tendons. This muscle type is often referred to as the voluntary muscle, as it can be consciously controlled. Smooth muscle is usually arranged in sheets or layers in tubular systems, such as arteries and veins (see Blood Vessels), the gastrointestinal and respiratory tracts, and the genitourinary tracts. The activities of the smooth muscles are not under conscious control rather they are coordinated by the autonomic (involuntary) nervous system. The cardiac muscle comprises the bulk of the heart wall proper and small amounts are found in the superior vena cava and pulmonary vein. The cardiac muscle is not under conscious control it has an automaticity center which responds to the autonomic nervous system when needed (see section Impulse Conduction). In the heart, cardiac muscle cells are joined in a network of fibers and are connected by gap junctions, which facilitate the conduction of electrical impulses through the cardiac muscle network. In addition to the typical cardiac myocytes, there are other cardiac muscle cells that are specialized to initiate, attenuate, or accelerate the electrical impulses for coordinated contraction of the cardiac network. 

In the peripheral nervous system, norepinephrine is an important neurotransmitter in the sympathetic branch of the autonomic system. Sympathetic nerve transmission operates below the level of consciousness in controlling physiological function of many organs and tissues of the body. The sympathetic system plays a particularly important role in regulating cardiovascular function in response to postural, exertional, thermal, and mental stress. With sympathetic activation, the heart rate is increased, peripheral arterioles are constricted, skeletal arterioles are dilated, and the blood pressure is elevated. In addition, sympathetic nerve stimulation dilates pupils inhibits smooth muscles of the intestines, bronchi, and bladder and closes the sphincters. Sympathetic signals work in balance with the parasympathetic portion of the autonomic nervous system to maintain a stable internal environment. 

The sympathetic nervous system is a subdivision of the autonomic nervous system (or visceral motor system), which provides automatic, involuntary regulation of smooth muscle, cardiac muscle, and glandular activity or secretions. Sympathetic nerve fibers reach the nasal mucosa, and when stimulated, sympathetic nerve terminals release norepineph-... 

Carbon dioxide is a rapid, potent stimulus to ventilation. Inhalation of 10% CO can produce minute volumes of 75 L/min in normal individuals. Carbon dioxide acts at multiple sites to stimulate ventilation. Elevated Pco causes bronchodilation, whereas hypocarbia causes constriction of airway smooth muscle these responses may play a role in matching pulmonary ventilation and perfusion. Circulatory effects of CO result from the combination of direct local effects and centrally mediated effects on the autonomic nervous system. The direct effects are diminished contractility of the heart and vascular smooth muscle (vasodilation). The indirect effects result from the capacity of CO to activate the sympathetic nervous system these indirect effects generally oppose the local effects ofCO. Thus, the balance of opposing local and sympathetic effects determines the total circulatory response to CO. The net effect of CO inhalation is an increase in cardiac output, heart rate, and blood pressure. In blood vessels, however, the direct vasodilating actions of carbon dioxide appear more important, and total peripheral resistance decreases when the Pco is increased CO also is a potent coronary vasodilator. Cardiac arrhythmias associated with increased Pco are due to the release of catecholamines. 

An abnormal, general elevation of sympathetic activity (termed either hyperactivity, hyper-reactivity or overreactivity) as the major cause of Raynaud s phenomenon in vibration-exposed workers has been advocated by Olsen (1990). In a recent paper, however, the same author (Olsen 1991) sees this as only one of several possible mechanisms leading to vibration-induced Raynaud s phenomenon. The active mechanism of digital artery closure mediated by central sympathetic reflexes is seen as predominant, but other active and passive mechanisms - such as abnormal adrenergic receptor activity of the smooth muscle cell or hypertrophy of vascular smooth muscle cells - are also envisaged as possible etiologic factors. An imbalance between the parasympathetic and sympathetic parts of the autonomic nervous system has been suggested to contribute to the development of VWF (Heinonen et al. 1987 Bovenzi 1990 Farkkila et al. 1990). 

---