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Chapter: Medical Physiology: Contraction and Excitation of Smooth Muscle

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Effect of Local Tissue Factors and Hormones to Cause Smooth Muscle Contraction Without Action Potentials

Probably half of all smooth muscle contraction is initiated by stimulatory factors acting directly on the smooth muscle contractile machinery and without action potentials.

Effect of Local Tissue Factors and Hormones to Cause Smooth Muscle Contraction Without Action Potentials

Probably half of all smooth muscle contraction is initiated by stimulatory factors acting directly on the smooth muscle contractile machinery and without action potentials. Two types of non-nervous and non–action potential stimulating factors often involved are (1) local tissue chemical factors and (2) various hormones.

Smooth Muscle Contraction in Response to Local Tissue Chemical Factors. We discuss control of contraction of the arterioles, meta-arterioles, and pre-capillary sphincters. The smallest of these vessels have little or no nervous supply. Yet the smooth muscle is highly contractile, responding rapidly to changes in local chemical conditions in the surrounding intersti-tial fluid.

In the normal resting state, many of these small blood vessels remain contracted. But when extra blood flow to the tissue is needed, multiple factors can relax the vessel wall, thus allowing for increased flow. In this way, a powerful local feedback control system controls the blood flow to the local tissue area. Some of the specific control factors are as follows:

1.     Lack of oxygen in the local tissues causes smooth muscle relaxation and, therefore, vasodilatation.

 

2.     Excess carbon dioxide causes vasodilatation.

 

3.     Increased hydrogen ion concentration causes vasodilatation.

Adenosine, lactic acid, increased potassium ions, diminished calcium ion concentration, and increased body temperature can all cause local vasodilatation.

Effects of Hormones on Smooth Muscle Contraction. Mostcirculating hormones in the blood affect smooth muscle contraction to some degree, and some have profound effects. Among the more important of these are norepinephrine, epinephrine, acetylcholine,angiotensin, endothelin, vasopressin, oxytocin, sero-tonin, and histamine.

A hormone causes contraction of a smooth muscle when the muscle cell membrane contains hormone-gated excitatory receptors for the respective hormone.Conversely, the hormone causes inhibition if the mem-brane contains inhibitory receptors for the hormone rather than excitatory receptors.

Mechanisms of Smooth Muscle Excitation or Inhibition by Hor-mones or Local Tissue Factors. Some hormone receptorsin the smooth muscle membrane open sodium or calcium ion channels and depolarize the membrane, the same as after nerve stimulation. Sometimes action potentials result, or action potentials that are already occurring may be enhanced. In other cases, depolari-zation occurs without action potentials, and this depo-larization allows calcium ion entry into the cell, which promotes the contraction.

Inhibition, in contrast, occurs when the hormone (or other tissue factor) closes the sodium and calciumchannels to prevent entry of these positive ions; inhi-bition also occurs if the normally closed potassiumchannels are opened, allowing positive potassium ionsto diffuse out of the cell. Both of these actions increase the degree of negativity inside the muscle cell, a state called hyperpolarization, which strongly inhibits muscle contraction.

Sometimes smooth muscle contraction or inhibition is initiated by hormones without directly causing any change in the membrane potential. In these instances, the hormone may activate a membrane receptor that does not open any ion channels but instead causes an internal change in the muscle fiber, such as release of calcium ions from the intracellular sarcoplasmic re-ticulum; the calcium then induces contraction. To inhibit contraction, other receptor mechanisms are known to activate the enzyme adenylate cyclase or guanylate cyclase in the cell membrane; the portions ofthe receptors that protrude to the interior of the cells are coupled to these enzymes, causing the formation of cyclic adenosine monophosphate (cAMP) or cyclicguanosine monophosphate (cGMP), so-called second messengers. The cAMP or cGMP has many effects, oneof which is to change the degree of phosphorylation of several enzymes that indirectly inhibit contraction. The pump that moves calcium ions from the sar-coplasm into the sarcoplasmic reticulum is activated, as well as the cell membrane pump that moves calcium ions out of the cell itself; these effects reduce the calcium ion concentration in the sarcoplasm, thereby inhibiting contraction.

Smooth muscles have considerable diversity in how they initiate contraction or relaxation in response to different hormones, neurotransmitters, and other substances. In some instances, the same substance may cause either relaxation or contraction of smooth muscles in different locations. For example, norepi-nephrine inhibits contraction of smooth muscle in the intestine but stimulates contraction of smooth muscle in blood vessels.


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