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. In Chapter 17, 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 interstitial 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.
Effects of Hormones on Smooth Muscle Contraction. Most circulating 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, serotonin, 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 membrane contains inhibitory receptors for the hormone rather than excitatory receptors.
Mechanisms of Smooth Muscle Excitation or Inhibition by Hormones or Local Tissue Factors. Some hormone receptors in 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, depolarization occurs without action potentials, and this depolarization 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 calcium channels to prevent entry of these positive ions; inhibition also occurs if the normally closed potassium channels are opened, allowing positive potassium ions to 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 of the receptors that protrude to the interior of the cells are coupled to these enzymes, causing the formation of cyclic adenosine monophosphate (cAMP) or cyclic guanosine monophosphate (cGMP), so-called second messengers. The cAMP or cGMP has many effects, one of 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.
Source of Calcium Ions That Cause Contraction (1) Through the Cell Membrane and (2) from the Sarcoplasmic Reticulum
Although the contractile process in smooth muscle, as in skeletal muscle, is activated by calcium ions, the source of the calcium ions differs; the difference is that the sarcoplasmic reticulum, which provides virtually all the calcium ions for skeletal muscle contraction, is only slightly developed in most smooth muscle. Instead, almost all the calcium ions that cause contraction enter the muscle cell from the extracellular fluid at the time of the action potential or other stimulus. That is, the concentration of calcium ions in the extracellular fluid is greater than 10-3 molar, in comparison with less than 10-7 molar inside the smooth muscle cell; this causes rapid diffusion of the calcium ions into the cell from the extracellular fluid when the calcium pores open. The time required for this diffusion to occur averages 200 to 300 milliseconds and is called the latent period before contraction begins. This latent period is about 50 times as great for smooth muscle as for skeletal muscle contraction.
Role of the Smooth Muscle Sarcoplasmic Reticulum. Figure 8-5 shows a few slightly developed sarcoplasmic tubules that lie near the cell membrane in some larger smooth muscle cells. Small invaginations of the cell membrane, called caveolae, abut the surfaces of these tubules. The caveolae suggest a rudimentary analog of the transverse tubule system of skeletal muscle. When an action potential is transmitted into the caveolae, this is believed to excite calcium ion release from the abutting sarcoplasmic tubules in the same way that action potentials in skeletal muscle transverse tubules cause release of calcium ions from the skeletal muscle longitudinal sarcoplasmic tubules. In general, the more extensive the sarcoplasmic re-ticulum in the smooth muscle fiber, the more rapidly it contracts.
Effect on Smooth Muscle Contraction Caused by Changing of Extracellular Calcium Ion Concentration. Although changing the extracellular fluid calcium ion concentration from normal has little effect on the force of contraction of skeletal muscle, this is not true for most smooth muscle. When the extracellular fluid calcium ion concentration falls to about 1/3 to 1/10 normal, smooth muscle contraction usually ceases. Therefore, the force of contraction of smooth muscle usually is highly dependent on extracellular fluid calcium ion concentration.
A Calcium Pump Is Required to Cause Smooth Muscle Relaxation. To cause relaxation of smooth muscle after it has contracted, the calcium ions must be removed from the intracellular fluids. This removal is achieved by a calcium pump that pumps calcium ions out
Sarcoplasmic tubules in a large smooth muscle fiber showing their relation to invaginations in the cell membrane called caveolae.
of the smooth muscle fiber back into the extracellular fluid, or into a sarcoplasmic reticulum, if it is present. This pump is slow-acting in comparison with the fast-acting sarcoplasmic reticulum pump in skeletal muscle. Therefore, a single smooth muscle contraction often lasts for seconds rather than hun-dredths to tenths of a second, as occurs for skeletal muscle.
Also see references for Chapters 5 and 6.
Blaustein MP, Lederer WJ: Sodium/calcium exchange: its physiological implications. Physiol Rev 79:763,1999.
Davis MJ, Hill MA: Signaling mechanisms underlying the vascular myogenic response. Physiol Rev 79:387, 1999.
Harnett KM, Biancani P: Calcium-dependent and calcium-independent contractions in smooth muscles. Am J Med 115(Suppl 3A):24S, 2003.
Horowitz A, Menice CB, Laporte R, Morgan KG: Mechanisms of smooth muscle contraction. Physiol Rev 76:967, 1996.
Kamm KE, Stull JT: Regulation of smooth muscle contractile elements by second messengers. Annu Rev Physiol 51:299, 1989.
Kuriyama H, Kitamura K, Itoh T, Inoue R: Physiological features of visceral smooth muscle cells, with special reference to receptors and ion channels. Physiol Rev 78:811, 1998.
Lee CH, Poburko D, Kuo KH, et al: Ca2+ oscillations, gradients, and homeostasis in vascular smooth muscle. Am J Physiol Heart Circ Physiol 282:H1571, 2002.
Rybalkin SD, Yan C, Bornfeldt KE, Beavo JA: Cyclic GMP phosphodiesterases and regulation of smooth muscle function. Circ Res 93:280, 2003.
Somlyo AP, Somlyo AV: Ca2+ sensitivity of smooth muscle and nonmuscle myosin II: modulated by G proteins, kinases, and myosin phosphatase. Physiol Rev 83:1325, 2003.
Stephens NL: Airway smooth muscle. Lung 179:333, 2001.
Walker JS, Wingard CJ, Murphy RA: Energetics of cross-bridge phosphorylation and contraction in vascular smooth muscle. Hypertension 23:1106,1994. Webb RC: Smooth muscle contraction and relaxation. Adv Physiol Educ 27:201, 2003.
Was this article helpful?