Excitation Contraction Coupling in Smooth Muscle
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Smooth muscle is distributed widely throughout the body and more variable in function than other muscle types. Smooth muscle is involved in the contractility of hollow organs such as gastrointestinal tract, bladder, blood vessels or the uterus. They are spindle shaped, with a single nucleus located in the middle of the cell. It has fewer actin and myosin myofilament present than in skeletal muscle. They do not have striated appearance. The distinct difference between a skeletal and smooth muscle occur in excitation contraction coupling; the similarity in both muscles is that calcium plays the starting role in other words initiate the process. Excitation contraction coupling is at term used to describe the physiological process of converting an electrical stimulus to a mechanical response. The general action process is that an action potential arrives to depolarise the cell membrane. This is achieved by mechanism specific to the muscle type, thus this depolarisation results in an increase in calcium; this increase in calcium activates calcium sensitive contractile proteins that then cause cell shortening by use of ATP.
Contracting coupling in smooth muscle refers primarily to the membrane intracellular calcium concentration which is enough to alter the contractile activities. Smooth muscle does not need neural input to function meaning it can function without the aid of the action potential. This is achieved by integrating a number of other stimuli such as humoral or paracrine, metabolic or physical stimuli and these are their examples: humoral (epinephrine, Angliostensin 2, AVP and endothelin) metabolic (example oxygen, carbondioxide, adenosine, potassium ions and hydrogen ions) and physical stimuli, examples are stress receptors and shear stress etc.
Smooth muscle contraction is however caused by stimuli which are neural. All neural input is involuntary (autonomic). During these, the excitation contraction coupling mechanism is as follows: parasympathetic input which uses the neurotransmitter acetylcholine. In smooth muscle, acetylcholine receptors are of the muscarinic receptor type and as such they are classified to be metabotropic, or G- protein or the second messenger coupled. Secondly, sympathetic input which makes use of a different neurotransmitter and its primary one is the nor-epinephrine. As the parasympathetic, all adrenergic receptors are also metabotropic. The consequent effects on the smooth muscle is based on the specific characteristics of the receptor activated which can be both parasympathetic input and sympathetic input be it either inhibitory (relaxing) or excitatory (contractile). The main mechanism responsible for the actual coupling involves variation in the sensitivity of calcium to specific cellular machinery. The smooth muscle cells shorten when the actin and myosin slide over one another during contraction. Some of the required calcium ions to initiate contractions in smooth muscle get into the cell by the means of extracellular fluid and from the sacroplasmic reticulum. The role of calcium ions in smooth muscle differ from that in skeletal muscle cells because there is no troponin molecules associated with actin fibres of the smooth muscle cells. A hormone combines with a hormone receptor and activates a G-protein mechanism or depolarisation of the plasma membrane occurs. An alpha sub unit opens the calcium ions channels in the plasma membrane or depolarisation opens calcium ion channels. Calcium ions diffuse through the calcium ion channels and combine with calmodium. The protein calmodium is binded with calcium ions that enter the cytoplasm. Calmodium molecules with calcium ions bound to them activates the enzyme called myosin kinase and this transfers a phosphate group from ATP to light myosin molecules on the heads of myosin molecules to activate contractile process. When myosin filaments have phosphate bound to them, formation, movement and detachment of cross bridge occurs. Elevated calcium ions in the sacroplasm of the smooth muscle cells result in the activation of myosin molecules and cross bridge formation. Calcium ion level in the sacroplasm of smooth muscle is reduced as calcium ions are actively transported across the plasma membrane inclusive of the plasma membrane of caveolae and into the sacroplasmic reticulum. Relaxation occurs when myosin phosphate removes phosphate from myosin (contraction of smooth muscles continue as long as there is calcium bound to calmodium and the myosin light chain remains phosphorylated) and this occurs in response to lower intercellular levels of calcium ions. The excitation contraction coupling of smooth muscle is significant in some treatments such as hypertension and intestinal spasm (colic). This is achieved by different mechanism; for intestinal spasm (colic), a drug containing atropine is taken to relieve contraction; atropine a muscarinic blocker binds with a receptor which inhibits the activation of phospholipase thus preventing the formation of disoglycerol and for hypertension; hypertension is caused by constriction of blood vessels and this may be relieved by intake of a calcium blocker, the calcium blocker binds with the calcium receptors of the cell thus preventing the calcium influx and increase of intracellular calcium, with low level of intracellular calcium, vasodilatation is now induced.
The contractility of hollow organs, such as blood vessels, the bladder, and gastrointestinal tract is done by the smooth muscle. Contraction coupling in smooth muscle basically is the intracellular events that meditate a change in the intracellular calcium ion concentrations. Smooth muscle contraction depends largely on the increase of the cytoplasmic calcium ion concentration. This change is brought about by the opening of the voltage dependent calcium channels or receptors operated calcium channels in order words allowing influx of calcium into the cell caused by depolarisation. This process of excitation contraction coupling in smooth muscle is a slow and a gradual process and not very quick as it is in excitation coupling in skeletal muscle.
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