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Lec 8 Physiology Dr Hanan Luay Smooth muscles Objectives 1-Describe the structural morphology of the smooth muscles and their types? 2-Explain the bases of contraction of smooth muscles? 3-list the factors affecting the smooth muscle contraction? 4- How does changing the length of smooth muscle affect its tension? Morphology: 1- Lack visible cross striations. 2- Actin and myosin are present. 3- There are dense bodies instead of Z lines. 4- Contain tropomyosin but toponin absent. 5- Poorly developed sarcoplasmic reticulum (so Ca2 released from this organelle may account for only the initial phase of smooth muscle contraction) 6- Few mitochondria so depend on glycolysis in their metabolism. Types: 1- Visceral smooth muscle (unitary or single unit). 2- Multi-unit smooth muscle. Unitary or visceral smooth muscles (or syncytial smooth muscles): It occurs in large sheets, has low-resistance bridges between individual muscle cells, and functions in a syncytial fashion, they contract together as a single unit. It is found primarily in the walls of hollow viscera. The cell membranes are joined by gap junctions through whom ions can flow freely from one muscle cell to another. Multi-unit smooth muscle: It is made up of individual units without interconnecting bridges. It is found in structures such as the iris of the eye, in which fine, graded contractions occur. It is not under voluntary control. 1 Electrical & Mechanical Activity: Visceral smooth muscle: It is characterized by the instability of its membrane potential and by the fact that it shows continuous, irregular contractions that are independent of its nerve supply. This maintained state of partial contraction is called tonus or tone. There is no true "resting" value for the membrane potential, but it averages about -50 mV, when the muscle active it becomes low and high during inhibition. Superimposed on the membrane potential are waves of various types: These are: -Slow sine wave-like. -Sharp spikes. -Pacemaker potentials. Thus, In addition to being graded, the excitation-contraction coupling in visceral smooth muscle is a very slow process compared with that in skeletal and cardiac muscle, in which the time from initial depolarization to initiation of contraction is less than 10 ms. The slowness of contraction is related to the fact that myosin ATPase in smooth muscle is slower in its action (splitting ATP for the cross-bridge cycle) than it is in striated muscle. 2 Molecular Basis of Contraction; 1-Binding of Ach to Muscarinic reseptors. 2-Ca2+ influx from the ECF via Ca2+ channels (the greater the depolarization, the more Ca2 will enter the cell and the stronger will be the smooth muscle contraction). 3-Ca2+ binds to calmodulin, and the resulting complex activates calmodulindependent myosin light chain kinase. This enzyme catalyzes the phosphorylation of the myosin light chain. 4-The phosphorylation allows the myosin ATPase to be activated, and actin slides on myosin, producing contraction. 5-Myosin is dephosphorylated by myosin light chain phosphatase in the cell. 6-Relaxation of the smooth muscle. 7- Dephosphorylation of myosin light chain kinase does not necessarily lead to relaxation of the smooth muscle. a latch bridge mechanism by which myosin cross-bridges remain attached to actin for some time after the cytoplasmic Ca2+ concentration falls. This produces sustained contraction with little expenditure of energy, which is especially important in vascular smooth muscle, and in the walls of hollow organs which must sustain contractions for long periods of time. 3 Stimulation of the smooth muscles: 1-Stretch: It contracts when stretched in the absence of any extrinsic innervations. Stretch is followed by a decline in membrane potential, an increase in the frequency of spikes and a general increase in tone. 2-Chemical mediators: Epinephrine or norepinephrine : The membrane potential usually becomes larger, the spikes decrease in frequency, and the muscle relaxes. Acetylcholin: Has an effect opposite to that of norepinephrine on the membrane potential acetylcholine causes the membrane potential to decrease and the spikes become more frequent, with an increase in tonic tension and the number of rhythmic contractions. Released by stimulation of cholinergic nerves (similar to cold and stretch in vitro). 3- Other chemicals: like progesterone which decreases the activity and estrogen which increase it (in uterine smooth muscles). 4-Thermal stimuli: like cold which causes spasm. Function of the Nerve Supply to Smooth Muscle: It has two important properties: (1) its spontaneous activity in the absence of nervous stimulation, and (2) Its sensitivity to chemical agents released from nerves locally or brought to it in the circulation. The function of the nerve supply is not to initiate activity in the muscle but rather to modify it (control). It has dual nerve supply from 2 divisions of the autonomic nervous system. Stimulation of one division usually increases smooth muscle activity, whereas stimulation of the other decreases it. (i.e if noradrenergic increase ,the Acetylcholine decrease and visa versa). Relation of Length to Tension; Plasticity: It is the variability of the tension it exerts at any given length. If a piece of visceral smooth muscle is stretched, it first exerts increased tension, if the 4 muscle is held at the greater length after stretching, the tension gradually decreases. It is consequently impossible to correlate length and developed tension accurately. In intact humans, For example, the tension exerted by the smooth muscle walls of the bladder can be measured at different degrees of distention as fluid is infused into the bladder via a catheter Initially there is relatively little increase in tension as volume is increased, because of the plasticity of the bladder wall. However, a point is eventually reached at which the bladder contracts forcefully. This phenomenon is called stress relaxation and reverse stress-relaxation. Its importance is that its ability to return to nearly its original force of contraction seconds or minutes after it has been elongated or shortened. Smooth muscles must be able to contract even when greatly stretched—in the urinary bladder, for example, the smooth muscle cells may be stretched up to two and a half times their resting length. The smooth muscle cells of the uterus may be stretched up to eight times their original length by the end of pregnancy. Striated muscles, because of their structure, lose their ability to contract when the sarcomeres are stretched to the point where actin and myosin no longer overlap. MULTI-UNIT SMOOTH MUSCLE: -It is nonsyncytial . -Contractions do not spread widely through it (discrete, fine and more localized). - Very sensitive to circulating chemical substances and is normally activated by chemical mediators (acetylcholine and norepinephrine). - Norepinephrine tends to persist in the muscle and to cause repeated firing of the muscle after a single stimulus rather than a single action potential. Therefore, the contractile response produced is usually an irregular tetanus rather than a single twitch. The simple muscle twitch resembles the twitch contraction of skeletal muscle except that its duration is ten times longer. The differences between the three types of the muscles: 5 Skeletal muscles Smooth muscles Cardiac muscles voluntary in voluntary in voluntary Site of action Attached to bones In the walls of viscera In the heart Morphology striated Not striated striated The Control cell shape Long cylindrical Speed of contraction Fast -slow Spindle shaped Very slow(crossbridge heads have less ATPase activity than in skeletal muscle). No Capable of spontaneous contraction Effect of nerve stimulation Connection slow yes Yes for some smooth muscles Excitation(contro Excitation or l of contraction) inhibition(modulation of contraction) Membrane refractory period Nuclei in each cell Cylindrical and branched Short Excitation or inhibition long many No anatomical or functional 6 single single Connected by gap Connected by intercalated between cells connections junctions and bridges . 7 discs