Smooth muscle.pptx

Smooth muscle

1. Smooth muscle By Dr A Amar Sandeep

2. content Types of Smooth Muscles Functional Organization Innervations of Smooth Muscles Electrical Properties Mechanism of Contraction Mechanical properties Smooth Muscle Hypertrophy Neural and Hormonal Influences

3. Types of Smooth Muscles Single-unit Smooth Muscle The muscle fibers in single-unit smooth muscles are connected to each other by gap junctions . They form the walls of hollow viscera Multiunit Smooth muscle They do not have gap junctions h Muscle The intrinsic muscles of the eye, precapillary sphincters, and piloerector muscles.

4. Functional Organization Circular Circular and longitudinal Circular, longitudinal and oblique

5. Structure Each smooth muscle fiber is a spindle-shaped cell, 100–300 µm long and 5–10 µm in diameter at the middle The cell derives energy mainly from glycolytic pathway The sarcoplasmic reticulum is well developed only in some types of smooth muscles; in others it is rudimentary. Myofilaments are organized differently. There are no sarcomeres and striations are not visible There is lack of an organized T tubular system. The cell membrane shows invaginations called caveolae that increase the surface area

6. Myofilaments Thick, thin and intermediate During the sliding-filament mechanism, the gap between the actin filaments reduces and the shortening force is transmitted through the dense bodies to the plasma membrane producing contraction of the muscle fiber

7. Innervations of Smooth Muscles Smooth muscles exhibit a spontaneous, slow wave rhythm. Neural stimulation only modulates (increases or decreases) this basic pattern . Branches of the autonomic nervous system innervate the smooth muscles, most of which are supplied by sympathetic as well as parasympathetic fibers

8. Electrical Properties The smooth muscles react to a variety of stimuli, which may be Neural (sympathetic or parasympathetic); H ormonal (circulating catecholamines , serotonin, histamine, angiotensin, vasopressin, oxytocin, estrogen , and progesterone); C hemical (hypoxia, hypercapnia , and H+ ); cold; and stretch.

9. Characteristic Electrical Activities The membrane potential of visceral smooth muscles is variable (no fixed resting potential), ranging from –30 mV to –70 mV with an average of –50 mV . Most of the visceral smooth muscles generate action potentials inherently; any stimulus acting on it only alters the rate and pattern of action potentials formed . The multiunit smooth muscles do not discharge spontaneously ; they also do not respond to stretch In some cells, in response to stimuli like hormones or mechanical stretch, the membrane potential shows a graded change that may culminate into an action potential.

10. Characteristic Electrical Activities

11. Excitatory junction potentials Pacemaker potential Some smooth muscle cells contract without any change in membrane potential.

12. Mechanism of Contraction Calcium Influx Calcium Release Binding of Calcium to Calmodulin Pumping Back of Calcium to the SR Calcium Efflux

13. Molecular Basis of Contraction & relaxation

14. Phasic Contraction Tonic Contraction Latch-Bridge Mechanism When MLCP-induced dephosphorylation of myosin light-chain takes place, it does not bring about dissociation of myosin from actin until the cytoplasmic calcium concentration falls below a critical level.

15. Mechanical properties Contractile Response Muscle Tone - basic slow wave rhythm Length–Tension Relationship - plasticity, the relationship is highly inconsistent.

16. Smooth Muscle Hypertrophy In pregnancy In hypertension Hypertrophy of urinary bladder in men due to enlargement of the prostate gland

17. Neural Influences Autonomic Control 1. Parasympathetic stimulation is excitatory, Ach acts by increasing the cytoplasmic Ca++ through phospholipase C and IP3 . 2. Sympathetic stimulation is inhibitory Acting via α receptors, NE increases calcium efflux from the cell. This leads to decline in cytoplasmic Ca++ and relaxation of the muscle . Acting via β receptors, NE stimulates adenylyl cyclase that increases formation of cAMP , which activates the enzyme cAMP-dependent protein kinase. This protein kinase as well as cAMP increase calcium uptake by the sarcoplasmic reticulum. This results in fall in cytoplasmic concentration of Ca++

18. Hormonal Influences Nitric oxide (NO) - The NO-receptor complex stimulates guanylyl cyclase and forms cGMP, which activates cGMPdependent protein kinase. This protein kinase produces relaxation by increasing calcium reuptake by SR, opening of Ca++activated K+ channels and decreasing IP3-induced Ca++ release by inhibiting phospholipases C . Angiotensin II acting via AT II receptors , vasopressin and endothelin stimulate contraction of smooth muscles by releasing IP3. Adenosine causes relaxation by increasing the level of cAMP .

19. Thank you