Vascular smooth muscle contraction & relaxation

    Cardiovascular Physiology Concepts
                                    Richard E. Klabunde, Ph.D.

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Vascular Smooth Muscle Contraction and Relaxation

The contractile characteristics and the mechanisms that cause contraction of vascular smooth muscle (VSM) are very different from cardiac muscle. VSM undergoes slow, sustained, tonic contractions, whereas cardiac muscle contractions are rapid and of relatively short duration (a few hundred milliseconds). While VSM contains actin and myosin, it does not have the regulatory protein troponin as is found in the heart. Furthermore, the arrangement of actin and myosin in VSM is not organized into distinct bands as it is in cardiac muscle. This is not to imply that the contractile proteins of VSM are disorganized and not well-developed. They are actually highly organized and well-suited for their role in maintaining tonic contractions and reducing lumen diameter.

Contraction in VSM can be initiated by mechanical, electrical, and chemical stimuli. Passive stretching of VSM can cause contraction that originates from the smooth muscle itself and is therefore termed a myogenic response. Electrical depolarization of the VSM cell membrane also elicits contraction, most likely by opening voltage dependent calcium channels (L-type calcium channels), which causes an increase in the intracellular concentration of calcium. Finally, a number of chemical stimuli such as norepinephrine, angiotensin II, vasopressin, endothelin-1, and thromboxane A₂ can cause contraction. Each of these substances bind to specific receptors on the VSM cell (or to receptors on the endothelium adjacent to the VSM), which then leads to VSM contraction. The mechanism of contraction involves different signal transduction pathways, all of which converge to increase intracellular calcium.

The mechanism by which an increase in intracellular calcium stimulates VSM contraction is illustrated in the figure to the right. An increase in free intracellular calcium can result from either increased flux of calcium into the cell through calcium channels or by release of calcium from internal stores (e.g., sarcoplasmic reticulum; SR). The free calcium binds to a special calcium binding protein called calmodulin. Calcium-calmodulin activates myosin light chain kinase (MLCK), an enzyme that is capable of phosphorylating myosin light chains (MLC) in the presence of ATP. Myosin light chains are 20-kD regulatory subunits found on the myosin heads. MLC phosphorylation leads to cross-bridge formation between the myosin heads and the actin filaments, and hence, smooth muscle contraction.

Intracellular calcium concentrations, therefore, are very important in regulating smooth muscle contraction. The concentration of intracellular calcium depends upon the balance between the calcium the enters the cells, the calcium that is released by intracellular storage sites (e.g., SR), and removal of calcium either back into storage sites or out of the cell. Calcium is re-sequestered by the SR by a ATP-dependent calcium pump. Calcium is removed from the cell to the external environment by either a ATP-dependent calcium pump or by the sodium-calcium exchanger.

RK Revised 04/01/2007

DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice.