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.
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.