Reduced contractile capacity of vascular smooth muscle: another mechanism of hypertension?
Hypertension has become a large burden of global development, but the mechanisms of it have still not been well elucidated. Increased contractility of vascular smooth cells induced by the overactivity of neurohormonal system or stress is one of the main and popular explanations until now. Smoothelin-B, recognized as the actin-binding protein, is only expressed in vascular smooth muscle cells and takes part in the contraction process of vascular smooth cells. Rensen et al. demonstrated that deficiency of smoothelin-B resulted in reduced contractile capacity of vascular smooth muscle and hypertension in mice, which provides us a novel fact in the pathogenesis of hypertension. Therefore, we proposed that reduced contractile capacity of vascular smooth muscle could result in hypertension, the mechanism of which might be related to normal cardiac output but blood retention induced by reduced vasoconstriction, impaired vasodilatation and decreased blood vessels. Studies are needed to demonstrate our hypotheses and further investigation and discussion should be focused on the treatment in these patients because beta-blockers, angiotensin-converting enzyme inhibitor or angiotensin receptor blocker may be not suitable for them.
Li
Shao-Hua
SH
Hypertension Division, FuWai Hospital and Cardiovascular Institute, 167 Beilishilu, Beijing 100037, PR China.
Hui
Ru-Tai
RT
D001158:Arteries / Q000503:physiopathology*; D003598:Cytoskeletal Proteins / Q000378:metabolism*; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D008955:Models, Cardiovascular; D009119:Muscle Contraction; D009124:Muscle Proteins / Q000378:metabolism*; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology*; D014661:Vasoconstriction; D014664:Vasodilation
D003598:Cytoskeletal Proteins; D009124:Muscle Proteins; C491050:Smtn protein, mouse