Abstract:
: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.
journal_name
Med Hypothesesjournal_title
Medical hypothesesauthors
Li SH,Hui RTdoi
10.1016/j.mehy.2009.01.038subject
Has Abstractpub_date
2009-07-01 00:00:00pages
62-4issue
1eissn
0306-9877issn
1532-2777pii
S0306-9877(09)00090-5journal_volume
73pub_type
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