Expression of smooth muscle myosin heavy chain B in cardiac vessels of normotensive and hypertensive rats

Item Type:	Article
Title:	Expression of smooth muscle myosin heavy chain B in cardiac vessels of normotensive and hypertensive rats
Creators Name:	Wetzel, U. and Lutsch, G. and Haase, H. and Ganten, U. and Morano, I.
Abstract:	We investigated expression of the 5'-spliced isoform of smooth muscle myosin heavy chain (SM-MHC-B) in smooth muscle cells of cardiac vessels of the left ventricle of normotensive (Wistar-Kyoto) and spontaneously hypertensive rats of the stroke-prone strain by immunofluorescence microscopy. In parallel, liver and bladder were studied for characterization of the nature of vessels expressing SM-MHC-B and for semiquantitative evaluation of its abundance. Smooth muscle cells were detected by staining with a monoclonal antibody specific for alpha-smooth muscle actin. Abundance of the SM-MHC-B isoform in these cells was evaluated by using an antibody raised against the seven-amino acid insert at the 25K/50K junction of the myosin head (a25K/50K) that specifically recognized SM-MHC-B. In the ventricle, a25K/50K immunoreactivity was observed in smooth muscle cells of precapillary arterioles but not in larger vessels or aorta. The a25K/50K immunoresponse of those vessels with the highest expression level of SM-MHC-B closely resembled the signal observed in the smooth muscle layer of urinary bladder known to preferentially express SM-MHC-B. Interestingly, in left ventricles of stroke-prone spontaneously hypertensive rats, there was a significantly reduced fraction of a25K/50K-positive precapillary arterioles compared with normotensive control rats.
Keywords:	Smooth Muscle, Myosin Heavy Chain, Hypertrophy, Hypertension, Cardiac Vessel, Animals, Rats
Source:	Circulation Research
ISSN:	0009-7330
Publisher:	American Heart Association
Volume:	83
Number:	2
Page Range:	204-209
Date:	27 July 1998
Official Publication:	http://circres.ahajournals.org/cgi/content/abstract/83/2/204
PubMed:	View item in PubMed

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