The aim of this study was to determine the phenotype of smooth muscle cells in the arteries of chronically hypertensive animals and to analyze the effects of treatments known to increase the survival of the animal without a clear effect on its hypertensive state. Stroke-prone spontaneously hypertensive rats (SHRSP) kept on a 1% sodium drinking solution were untreated or treated with one of two diuretics, indapamide (3 mg/kg per day) or hydrochlorothiazide (20 nig/kg per day), from 6 to 13 weeks of age. Phenotype was characterized by the immunolabeling of arteries with antibodies raised against a cellular form (EIIIA) of fibronectin, <*-smooth muscle actin, and nonmuscle myosin. We demonstrated that phenotypes of smooth muscle cells of the SHRSP differ from those found in Wistar-Kyoto rats. The difference in phenotype is specific for the vessel type: ie, an increased expression of nonmuscle myosin in the aorta and of both EIIIA fibronectin and nonmuscle myosin in the coronary arteries. The two diuretics (1) had no effect on blood pressure, (2) prevented or did not prevent the increase in medial thickness, and (3) prevented changes in both smooth muscle cell phenotype and ischemic tissular lesions. Taken and/or hyperplasia of medial smooth muscle cells, develops in salt-loaded stroke-prone spontaneously hypertensive rats (SHRSP). 1 -2 Cardiac hypertrophy in hypertensive rats is correlated with a shift in the myosin heavy chain pattern of striated cardiac myocytes toward a fetal phenotype.3 Both quantitative and qualitative alterations may be normalized by antihypertensive treatment. 4 Changes in the phenotype of smooth muscle cells occur in vivo during ontogenesis.58 A well-differentiated phenotype is predominant in the vessels when cells contract in response to chemical and mechanical stimuli and are involved in the control of blood pressure and flow. At this stage, a-smooth muscle actin (aSM-actin) and smooth muscle myosin heavy chain (SM2) are the major contractile protein isoforms expressed in human, rat, or rabbit smooth muscle cells.6 -8 " A phenotypic shift in the expression of the contractile proteins 1 " 12 ' 3 and of a protein of the extracellular matrix, fibronectin, 14 toward the forms expressed in the fetus is observed in the aorta during the early phase of atherogenesis. Changes in the expression of fibronectin isoforms also occur in the coronary arteries and aorta as a result of pressure overload. In vivo, the heterogeneity of the smooth muscle cell phenotype throughout the vascular system in normotensive conditions 1718 would suggest specific changes in the phenotype of the smooth muscle cells as a result of hypertension. Therefore, the present study was conducted to determine whether an increase in size of the aortic and coronary artery mediae in SHRSP is associated with changes in the phenotype of the smooth muscle cells.It has been shown in the salt-loaded SHRSP that several types of drugs, such as angiotensin converting enzyme inhibitors, 1 /3-blockers, 19 and diuretics, 2 prevent the occurren...
The quantity and the electrophoretic characteristics of desmin were analyzed in a familial skeletal muscle disorder, characterized by the intra-sarcoplasmic accumulation of an electron-dense granulo-filamentous material facing the Z-lines and reacting strongly with polyclonal anti-desmin antibodies. The analysis was performed on biopsies from the deltoid muscles of 4 patients, members of 2 families. In the 4 biopsies, an increase in the relative amount of desmin compared to that of actin or insoluble proteins (3 fold) and in the number of isovariants (6 instead of 3) was observed. The isovariants of desmin were similar to those described in Purkinje fibres of the heart as a phosphorylated form of the protein [(1987) Eur. J. Cell Biol. 44, 68-78]. Therefore, post-translational events could affect both the polymerization and the amount of desmin filaments in this autosomal dominant familial myopathy.
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