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Hypertensive renal damage: Modulation expression of smooth muscle myosin heavy chain isoforms
Author(s) -
SUZUKI Naoe,
KIMURA Kenjiro,
NAGAI Ryozo,
OHBA Shigeyoshi,
MISE Naobumi,
HIROI Junko,
TOJO Akihiro,
HIRATA Yasunobu,
NAGAOKA Akinobu,
GOTO Atsuo,
OMATA Masao
Publication year - 1997
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1111/j.1440-1797.1997.tb00224.x
Subject(s) - afferent arterioles , myosin , endocrinology , medicine , vascular smooth muscle , actin , gene isoform , immunohistochemistry , phenotype , microbiology and biotechnology , chemistry , receptor , biology , smooth muscle , angiotensin ii , biochemistry , gene
Summary: The aim of this study was to determine the phenotypic modulation in preglomerular vascular smooth muscles and glomerular cells in hypertension. Eight‐week‐old stroke‐prone spontaneously hypertensive rats (SHRSP) fed high sodium pellets (3%) were untreated or treated with a calcium antagonist, manidipine HCI (2 mg/kg per day), for 8 weeks. the expression of myosin heavy chain isoforms (MHC), SM2 (muscletype) and SMemb (non‐muscle‐type) or α‐actin was examined by the immunohistochemical technique. In normotensive Wistar‐Kyoto rats, both SM2 and α‐actin were expressed equally in the smooth muscles of preglomerular vessels, and SMemb was expressed slightly in the glomerular epithelial cells. In the SHRSP, however, the expression of SM2 and α‐actin was significantly decreased or disappeared in the afferent arterioles, depending on the degree of vascular damage. In damaged glomeruli, SMemb and α‐actin were newly expressed in mesangial cells. Manidipine HCI attenuated the renal damage and restored the expression of α‐actin in the afferent arterioles. There was a significant correlation between the glomerular damage and the attenuation of SM2 expression (r=0.87). In conclusion, phenotypic modulation of vascular smooth muscles occurred in hypertensive renal damage and was correlated with the glomerular damage, where the phenotypic modulation also took place in the mesangial cells. These results indicate that the phenotypic modulations revealed by the expression of myosin isoforms might play an important role in the development of hypertensive renal damage.