Localization of α1(I) Collagen mRNA in Myocardium from the Spontaneously Hypertensive Rat During the Transition from Compensated Hypertrophy to Failure

Spontaneously hypertensive rats (SHR) commonly develop impairment of myocardial function between ages 18–24 months. Isolated muscle studies demonstrate depressed myocardial contractility and increased passive stiffness. Studies of the extracellular matrix in SHR with failure (SHR-F) demonstrate an increased expression of genes encoding extracellular matrix components (ECM), hydroxyproline concentration and fibrosis relative to age-matched non-failing animals. In the present study, tissue sections of hearts from SHR-F, non-failing SHR (SHR-NF) and non-hypertensive Wistar Kyoto rats (WKY) were hybridized with a cDNA probe forα1(I) collagen mRNA, which was found by Northern blot analysis to be elevated in SHR-F relative to hearts from control animals.In situhybridization studies demonstrate increased perivascular and interstitial collagenα1(I) gene expression in myocardium from the SHR relative to WKY. In addition, failing hearts from the SHR demonstrate focalα1(I) collagen mRNA accumulation in the endocardium and at sites of degenerating single myocardial cells.