BIOCHEMICAL REMODELING OF COLLAGEN IN THE HEART OF SPONTANEOUSLY HYPERTENSIVE RATS - PROMINENT INCREASE IN TYPE-V COLLAGEN

To determine how collagen is remodeled in the heart during the development of cardiac hypertrophy, the collagen concentration and the proportions of types I, III, and V collagen were analyzed in the hearts of 10-, 20-, 32-, and 40-week-old spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. The collagen concentration was calculated after the hydroxyproline content was measured and the proportions of types I, III, and V collagen were determined by non-interrupted SDS-polyacrylamide gel electrophoresis (SDS-PAGE). There was no significant difference between the collagen concentrations in 10-week-old SHR and WKY. At 20 weeks, the collagen concentration in the hearts of the SHR had-decreased significantly (p<0.01) when compared to that in the WKY, at 40 weeks, this concentration in SHR had increased significantly (p<0.05) when compared to that in the WKY. Type V collagen in WKY increased with age and type I collagen in the 20- and 40-week-old WKY decreased significantly (p<0.05) when compared to that in the 10-week-old WKY. However, the proportion of type I collagen in the 20-week-old WKY did not differ from that of the 40-week-old WKY. There was no significant difference between the proportions of the various types of collagen in 10-week-old SHR and those in age- and sex-matched WKY. However, the proportion of type V collagen in the 20- and 40-week-old SHR was significantly (p<0.01) higher than that in age- and sex-matched WKY. Moreover, the proportion of type I collagen in the 40-week-old SHR was significantly (p<0.01) lower than that in age- and sex-matched WKY. The III/I ratio of the 40-week-old SHR was significantly higher than that of age-matched WKY (p<0.05). These results show qualitatively and quantitatively that collagen is remodeled as cardiac hypertrophy develops and that there is a prominent increase in type V collagen. This suggests that type V collagen is involved in the pathogenesis of cardiac hypertrophy in SHR.