Cardiac protein kinase C expression in two models of cardiac hypertrophy associated with an activated cardiac renin-angiotensin system: effects of experimental hyperthyroidism and genetic hypertension (the mRen-2 rat).

There is evidence for a role of protein kinase C (PKC) in the development of cardiac hypertrophy. We examined the expression of individual PKC isoforms in the adult rat heart in two distinct, well-characterised in vivo models of cardiac hypertrophy associated with an activated cardiac renin-angiotensin system, namely experimental hyperthyroidism and the TGR(mRen2)27 rat. The cardiac expression of a range of PKC isoforms (PKC-alpha, PKC-omega, PKC-epsilon, PKC-gamma, and PKC-tau) was examined by immuno-blotting. Our work demonstrates that the expression of total cardiac nPKC-omega and nPKC-epsilon relative to protein is selectively and differentially modified in these models. A consistent up-regulation of nPKC-omega in conjunction with overall down-regulation of nPKC-epsilon was observed in both models. The expression of other PKC isoforms was unaffected. The divergent responses of the expression of the two nPKC isoforms to an activated cardiac renin-angiotensin system in vivo in adulthood suggest that these individual nPKC isoforms subserve specific roles in the response.