Biochemical alterations in cardiac hypertrophy.
In both two-kidney, one clip renal hypertensive rats (RHR) and spontaneously hypertensive rats (SHR) with myocardial hypertrophy, inotropic responsiveness to adenylate cyclase mediated agonists, such as isoproterenol and glucagon is decreased, as is the responsiveness to phenylephrine acting via alpha 1 adrenergic receptors. However, defects in the excitation response pathway differ in the two hypertensive models. In SHR beta-adrenergic receptors are decreased, alpha 1 receptors increased, cyclase activity is unchanged but c-AMP stimulated protein kinase is decreased. In RHR beta-receptors are increased, alpha 1 receptors decreased, adenylate cyclase activity decreased due to decreased nucleotide regulatory protein activity, and microsomal cAMP stimulated protein kinase is increased. We conclude that, although functional changes in hypertensive cardiac hypertrophy are similar, the underlying biochemical alterations are different. The shift in balance between alpha- and beta-adrenergic pathways may be a compensatory mechanism and play a role in the pathophysiology of cardiac hypertrophy.
D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism*; D004082:Dihydroalprenolol / Q000378:metabolism; D006973:Hypertension / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D011224:Prazosin / Q000378:metabolism; D011494:Protein Kinases / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D011941:Receptors, Adrenergic / Q000032:analysis / Q000378:metabolism; D013997:Time Factors
D011941:Receptors, Adrenergic; D004082:Dihydroalprenolol; D011494:Protein Kinases; D011224:Prazosin