Adenylate cyclase activity during development and reversal of XXXX .

@entity101 @entity35 @entity1184 @entity1283 @entity377 @entity3044
Inotropic responses to @entity3044 of hypertrophied hearts have been shown to be decreased. We have previously reported that in 13-week-old spontaneously @entity101 @entity35 (SHR) this decrease is probably due to decreased beta-adrenergic receptor number, while in hearts from two kidney-one clip renal @entity101 @entity35 (2K-1C RHR), this is due to a decreased @entity377 regulatory protein activity. We now show that changes in 2K-1C RHR are time dependent. One week after instituting development of @entity101 the heart is already hypertrophied. Biochemical changes consistent with decreased glucagon receptors are seen, as well as beginning changes consistent with decreases in the @entity377 regulatory protein activity. By two weeks this is more evident. @entity1184 and biochemical changes can be reversed up to six weeks, but by ten weeks the activity of the catalytic subunit of the adenylate cyclase system is decreased. In 1K-1C RHR, biochemical changes in the cyclase system are accelerated as compared with the 2K-1C model. In SHR, changes in 24-week-old @entity35 are the same as in the 13-week-old @entity35 . It is concluded that in @entity1283 associated with different models of @entity101 the decreased inotropic responsiveness to @entity3044 is associated with different biochemical defects in the beta-adrenergic receptor response coupling pathway, and that reversal in function occurs only when there is no apparent change in the catalytic subunit of the adenylate cyclase complex.
