Increased aortic pressure accelerates ribosome formation in the heart through a cAMP-dependent mechanism, providing insight into pressure-induced cardiac remodeling.
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Should not alter clinical hypertension management; leaves open cAMP mediation of pressure-induced ribosome formation for mechanistic studies.
Elevation of aortic perfusion pressure from 60 to 120 mmHg in beating and arrested rat hearts raised cAMP content and increased rates of ribosome formation but had no effect on total protein synthesis during 1 h of perfusion. The activity of adenosine 3',5'-cyclic monophosphate (cAMP)-dependent protein kinase increased as perfusion pressure was elevated in arrested hearts. A regulatory link between increased cAMP content and accelerated ribosome formation was hypothesized to exist. When hearts were arrested with tetrodotoxin and exposed to 0.2 mM methacholine, a muscarinic-cholinergic agonist that blocked pressure-induced increases in cAMP content, elevation of aortic pressure to 120 mmHg failed to increase the rate of ribosome formation. When aortic pressure was maintained at 60 mmHg, exposure of beating hearts to glucagon increased cAMP content and mimicked the effect of elevated aortic pressure to accelerate rates of ribosome formation. These studies support the hypothesis that increased aortic pressure preferentially accelerates rates of ribosome formation by a cAMP-dependent mechanism.
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Watson et al. (1989) studied this question.
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