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Horn EM, Corwin SJ, Steinberg SF, et al. Reduced lymphocyte stimulatory guanine nucleotide regulatory protein and beta-adrenergic receptors in congestive heart failure and reversal with angiotensin converting enzyme inhibitor therapy. Circulation. 1988;78(6):1373-9doi: 10.1161/01.cir.78.6.1373.
Horn, E. M., Corwin, S. J., Steinberg, S. F., Chow, Y. K., Neuberg, G. W., Cannon, P. J., Powers, E. R., & Bilezikian, J. P. (1988). Reduced lymphocyte stimulatory guanine nucleotide regulatory protein and beta-adrenergic receptors in congestive heart failure and reversal with angiotensin converting enzyme inhibitor therapy. Circulation, 78(6), 1373-9. https://doi.org/10.1161/01.cir.78.6.1373
Horn, E M, et al. "Reduced lymphocyte stimulatory guanine nucleotide regulatory protein and beta-adrenergic receptors in congestive heart failure and reversal with angiotensin converting enzyme inhibitor therapy." Circulation vol. 78,6 (1988): 1373-9. doi: https://doi.org/10.1161/01.cir.78.6.1373
Horn EM, Corwin SJ, Steinberg SF, Chow YK, Neuberg GW, Cannon PJ, Powers ER, Bilezikian JP. Reduced lymphocyte stimulatory guanine nucleotide regulatory protein and beta-adrenergic receptors in congestive heart failure and reversal with angiotensin converting enzyme inhibitor therapy. Circulation. 1988 Dec;78(6):1373-9. doi: 10.1161/01.cir.78.6.1373. PMID: 2847884.
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Circulation. 1988 Dec;78(6):1373-9. doi: 10.1161/01.cir.78.6.1373.

Reduced lymphocyte stimulatory guanine nucleotide regulatory protein and beta-adrenergic receptors in congestive heart failure and reversal with angiotensin converting enzyme inhibitor therapy.

Circulation

E M Horn, S J Corwin, S F Steinberg, Y K Chow, G W Neuberg, P J Cannon, E R Powers, J P Bilezikian

Affiliations

  1. Department of Medicine, Columbia University, College of Physicians and Surgeons, New York, NY 10032.

PMID: 2847884 DOI: 10.1161/01.cir.78.6.1373

Abstract

Adrenergic hyporesponsiveness in congestive heart failure has been understood previously in terms of a reduction in beta-adrenergic receptors. We have examined another hypothesis, one that states the stimulatory guanine nucleotide regulatory protein (Gs) that couples the beta-adrenergic receptor to adenylate cyclase activity is also decreased in congestive heart failure. In addition to the 40% decrease in lymphocyte beta-adrenergic receptors in patients in congestive heart failure (5.9 +/- 0.7 vs. 9.7 +/- 1.4 fmol/mg, p less than 0.05), we found an 80% decrease in levels of Gs compared with age- and sex-matched healthy control subjects (72.5 +/- 19 vs. 376 +/- 73 fmol/mg, p less than 0.05). Myocardial Gs levels correlated significantly with lymphocyte Gs levels. We also assessed the hypothesis that reductions in beta-adrenergic receptors and in Gs are reversible after successful therapy with angiotensin converting enzyme inhibitors. Treatment with either captopril or lisinopril was associated with clinical improvement, an increase in beta-adrenergic receptor density (from 5.5 +/- 0.7 to 8.7 +/- 1.5 fmol/mg), and a twofold increase in Gs levels (p less than 0.05). Thus, the data are compatible with Gs serving as an adaptable and reversible regulator of the adrenergic response in congestive heart failure. In view of the fact that Gs is a transducing element common to all hormones that stimulate cyclic adenosine 5'-monophosphate production, the observations could extend to other abnormal neurohumoral mechanisms in congestive heart failure.

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