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Research Article Free access | 10.1172/JCI117219

Downregulation of adenylylcyclase types V and VI mRNA levels in pacing-induced heart failure in dogs.

Y Ishikawa, S Sorota, K Kiuchi, R P Shannon, K Komamura, S Katsushika, D E Vatner, S F Vatner, and C J Homcy

Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York 10032.

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Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York 10032.

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Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York 10032.

Find articles by Kiuchi, K. in: JCI | PubMed | Google Scholar

Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York 10032.

Find articles by Shannon, R. in: JCI | PubMed | Google Scholar

Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York 10032.

Find articles by Komamura, K. in: JCI | PubMed | Google Scholar

Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York 10032.

Find articles by Katsushika, S. in: JCI | PubMed | Google Scholar

Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York 10032.

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Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York 10032.

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Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York 10032.

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Published May 1, 1994 - More info

Published in Volume 93, Issue 5 on May 1, 1994
J Clin Invest. 1994;93(5):2224–2229. https://doi.org/10.1172/JCI117219.
© 1994 The American Society for Clinical Investigation
Published May 1, 1994 - Version history
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Abstract

We have shown that the heart expresses two distinct forms of adenylylcyclase mRNA, types V and VI. In this study we have characterized the expression of these two mRNA species in heart failure generated by overdrive pacing at a rate of 240 beats/min. After 4 wk, left ventricular end-diastolic pressure and heart rate increased significantly with the appearance of signs of heart failure, i.e., edema, ascites, and exercise intolerance. Basal as well as forskolin-stimulated adenylylcyclase activities decreased significantly, which was accompanied by a reduction in the steady state mRNA levels of adenylylcyclase types V and VI. These data suggest that in this model of cardiomyopathy, the downregulation of adenylylcyclase catalytic activity results, at least in part, from a reduction in the steady state levels of types V and VI adenylylcyclase mRNA levels.

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