AJP - Heart and Circulatory Physiology, Vol 246, Issue 1 31-H36, Copyright © 1984 by American Physiological Society
Norepinephrine increases beta-receptors and adenylate cyclase in canine myocardium
W. J. Raum, M. M. Laks, D. Garner, M. H. Ikuhara and R. S. Swerdloff
Norepinephrine, a known inducer of myocardial hypertrophy, was found to
have marked effects on the myocardial adrenergic system, which occurred
prior to the development of a significant increase in heart weight. The
chronic subhypertensive infusion (1.4 microgram/min) in free-roaming dogs
produced a threefold increase in plasma norepinephrine (determined by
radioimmunoassay). After 3 mo of infusion, right and left ventricular
norepinephrine content (ng/mg protein) decreased significantly by twofold
(right, 2.50 +/- 0.24; left, 2.08 +/- 0.36) compared with controls (right,
4.76 +/- 1.48; left, 4.65 +/- 1.49), and beta-receptor density
(125I-pindolol) increased (right, 0.122 +/- 0.029; left, 0.153 +/- 0.021)
over the controls (right, 0.082 +/- 0.015; left, 0.069 +/- 0.008 pmol/mg
protein). Accompanying the beta-receptor changes, isoproterenol-stimulated
adenylate cyclase activity also increased significantly [right, 29.2 +/-
2.1; left, 29.5 +/- 1.0 vs. controls, right, 13.8 +/- 1.1; left, 20.2 +/-
2.2 pmol adenosine 3',5'-cyclic monophosphate (cAMP) generated X min-1 X mg
protein-1]. Because the above changes occurred in the absence of cardiac
hypertrophy, it suggests that alterations in the myocardial adrenergic
system are dependent on the stimulus (in this case norepinephrine) invoking
the change and not the degree of hypertrophy. It also suggests that changes
in the adrenergic system may not directly reflect the mechanism involved in
the development of hypertrophy.
