AJP - Heart and Circulatory Physiology, Vol 249, Issue 4 814-H819, Copyright © 1985 by American Physiological Society
Renal hypertension impairs inotropic isoproterenol effect without beta-receptor changes
O. A. Gende, A. Mattiazzi, M. C. Camilion, P. Pedroni, C. Taquini, H. Gomez Llambi and H. E. Cingolani
Experiments were performed in male Wistar rats with renovascular
hypertension (167 +/- 4.2 mmHg) produced by clipping the renal artery for a
3-wk period (2-kidney, 1-clip Goldblatt). The results were compared with
those obtained in age-matched normotensive controls. Hypertension of 3-wk
duration elicited a significant increase in ventricular weight (1.01 +/-
0.02 g) with respect to the controls (0.82 +/- 0.01 g) but had no
significant effect on body weight. The inotropic responsiveness to
beta-adrenergic stimulation was diminished in papillary muscles from renal
hypertensive rats: the maximum increase in the maximal rate of rise of
tension produced by isoproterenol was 27.39 +/- 5.4 and 11.77 +/- 2.91 g X
mm-2 X s-1 (P less than 0.05) in control and hypertensive animals,
respectively. Similar results were obtained when the estimated maximal
velocity of shortening of the contractile element (Vmax) was used to assess
myocardial contractility. The inotropic response to CaCl2 was also
significantly depressed in the 2-kidney, 1-clip rats. However, the relaxant
and the chronotropic responses to isoproterenol were not significantly
modified in the Goldblatt rats. Assays of beta-adrenergic receptors to
l-[3H]dihydroalprenolol binding, showed no significant changes in the
number (expressed per mg of membrane protein) or in the affinity of the
beta-receptors. These results suggest that at an early stage of the renal
hypertensive model the impaired inotropic response to isoproterenol is not
mediated by an alteration of the beta-receptors and should be searched at a
postreceptor adenyl cyclase level.
