Reduction of cardiac hypertrophy in renal hypertensive rabbits with pindolol
Cimini, C.M.; Gonzalez, M.A.; Weiss, H.R.
Journal of Pharmacology and Experimental Therapeutics 257(2): 541-546
1991
ISSN/ISBN: 0022-3565 PMID: 1827840 Document Number: 383405
Arterial pressure, cardiac mass and coronary flow reserves were measured in untreated and chronically pindolol-treated rabbits, prepared as either one-kidney one clip (1K1C) hypertensive or uninephrectomzied (sham) controls. Pindolol (200 .mu.g/kg/day) was administered for either 23 or 30 days, beginning 1 week after, or the day of initial surgery, respectively. Coronary flow was measured, at day 30, using radioactive microspheres, during base-line and adenosine infusion (0.4 mg/kg/min) in anesthetized open-chest preparations. Heart weight of untreated 1K1C animals (9.13 .+-. 0.73 g) was significantly greater than the controls (7.19 .+-. 0.77 g). Myocardial mass of 1K1C (9.93 .+-. 0.86 g) and sham controls (7.40 .+-. 0.31 g) were unaffected by chronic pindolol for 23 days. Cardiac hypertrophy was prevented in 1K1C animals treated with pindolol for 30 days (7.53 .+-. 1.28 g). Untreated 1K1C animals were hypertensive compared to sham controls (116 .+-. 12 and 78 .+-. 7 mm Hg) and neither pindolol regime affected blood pressure. Bradycardia was evident in all pindolol-treated animals. Base-line coronary flow was higher in the untreated 1K1C animals compared to untreated controls (228 .+-. 43 vs. 182 .+-. 31 ml.min/100 g). After chronic pindolol treatments, 1K1C base-line blood flows were reduced (158 .+-. 48 and 175 .+-. 59 ml/min/100 g, for 23- and 30-day protocols). Adenosine vasodilated flows were not different between the untreated 1K1C and sham animals and were not affected by pindolol treatment. Therefore, hypertension and cardiac hypertropy were dissociable in this model when pindolol was administered from the onset of hypertension. This suggests immediate involvement of beta adrenergic activation in the development of hypertrophy. Flow reserves were restored toward control, independent of myocardial mass.