Improvement of cardiac contractile response to beta-adrenergic stimulation in normal and two-kidney, one-clip hypertensive rats treated with nitrendipine.
To evaluate the effect of nitrendipine on cardiac hypertrophy and inotropic response to isoproterenol in two-kidney, one-clip (2K,1C) renovascular hypertension, male Wistar rats (n = 56) were divided into a clipped group (K) (n = 28) and a sham group (S) (n = 28). Twenty-one days after surgery, the rats were placed in metabolic cages where they received either a normal diet (S and K rats) or a similar one containing N (18 mg/day) (SN and KN rats) during 3 weeks. Arterial pressure and body weight were measured twice a week. At the end of the experimental period, the hearts were excised, the ventricles were weighed, and cardiac proteins were measured by the Lowry method in seven hearts of each group. In the remaining hearts, the left ventricular papillary muscle was excised and mounted in a bath where the developed tension (dt) and the maximal rate of rise of developed tension (+T) were recorded in basal conditions, and after cumulative doses of isoproterenol (10(-11) to 10(-4) M). The arterial pressure, ventricular weight, and cardiac proteins were similar in S, SN, and KN groups and were significantly higher in the K group (p less than 0.05). No difference in the basal values of +T and dt were observed among the four groups. The increment in +T after isoproterenol was higher in treated (KN and SN) than in nontreated (K and S) groups (p less than 0.05). In conclusion, nitrendipine enhances the contractile response to isoproterenol and reverses the cardiac hypertrophy in the 2K, 1C model.