Hypertension without cardiac hypertrophy does not induce a cardiac baroreflex deficit.

Abstract

To investigate the effects of prolonged hypertension in the absence of cardiac hypertrophy on the blood pressure-heart rate reflex during acute and chronic NO synthase blockade. Male Wistar rats were treated acutely with N omega-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg intraperitoneally) or chronically with L-NAME (2.5-3 weeks, 50 mg/kg per day orally). The cardiac baroreceptor reflex was assessed in previously instrumented conscious rats by using a 'steady-state' method that involved alternating vasoactive drug-induced stepwise increases and decreases in mean arterial pressure with methoxamine and sodium nitroprusside. Following baroreflex assessment, the rats were killed by an overdose of anaesthetic, their hearts were removed and the left ventricle plus septum separated from the heart and weighed. The arterial pressure at one-half of the heart rate range was shifted to higher arterial pressures, consistent with the increase in the operating point of mean arterial pressure following NO synthase blockade. No change in any of the baroreflex parameters could be detected despite prolonged L-NAME-induced hypertension. On the basis of the study criteria, the data from one rat were not included in the group analysis because of the presence of cardiac hypertrophy. The results of the present study indicate that increased blood pressure alone, either acutely or chronically, is not a sufficient stimulus to induce a baroreflex deficit.