HYPERTENSION WITHOUT CARDIAC-HYPERTROPHY DOES NOT INDUCE A CARDIAC BAROREFLEX DEFICIT

Objective 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, Methods Male Wistar ra ts 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 we eks, 50 mg/kg per day orally), The cardiac baroreceptor reflex was ass essed in previously instrumented conscious rats by using a 'steady-sta te' 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 th e left ventricle plus septum separated from the heart and weighed. Res ults The arterial pressure at one-half of the heart rate range was shi fted to higher arterial pressures, consistent with the increase in the operating point of mean arterial pressure following NO synthase block ade, No change in any of the baroreflex parameters could be detected d espite prolonged L-NAME-induced hypertension, On the basis of the stud y criteria, the data from one rat were not included in the group analy sis because of the presence of cardiac hypertrophy. Conclusions The re sults of the present study indicate that increased blood pressure alon e, either acutely or chronically, is not a sufficient stimulus to indu ce a baroreflex deficit.