1. The chronic inhibition of nitric oxide synthesis by N omega-nitro-L-arginine-methyl ester (L-NAME) leads to arterial hypertension accompanied by a significant increase in cardiac sympathetic tone and an almost complete abolition of the vagal tone in conscious adult male Wistar rats. The main aim of the present study was to examine the baroreceptor heart rate reflex function in L-NAME-treated rats (N = 10). 2. Spontaneous daily oral intake of L-NAME (1 mg/ml for 6 days) caused marked hypertension and tachycardia (176 +/- 5 mmHg and 418 +/- 16 bpm), when compared to untreated rats (111 +/- 2 mmHg and 354 +/- 8 bpm). 3. Baroreflex gain was determined in conscious freely moving rats by sigmoidal curve fitting analysis using alternate intravenous injections of phenylephrine (0.2-10.0 micrograms/kg) and sodium nitroprusside (0.5-20.0 micrograms/kg) to produce pressor-induced bradycardia and depressor-induced tachycardia, respectively. The baroreflex gain (sensitivity) was significantly enhanced in L-NAME-treated rats compared to control rats (10.9 +/- 2.5 vs 4.5 +/- 0.3 bpm/mmHg, respectively) mainly due to exaggerated reflex bradycardia responses to increases in arterial hypertension. 4. The data indicate that chronic inhibition of nitric oxide synthesis enhances the bradycardic component of the baroreflex function.