ATRIAL NATRIURETIC FACTOR AND ARTERIAL BARORECEPTOR REFLEXES IN UNANESTHETIZED RATS

The modulation exerted by atrial natriuretic factor (ANF) on the cardiac and vascular influences of arterial baroreceptors was investigated in two groups of unanesthetized, chronically instrumented normotensive rats. In group 1, the reflex control of heart rate was assessed by graded baroreceptor stimulations and deactivations obtained by intravenous boluses of phenylephrine and nitroprusside. Under either circumstance, baroreceptor reflex sensitivity was expressed as the linear regression slope relating the chronotropic responses to the drug-induced mean arterial pressure changes. In group 2, right common carotid occlusion was performed in rats with their aortic and left carotid sinus baroreceptors denervated to assess the baroreceptor control of blood pressure; the reflex response was quantitated as the peak blood pressure rise observed during the maneuver. The reflex studies were performed before and during atriopeptin III infusion (0.15-0.20 μ/kg/min for 60 minutes). ANF augmented the bradycardic response to phenylephrine by 102.5±29% (p<0.01), reduced the tachycardic response to nitroprusside by 67.7±6.4% (p<0.01), and failed to modify the pressor response to carotid occlusion (-6.8±2.1%, p=NS). In a separate group of rats infused with low dose nitroprusside, no change in the baroreceptor-heart rate reflex was observed. ANF infusion (0.20 μg/kg/min) performed in further separate groups of conscious rats raised plasma ANF to 480±58 fmol/ml. Values in control vehicle-infused rats were 50±8 fmol/ml. Vascular reactivity (pressor response to intravenous phenylephrine boluses in anesthetized, sinoaortic-denervated rats) was only minimally reduced by ANF. It is concluded that ANF at doses within the pathophysiological range exerts a complex modulatory effect on arterial baroreceptor reflexes, consisting of potentiation of the cardioinhibitory, no change of the vascular, and depression of the cardioexcitatory reflex influences. These data may have pathophysiological implications in high ANF release states.