INFLUENCE OF THE BARORECEPTOR REFLEX ON THE MODULATION OF NORADRENALINE OVERFLOW THROUGH PREJUNCTIONAL RECEPTORS IN THE PORTAL-VEIN OF FREELY MOVING RATS

1 The effects of alterations in mean arterial blood pressure (MAP), as induced by vasoactive drugs, on heart rate (HR), basal noradrenaline concentration and electrically evoked noradrenaline overflow and on bl ood flow in the portal vein of freely moving rats, were investigated. 2 By infusion of sodium nitroprusside or phenylephrine (0.5, 1.0 and 2 .5 mu g kg(-1) min(-1)), MAP was altered over a range of 50 to 150 mmH g. The resulting changes in HR showed a sigmoidal relationship with MA P. Noradrenaline overflow increased linearly when MAP was decreased; w hen MAP was increased, however, noradrenaline levels only decreased to 70% and reached a plateau from 125 mmHg onwards. 3 Nitroprusside (2.5 mu g kg(-1) min(-1)) and fenoterol (0.25 mg kg(-1)) decreased MAP to the same extent (- 46 mmHg). HR and basal noradrenaline concentration, however, were increased to a higher extent by fenoterol (+ 192 beats min(-1); + 373 pg ml(-1), respectively) than by nitroprusside (+ 78 be ats min(-1); + 206 pg ml(-1), respectively). Electrically evoked overf low was not changed at all after nitroprusside, whereas fenoterol indu ced an increase to 206% of control. 4 Phenylephrine (2.5 mu g kg(-1) m in(-1)) and angiotensin II (1 mu g kg(-1) min(-1)) increased MAP to th e same extent (to 155 and 161 mmHg, respectively). Basal noradrenaline concentration decreased by 30% after phenylephrine, whereas angiotens in II increased noradrenaline levels to 226% of control. Evoked noradr enaline overflow was not changed after phenylephrine but was increased to 204% of control after angiotensin II. 5 Portal venous blood flow ( 15.3 ml min(-1)) was not affected after brisk changes in MAP induced b y nitroprusside (2.5 mu g kg(-1) min(-1)), fenoterol (0.25 mg kg(-1)) or phenylephrine (2.5 mu g kg(-1) min(-1)). 6 The results showed that the electrically evoked overflow of endogenous noradrenaline in the po rtal vein of the freely moving rat is not influenced by baroreceptor r eflex-induced changes in basal noradrenaline overflow. As a consequenc e, the prejunctional effects of drugs on the electrically evoked overf low are only of local origin. Portal venous blood flow is not changed by brisk changes in MAP or electrical stimulation, therefore no change s in noradrenaline spillover from nerve terminals are expected. Howeve r, the enhancement of basal noradrenaline overflow from numerous perip heral sympathetic junctions as seen with fenoterol and angiotensin II, is augmented or dampened, respectively, by baroreceptor reflex-mediat ed changes of sympathetic activity.