SUMMARYWe studied the effect of a-adrenergic stimulation, using phenylephrine, on basal and isoproterenol-provoked renin secretion in the isolated perfused rat kidney. Infusion of phenylephrine increased renal perfusion pressure and prevented the response in renin secretion to isoproterenoL No suppression of basal secretion was observed. Renal vasoconstriction was abolished, and the response in renin secretion to isoproterenol was restored by a-adrenoceptor blockade with phenoxybenzamine. In contrast, when renal vasoconstriction was prevented by dihydralazine, suppression of renin release by phenylephrine still occurred. These observations support an inhibitory effect of a nonvascular aadrenergic mechanism on renin release. We suggest that the a receptor mediating this effect is related directly to the juxtaglomerular cell. Ore Res 45: [435][436][437][438][439] 1979 INTRARENAL ft adrenoceptors play an important role in the stimulation of rerun release by catecholamines. Studies with isoproterenol in the isolated rat kidney (Vandongen et aL, 1973;Vandongen and Greenwood, 1975) and in rat kidney slices (Weinberger et al., 1975;Capponi and Vallotton, 1976) suggest a direct effect on renin secretion without the intervention of a vascular baroreceptor.In contrast, several reports have indicated an opposite, inhibitory role for a adrenoceptors on renin release (Capponi and Vallotton, 1976;Vandongen and Peart, 1974a;Pettinger et al., 1976;Fray and Mayer, 1977). Since renal vasoconstriction invariably accompanies a-adrenergic stimulation, the involvement of a baroreceptor mechanism indirectly suppressing renin release cannot be excluded.In this study, we have attempted to determine the existence of a direct inhibitory effect of a-adrenergic stimulation on renin release by dissociating the renin suppressing and vasoconstrictor actions of phenylephrine infused into the isolated rat kidney. MethodsMale Wistar rats (200-300 g), maintained on a regular diet, were anesthetized with sodium pentobarbital (0.1 mg/g, im) and heparinized (50-100 U, iv). Through a midline incision, the abdominal vessels and the left kidney were exposed, and beveled Teflon cannulas were inserted in the aorta and the vena cava to the junction with the left renal artery and vein, respectively. This procedure permitted perfusion of the kidney without interruption of blood flow. With perfusion fluid flowing, the aorta and the vena cava were tied above the left renal vessels, allowing selective perfusion of the left kidney in situ. The perfusion fluid was delivered as pulsatile flow by a roller pump from a reservoir containing Krebs-Ringer saline with dextran (moL wt. 70,000; Pharmacia) 36 g/liter, oxygenated with 95% 02-5% CO 2 and maintained at 37°C. Perfusion pressure (mm Hg) was continuously recorded, and flow rates (ml/min) were obtained by direct measurement of the venous effluent perfusate. All infusions were given at 0.04 ml/min. After commencing perfusion, we infused either saline (0.16 mol/ liter NaCl) or phenylephrine diluted in saline (10...

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1. The effect of alpha-adrenergic stimulation, with phenylephrine, on isoprenaline-provoked renin secretion was studied in the isolated perfused rat kidney. 2. Infusion of phenylephrine increased renal perfusion pressure and prevented renin secretion in response to isoprenaline. 3. Renal vasoconstriction was abolished and the response in renin secretion to isoprenaline was restored by alpha-adrenoreceptor blockade with phenoxybenzamine. 4. In contrast, when renal vasoconstriction was prevented by dihydrallazine, suppression of renin release by phenylephrine still occurred. 5. These observations support an inhibitory effect of a non-vascular alpha-adrenergic mechanism on renin release. It is suggested that the alpha-receptor mediating this effect is directly related to the renin-producing juxtaglomerular cell.