Failure of α-adrenergic stimulation by phenylephrine to enhance renin secretion in the isolated rat kidney

Strang, K. D.; Vandongen, R.; Poessè, M H; Birkenhäger, W. H.

doi:10.1016/0014-2999(77)90083-8

Cited by 3 publications

(2 citation statements)

References 14 publications

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“…It is evident that only /8-adrenergic stimulated renin secretion is suppressed, with basal levels relatively unaffected, despite similar increases in renal perfusion pressure. This is not due to the shorter duration of renal vasoconstriction, since more prolonged infusion of phenylephrine in another study did not influence basal secretion (Strang et al, 1977). Suppression of basal levels also was not seen during administration of norepinephrine in vasoconstrictor doses (Vandongen and Peart, 1974a).…”

Section: Discussionmentioning

confidence: 86%

Suppression of renin secretion in the rat kidney by a nonvascular alpha-adrenergic mechanism.

Vandongen¹,

Strang²,

Poessè³

et al. 1979

Circulation Research

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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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Section: Discussionmentioning

confidence: 86%

Suppression of renin secretion in the rat kidney by a nonvascular alpha-adrenergic mechanism.

Vandongen¹,

Strang²,

Poessè³

et al. 1979

Circulation Research

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“…A complex interaction between the renin-angiotensin system and the sym-pathetic nervous system has been described in a variety of experiments, both in vitro (Peach 1971) and in vivo . It also is well established that renin release is at least partially adrenergically mediated, being activated through /J-adrenergic receptors (Winer et al, 1969) and inhibited by a-adrenergic receptors (Pettinger et al, 1976, Strang et al, 1977. These data indicate that the renin-angiotensin and the adrenergic systems are interrelated, and that any hemodynamic effects attributed to changes in one system also may be affected by concomitant alterations in the other.…”

mentioning

confidence: 88%

Acute renovascular hypertension in conscious dogs. Interaction of the renin-angiotensin system and sympathetic nervous system in systemic hemodynamics and regional blood flow responses.

Gavras¹,

Liang²

1980

Circulation Research

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The effects of acute renovascular hypertension on the sympathetic nervous system, regional blood flow and cardiac function were studied in conscious dogs submitted to renal artery occlusion by inflation of a cuff implanted previously around one renal artery. We then compared the alterations in plasma renin and catecholamine levels and in the various hemodynamic parameters induced by those maneuvers in intact dogs, to those in dogs pretreated with alpha- and beta-adrenergic receptor blockers. Subsequently, the converting enzyme inhibitor teprotide was administered to inhibit angiotensin formation in both experiments. Our results suggest that both the renin-angiotensin system and the sympathetic system contribute to the rise in blood pressure. The hemodynamic changes and alterations in regional blood flows accompanying this acute hypertension appear to be due mostly to the increase in plasma angiotensin, since prior adrenoceptor blockade only attenuated their magnitude but did not alter their direction. However, angiotensin-induced coronary vasoconstriction was observed only in adrenergically blocked but not intact animals, probably because of the protective effect of baroreceptor-mediated reflex sympathetic coronary vasodilation.

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Effects of Adrenergic Activators and Inhibitors on Kidney Function

Oßwald¹,

Greven²

1981

Adrenergic Activators and Inhibitors

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Failure of α-adrenergic stimulation by phenylephrine to enhance renin secretion in the isolated rat kidney

Cited by 3 publications

References 14 publications

Suppression of renin secretion in the rat kidney by a nonvascular alpha-adrenergic mechanism.

Suppression of renin secretion in the rat kidney by a nonvascular alpha-adrenergic mechanism.

Acute renovascular hypertension in conscious dogs. Interaction of the renin-angiotensin system and sympathetic nervous system in systemic hemodynamics and regional blood flow responses.

Effects of Adrenergic Activators and Inhibitors on Kidney Function

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