Mechanism of Effect of Prostaglandin E1 on Renal Water Excretion

Berl, Tomás; Schrier, Robert W.

doi:10.1172/jci107203

Cited by 63 publications

(31 citation statements)

References 17 publications

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“…Some authors (21) have suggested that catecholamines may directly suppress the release of vasopressin. While the results of recent investigations suggest that the effect of isoproterenol (17) and prostaglandin (22) on vasopressin release is mediated indirectly as a consequence of alterations in systemic hemodynamics, the present results do not exclude a direct central effect of norepinephrine on vasopressin release. Alternatively, however, the increase in systemic arterial pressure which occurred during the intravenous infusion of norepinephrine could have caused a suppression of vasopressin release or initiated a reflex which in turn led to a diminution in vasopressin release.…”

Section: Resultscontrasting

confidence: 99%

See 1 more Smart Citation

Mechanism of Effect of Alpha Adrenergic Stimulation with Norepinephrine on Renal Water Excretion

Schrier¹,

Berl²

1973

J. Clin. Invest.

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A B S T R A C T The present study was undertaken to investigate the mechanism whereby alpha adrenergic stimulation with intravenous norepinephrine results in a water diuresis. Renal perfusion pressure was kept constant in all experiments by adjustment of a suprarenal aortic clamp. In hydropenic anesthetized dogs the intravenous infusion of norepinephrine (0.5 /g/kg per min) was associated with a mean decrease in urinary osmolality from 616 to 126 mosmol/kg (P < 0.001) which increased to 532 mosmol/kg (P < 0.001) after the infusion was discontinued. During the same period of time the mean free water clearance increased from -0.437 to 1.59 (P < 0.001) and then returned to -0.314 ml/min (P <0.001) after cessation of the infusion. This diuretic effect occurred in both innervated and denervated kidneys and was not ing 20-30 AU/kg per min of vasopressin. These results thus indicate that the water diuresis associated with intravenous norepinephrine is mediated primarily by suppression of vasopressin release rather than by changes in renal hemodynamics, renal innervation, or an effect of norepinephrine on the water permeability of the tubular epithelium.

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Section: Resultscontrasting

confidence: 99%

“…METHODS 33 experiments were performed in 22 mongrel dogs of either sex weighing [20][21][22][23][24][25][26][27][28][29][30] kg. Food was withheld 18 h before study but water was allowed ad lib.…”

Section: Introductionmentioning

confidence: 99%

Mechanism of Effect of Alpha Adrenergic Stimulation with Norepinephrine on Renal Water Excretion

Schrier¹,

Berl²

1973

J. Clin. Invest.

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“…30 experiments were performed in 19 mongrel dogs of either sex weighing [20][21][22][23][24][25][26][27][28][29][30] kg. Food was withhetd from these animals for 18 h before study, but water was allowed ad lib.…”

Section: Methodsmentioning

confidence: 99%

Mechanism of Stimulation of Vasopressin Release during Beta Adrenergic Stimulation with Isoproterenol

Berl¹,

Cadnapaphornchai²,

Harbottle³

et al. 1974

J. Clin. Invest.

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A B S T R A C T Recent studies have demonstrated that the antidiuresis associated with intravenous (i.v.) infusion of the beta adrenergic agonist, isoproterenol (ISO), is mediated by release of endogenous vasopressin. To examine whether beta-adrenergic stimulation causes vasopressin release by a direct cerebral action, ISO was infused into the carotid artery in a dose estimated to equal the amount of catecholamine reaching the cerebral circulation in the i.v. studies. This intracarotid infusion did not alter renal or systemic hemodynamics, urinary osmolality (Uosm) or free-water clearance (CH20). Although renal perfusion pressure was maintained constant in all experiments i.v. ISO was consistently associated with a decrease in total peripheral resistance and systemic arterial pressure as cardiac output increased. To investigate whether the decrease in cerebral perfusion pressure with i.v. ISO might be responsible for vasopressin release, the carotid arteries were bilaterally constricted both above and below the carotid sinus to lower carotid perfusion pressure by a mean of 25 mmHg, a decrement comparable to that observed during i.v. ISO. Constriction of the carotid arteries above the carotid sinus did not affect Uosm or CHIo, while constriction below the sinus was associated with an antidiuresis as Uosm increased from 155±25 to 385+58 mosmol/kg (P < 0.001) and CH2o decreased from 1.20 to -0.44 ml/min (P < 0.001). This antidiuresis was not significantly different from that observed during i.v. ISO. Since these results suggested that changes in autonomic neural tone from arterial baroreceptors are responsible for vasopressin release with i.v. ISO, studies were performed in animals with denervated baroreceptors. While sham-operated animals and animals with bilateral cervical vagotomy showed a reversible antidiuresis with i.v. ISO infusion, dogs with complete denervation of arterial baroreceptors did not show a significant alteration in renal water excretion (Uosm, 187 to 182 mosmol/kg and CH0o, 0.59 to 0.74 ml/min). The results therefore indicate that ISO stimulates vasopressin release by altering baroreceptor tone rather than by a direct central or depressor effect of the catecholamine. These same baroreceptor pathways have been recently shown to be involved in the suppression of vasopressin release with norepinephrine and may well be the common pathway whereby nonosmotic stimuli control vasopressin release.

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“…They concluded that a sudden variation in blood pressure is probably the most important stimulus for vasopressin secretion. Infusion of PGE1 generally induces diuresis, but Berl and Schrier (28) reported that the intravenous administration of PGE1 in a high dose (7 /tg/min) produced an antidiuresis, and suggested that this antidiuresis was due to the release of ADH provoked by the systemic hemodynamic effects of the high intravenous dose of PGE1, because the antidiuretic effect of intravenous PGE1 was not observed in hypophysectomized dogs. The antidiuresis induced by the high intravenous dose of PGI2…”

Section: Discussionmentioning

confidence: 99%

Effects of prostaglandin E2, I2 and F2.ALPHA. on systemic and renal hemodynamics, renal function and renin secretion in anesthetized dogs.

Hashimoto

1980

Jpn.J.Pharmacol

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Abstract-Effects of intrarenal-arterial (i.r.a.) and intravenous (i.v.) infusions of PGE2, 12 and Fza on systemic blood pressure (BP), heart rate (HR), renal blood flow (RBF), urine volume (UV), renal function and plasma renin activity (PRA) of the renal venous blood (RVPRA) were investigated. A dose-dependent fall in BP was observed with PGE2 and 12 and was accompanied by a tachycardia (PGE2<12, i.r.a. 12, i.r.a.>i.v.), however, antidiuresis was observed with the highest intravenously given dose of PGI2 (300 ng/kg/min) such being ascribed to a pronounced hypotension. Changes in electrolyte excretion induced by PGE2 and 12 were similar to the pattern of those in RBF or UV. Neither PGE2 or 12 produced any significant changes in the glomerular filtration rate (GFR). The diuretic effect of PGE2 and Fza correlated with osmolar clearance (Cos,71) (r-0.89, p<0.01 ; r=0.55, p<0.01) and free water clearance (Cixzo) (r=0.52, p<0.01 ; r=0.83, p<0.01), whereas that of PGI2, only with Cosm (r=0.74, p<0.01).PGF2a produced the weakest changes in the parameters described above. PGE2 and 12 (30 ng/kg/min, i.r.a.), but not PGF2a, produced a significant elevation of RVPRA without any significant change in BP. These findings suggest that PGE2 plays a primary role in the kidney, whereas PG12 is important in the regu lation of the systemic circulation, and that PGE2, 12 and F2a all have different modes of action in producing diuresis. Both PGE2 and 12 may participate in the control of renin secretion. PGI2 (prostacyclin; originally called PGX) was first labelled as an unstable substance that inhibited platelet aggregation (1) and has been shown to be synthesised in arteries, veins, heart, kidney and other tissues in different species including humans (1-5). This PG has a different biological property from PGE2, since PGI2 survives the inactivation in the lung (6), while PGE2 is largely inactivated during a single passage through the lung (7), and is thought to be a circulating hormone. PGI2 causes vasodilatation in rats (8) and dogs (9), and has a vasodepressor action of approximately 4-8, 2 and 10 times greater than that of PGE2 in rats, rabbits (10) and dogs (11), respectively. The renal action of PGI2 has, however, been less intensely investigated. There is no systematic comparison of the renal effects of PGE2, 12 and F2,1 in extensive dose ranges, and to my knowledge, there are no reports dealing with the renal effects of PGI2 in relation to its systemic and renal hemodynamic effects.In the present study, an attempt was made to delineate the direct action of PG's on the excretory function of the kidney, differentiating it from hemodynamic intervention. For that purpose, the effects of PGE2, 12 and F2, on systemic and renal hemodynamics and renal

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Mechanism of Effect of Prostaglandin E1 on Renal Water Excretion

Cited by 63 publications

References 17 publications

Mechanism of Effect of Alpha Adrenergic Stimulation with Norepinephrine on Renal Water Excretion

Mechanism of Effect of Alpha Adrenergic Stimulation with Norepinephrine on Renal Water Excretion

Mechanism of Stimulation of Vasopressin Release during Beta Adrenergic Stimulation with Isoproterenol

Effects of prostaglandin E2, I2 and F2.ALPHA. on systemic and renal hemodynamics, renal function and renin secretion in anesthetized dogs.

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