Prostaglandins and the Kidney

McGiff, John C.; Itskovitz, Harold D.

doi:10.1161/01.res.33.5.479

Cited by 124 publications

(36 citation statements)

References 57 publications

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“…This is compatible with the data of Lipson and Sharp (24), who found that the application of PGE to the serosal side of the toad bladder increased short circuit current and sodium transport. These findings are of major interest, because of the view that the renal action of PGE is primarily at the local site of production in the renal medulla (25). In this regard, the data in Table I suggest that the natriuretic action of prostaglandin inhibition is most likely beyond the distal tubule since urinary volume and potassium excretion were not increased, while urinary sodium concentration rose fourfold.…”

Section: Re Sultsmentioning

confidence: 90%

The effect of inhibition of prostaglandin synthesis on urinary sodium excretion in the conscious dog.

Kirschenbaum¹,

Stein²

1976

J. Clin. Invest.

115

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A B S T R A C T Studies were performed to determine the effect of decreased endogenous release of renal prostaglandins on urinary sodium excretion. Two structurally dissimilar inhibitors of prostaglandin synthesis were employed, and studies were performed in conscious dogs allowed to recover from prior surgical instrumentation. Either meclofenamate (2 mg/kg) or the competitive prostaglandin inhibitor RO 20-5720 (1 mg/kg) was given to seven unanesthetized dogs undergoing a water diuresis. The administration of either prostaglandin inhibitor did not alter glomerular filtration rate, renal plasma flow, urinary volume, or potassium excretion. Sodium excretion, however, increased from 32 to 130 ueq/min (P <0.02). Essentially, the entire increase in sodium excretion was due to an increase in urinary sodium concentration from 7.7 to 28.3 meq/liter (P < 0.02). On a different day, the same animals were studied before and after administration of the diluent of the prostaglandin inhibitor. No change was noted in sodium excretion or any other parameter.Thus, these findings suggest that prostaglandin inhibition in the conscious dog is associated with a natriuresis without a change in urinary volume or potassium excretion during water diuresis. This may indicate that the natriuresis was due to diminished sodium reabsorption beyond the distal tubule.

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Section: Re Sultsmentioning

confidence: 90%

The effect of inhibition of prostaglandin synthesis on urinary sodium excretion in the conscious dog.

Kirschenbaum¹,

Stein²

1976

J. Clin. Invest.

115

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“…The activity of the prostaglandin synthetase in rat papilla and medulla is less than in rabbit kidney papilla and medulla. Increased synthesis of renal PGE2, in vivo, could possibly modulate the blood pressure and thereby minimize its deleterious effects on the renal vasculature through the vasodilatory and natriuretic properties of PGE2 (6). The potential actions of enhanced PGFi.…”

Section: Discussionmentioning

confidence: 99%

“…The major renal prostaglandin which could serve an antihypertensive function is prostaglandin E2 (PGE2)1 since it is vasodilatory and natriuretic in most species (2). Although PGA2 also shares these pharmocologic properties (4), there is considerable disagreement about the physiologic importance and biochemical origin of PGA2 (5,6). Previous publications have asserted that renal prostaglandin secretion increases in experimental hypertension (3,(7)(8)(9) or contrariwise that prostaglandin production by the kidney decreases in hypertension (10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

Renal prostaglandin synthesis in the spontaneously hypertensive rat.

Dünn¹

1976

J. Clin. Invest.

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A B S T R A C T Tlhe precise role of the kidney in spontaneous experimental hypertension is unknown. We have analyzed the rates of renal prostaglandin synthesis by utilizing a spontaneously hypertensive rat model. The synthetic rate of prostaglandin E2, prostaglandin F2a, and prostaglandin A2-like products was measured in vitro with renal microsomes. In the rabbit and rat there is a steep gradient of microsomal prostaglandin synthetase from papilla to cortex with highest activities in the papilla. Comparison of the activity of prostaglandin synthetase in medullary microsomes from normotensive and hypertensive rats showed accelerated synthesis in the spontaneously hiypertensive rat. These differences appeared after several months of age, were statistically significant from 3 mo of age and, on the average, represented at least a twofold increase of in vitro activity.All classes of prostaglandins were involved with increased synthesis of prostaglandin E2, prostaglandin F2, and prostaglandin A2-like material. These data reenforce and extend previous work showing alterations of granularity and presumably prostaglandin synthesis in renal medullary interstitial cells in various experimental hypertensions.We also measured renal tissue content of prostaglandin E and prostaglandin A-prostaglandin B by radioimmunoassay. Swift and careful handling of the tissue was necessary to avoid extensive postmortem synthesis of prostaglandins. In rapidly-frozen medullary tissue only prostaglandin E was detectable in concentrations ranging from 10 to 200 pg/mg tissue. No significant differences were found in the medullary content of Presented at the second U.S.-Japan seminar on the spontaneously hypertensive rat, April 1976, Newport Beach, Calif.

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“…Prostaglandin E2 is the most abundant renal prostaglandin and is a potent vasodilator (Lee, Crowshaw, Takman, Attrep & Gougoutas, 1967;Daniels, Hinman, Leach & Muirhead, 1967). Consequently, it has been postulated that this prostaglandin has a physiological role in blood flow regulation in the kidney (McGiff, Crowshaw, Terragno & Lonigro, 1970;Lonigro, Terragno, Malik & McGiff, 1973;McGiff & Itskovitz, 1973;Herbaczynska-Cedro & Vane, 1973Larsson & Anggard, 1974;Needleman, Douglas, Jalsetik, Stoecklein & Johnson, 1974). It has in addition been shown that both renal nerve stimulation (RNS) and catecholamine administration increase the output of prostaglandins in the renal venous effluent of rabbits, prostaglandin E2 being most abundant (Davis & Horton, 1972;Needleman et al, 1974).…”

Section: Introductionmentioning

confidence: 99%

Evidence for Prostaglandin Mediated Prejunctional Control of Renal Sympathetic Transmitter Release and Vascular Tone

Frame

Hedqvist

1975

British J Pharmacology

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I Prostaglandin E2 dose-dependently and reversibly inhibited the noradrenaline overflow resulting from nerve stimulation of the rabbit kidney. 2 The magnitude of this inhibition varied inversely with the frequency of stimulation employed. 3 The prostaglandin synthesis inhibitors, indomethacin and meclofenamic acid, both increased the transmitter overflow resulting from renal nerve stimulation, suggesting that endogenous prostaglandin has a role in the regulation of transmitter release. 4 In the presence of indomethacin, the inhibitory effect of exogenous prostaglandin E2 was enhanced. 5 The prostaglandin precursor, arachidonic acid, also caused a significant, dose-dependent and reversible inhibition of transmitter overflow. This inhibition became insignificant when arachidonic acid was applied in the presence of indomethacin, suggesting that the inhibition was mediated by newly formed prostaglandin rather than by arachidonic acid itself. 6 It is proposed that newly formed prostaglandin controls noradrenaline release primarily from inner cortical nerve endings, thereby maintaining juxtamedullary blood flow under periods of increased sympathetic nerve activity.

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Prostaglandins and the Kidney

Cited by 124 publications

References 57 publications

The effect of inhibition of prostaglandin synthesis on urinary sodium excretion in the conscious dog.

The effect of inhibition of prostaglandin synthesis on urinary sodium excretion in the conscious dog.

Renal prostaglandin synthesis in the spontaneously hypertensive rat.

Evidence for Prostaglandin Mediated Prejunctional Control of Renal Sympathetic Transmitter Release and Vascular Tone

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