Opposition of the vasopressin-induced vasoconstriction in the isolated perfused rat kidney by some prostaglandins

Pace-Asciak, Cecil R.; Rosenthal, A.

doi:10.1016/0090-6980(81)90066-6

Cited by 13 publications

(2 citation statements)

References 10 publications

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“…angiotensin), PGE2 will dilate the renal vasculature (Inokuchi & Malik, 1984;Pace-Asciak & Rosenthal, 1981) by possibly preferentially activating EP2 receptors.…”

Section: Discussionmentioning

confidence: 99%

Effects of endogenous and synthetic prostanoids, the thromboxane A₂ receptor agonist U‐46619 and arachidonic acid on [³H]‐noradrenaline release and vascular tone in rat isolated kidney

Schollmeyer

1989

British J Pharmacology

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1 Rat kidneys were perfused with Krebs-Henseleit solution and the perfusion pressure was monitored. After incubation with [3H]-noradrenaline the renal nerves were stimulated. The stimulationinduced (S-I) outflow of radioactivity was taken as an index of noradrenaline release. The effect of prostaglandins on perfusion pressure, pressor responses to renal nerve stimulation (RNS) and S-I outflow of radioactivity was assessed.2 Prostaglandin E2 (PGE2, 0.06 and 0.6pM), PGF2. (0.6 gM), PGI2 (0.6 and 3.uM) and iloprost (0.6.uM) increased perfusion pressure and enhanced pressor responses to RNS. These facilitatory effects of the prostaglandins were not a result of an enhanced transmitter release. In contrast, PGE2 dose-dependently inhibited, whereas the other prostaglandins failed to modulate S-I outflow of radioactivity. PGE2 (0.6 M) also enhanced pressor responses to exogenous noradrenaline. 3 Arachidonic acid (1 pm) increased perfusion pressure and enhanced pressor responses to RNS. These effects were abolished in the presence of indomethacin (10 pm) suggesting that local production of prostaglandins from exogenous arachidonic acid was responsible for this facilitation.However, arachidonic acid (1 ym) did not modulate S-I outflow of radioactivity. Arachidonic acid (10ym)p despite causing a marked increase in perfusion pressure, failed to alter pressor responses to RNS and only slightly inhibited S-I outflow of radioactivity.4 The thromboxane A2 (TxA2) receptor agonist U-46619 (0.1 pM) increased vascular tone and enhanced pressor responses to RNS. These effects were blocked by the newly developed selective TxA2 receptor antagonist, daltroban (BM 13505; 3 pm), suggesting that these facilitatory effects of U-46619 were due to activation of TxA2 receptors. However, U46619 failed to alter the S-I outflow of radioactivity from rat isolated kidney. 5 The ax-adrenoceptor agonist methoxamine (1 pM) also increased perfusion pressure and enhanced pressor responses to RNS without affecting the S-I outflow of radioactivity in the presence of the prostaglandin synthesis inhibitor indomethacin (10pM). 6 The results suggest that PGE2 modulates noradrenaline release through an inhibitory prejunctional receptor mechanism. There is no evidence for prejunctional PGF2., PGI2 or TxA2 receptors in the rat isolated kidney. All prostaglandins increased vascular tone in the rat isolated kidney and this alone may provide a condition for enhanced pressor responses to RNS since methoxamine also enhanced pressor responses to RNS without affecting S-I outflow of radioactivity. It is probable that postjunctionally active PGF2 and PGI2 is formed locally from exogenous arachidonic acid, but not enough prejunctionally active PGE2 is synthesized to modulate renal transmitter release.

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“…angiotensin), PGE2 will dilate the renal vasculature (Inokuchi & Malik, 1984;Pace-Asciak & Rosenthal, 1981) by possibly preferentially activating EP2 receptors.…”

Section: Discussionmentioning

confidence: 99%

Effects of endogenous and synthetic prostanoids, the thromboxane A₂ receptor agonist U‐46619 and arachidonic acid on [³H]‐noradrenaline release and vascular tone in rat isolated kidney

Schollmeyer

1989

British J Pharmacology

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“…Hedqvist (1981) has put forward evidence suggesting that prostaglandins, particularly PGE2, are significant trans-synaptic modulators of noradrenergic secretion and may help maintain the functional integrity of the effector organ. Whether the modulation of adrenergic transmission by prostaglandins in the isolated perfused kidney is inhibiting or augmentary appears to depend both on the species (Malik & McGiff, 1975) and on the tone of the renal vasculature (Pace-Asciak & Rosenthal, 1981).…”

Section: Introductionmentioning

confidence: 99%

Effect of bumetanide, frusemide and prostaglandin E₂ on the isolated perfused kidney of rat and rabbit

Foy

Nuhu

1984

British J Pharmacology

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1 Rat and rabbit kidneys were isolated, perfused via the renal artery with Krebs solution and perfusion pressure monitored. Dose-response curves to noradrenaline administered as bolus doses or frequency-response curves from transmural arterial electrical stimulation were obtained. 2 A 1 h continuous infusion of bumetanide (0.1 lg ml1) increased the sensitivity of rat kidney vessels to noradrenaline, an effect also seen when bumetanide and flurbiprofen (6 ,tgmlP) were simultaneously perfused. In the rabbit there was a decreased sensitivity to both electrical stimulation and noradrenaline.3 A 1 h continuous infusion of frusemide (6 tg ml-) only altered the effects of electrical stimulation. An increased sensitivity in the rat (abolished by flurbiprofen) and a decreased sensitivity in the rabbit kidney was observed. 4 A 1 h continuous infusion of prostaglandin (PG)E2 (2 ng ml1) increased the sensitivity of rat kidney to both types of stimuli but caused a reduction in the responsiveness of the rabbit kidney to electrical stimuli only. Addition of flurbiprofen only slightly modified these results. 5 The results emphasize and confirm the fundamental difference in reactivity of the rat and rabbit kidney. 6 Bumetanide and frusemide, two ostensibly similar loop diuretics, show significantly different effects on these preparations suggesting that any modification by non-steroidal anti-inflammatory drugs cannot wholly be explained by similar PGE2 induced haemodynamic changes.

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Renal Prostaglandins and Other Eicosanoids

Conrad

Dünn

1992

Comprehensive Physiology

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The sections in this article are: Biochemistry Eicosanoid Synthesis Eicosanoid Degradation Lipoxygenase and Epoxygenase Derivatives of Arachidonic Acid Sites of Renal Eicosanoid Synthesis Mechanism of Peptide Hormone Stimulation of Eicosanoid Synthesis Eicosanoid Receptors and Mechanism of Action of Eicosanoids Prostaglandin Excretion and Secretion Influence of Prostaglandins on Renal Blood Flow and Glomerular Filtration Rate Administration of Prostaglandins and Their Precursors Influence of Cyclooxygenase Inhibition on Renal Blood Flow and Glomerular Filtration Role of Prostaglandins in Renal Autoregulation and Tubuloglomerular Feedback Hormonal Stimulation of Renal Prostaglandin Synthesis Peptide Hormones and Prostaglandin Interactions in the Control of Renal Blood Flow Some Conditions in Which Prostaglandins Exert an Important Vasodilatory Action Summary: Prostaglandins and Renal Hemodynamics Prostaglandins and Renal Water Excretion Capacity of Renal Prostaglandins to Modulate Water Excretion in the Presence of Vasopressin Capacity of Renal Prostaglandins to Modulate Water Excretion When Vasopressin Is Absent or Severely Reduced Vasopressin and Vasopressin Analogs Stimulate Prostaglandin Synthesis in the Kidney Mechanisms by Which Prostaglandins Modulate Renal Water Excretion Prostaglandin Antagonism of AVP ‐Stimulated Water Flow: A Physiologic Phenomenon Mediated through the cyclic‐ AMP System? Summary: Prostaglandins and Renal Water Excretion Staglandins and Sodium Excretion Influence of Prostaglandins and Arachidonic Acid on Renal Sodium Excretion Cyclooxygenase Inhibition and Renal Sodium Excretion Effect of Sodium Intake on Renal Prostaglandin Synthesis and Excretion Nephron Sites Where Prostaglandins Oppose Sodium Absorption Summary: Prostaglandins and Sodium Excretion Contribution of Prostaglandins to the Renal Release of Renin Effects of Exogenous Prostaglandins and Arachidonic Acid on Renal Renin Release Influence of Cyclooxygenase Inhibition on Renal Renin Release Renin Release by the β‐Adrenergic, Renal Baroreceptor, and Macula Densa Mechanisms: Role of Prostaglandins Summary: Prostaglandins and Renin Release Prostaglandins as Mediators of Erythropoietin Release Effect of Prostaglandins on Tubular Transport of Calcium, Phosphate, and Magnesium, and on Renal Ammoniagenesis Calcium Phosphate Magnesium Renal Ammoniagenesis

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Opposition of the vasopressin-induced vasoconstriction in the isolated perfused rat kidney by some prostaglandins

Cited by 13 publications

References 10 publications

Effects of endogenous and synthetic prostanoids, the thromboxane A₂ receptor agonist U‐46619 and arachidonic acid on [³H]‐noradrenaline release and vascular tone in rat isolated kidney

Effects of endogenous and synthetic prostanoids, the thromboxane A₂ receptor agonist U‐46619 and arachidonic acid on [³H]‐noradrenaline release and vascular tone in rat isolated kidney

Effect of bumetanide, frusemide and prostaglandin E₂ on the isolated perfused kidney of rat and rabbit

Renal Prostaglandins and Other Eicosanoids

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Opposition of the vasopressin-induced vasoconstriction in the isolated perfused rat kidney by some prostaglandins

Cited by 13 publications

References 10 publications

Effects of endogenous and synthetic prostanoids, the thromboxane A2 receptor agonist U‐46619 and arachidonic acid on [3H]‐noradrenaline release and vascular tone in rat isolated kidney

Effects of endogenous and synthetic prostanoids, the thromboxane A2 receptor agonist U‐46619 and arachidonic acid on [3H]‐noradrenaline release and vascular tone in rat isolated kidney

Effect of bumetanide, frusemide and prostaglandin E2 on the isolated perfused kidney of rat and rabbit

Renal Prostaglandins and Other Eicosanoids

Contact Info

Product

Resources

About

Effects of endogenous and synthetic prostanoids, the thromboxane A₂ receptor agonist U‐46619 and arachidonic acid on [³H]‐noradrenaline release and vascular tone in rat isolated kidney

Effects of endogenous and synthetic prostanoids, the thromboxane A₂ receptor agonist U‐46619 and arachidonic acid on [³H]‐noradrenaline release and vascular tone in rat isolated kidney

Effect of bumetanide, frusemide and prostaglandin E₂ on the isolated perfused kidney of rat and rabbit