Effect of bumetanide, frusemide and prostaglandin E<sub>2</sub> on the isolated perfused kidney of rat and rabbit

Foy, J. M.; Nuhu, Saleh

doi:10.1111/j.1476-5381.1984.tb16455.x

Cited by 7 publications

(1 citation statement)

References 24 publications

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“…This vasoconstrictor effect of PGE2 is in accord with results of other workers using isolated rat tissues. In the rat liver (Haussinger et al, 1987) and kidney (Malik & McGiff, 1975;Foy & Nuhu, 1984) stimulation periods (S, and S2) each at 1Hz for 30s. Drugs were added 15min before S2.…”

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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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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Effects of Diuretics on Renal Function

Puschett

Winaver

1992

Comprehensive Physiology

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The sections in this article are: Diuretic Effects on Renal Hemodynamics Drugs That Primarily Alter Glomerular Function Drugs That Primarily Alter Tubular Function Diuretic Effects on Intrarenal Blood Flow Distribution Diuretic Interactions with the Renin–Angiotensin‐Aldosterone system Diuretic Interactions with Prostaglandin Synthesis and with the Inhibition of Prostaglandin Synthetase Nephron Sites of Action and Effects of Diuretics on Solute Excretion Review and Comparison of Methodologies Utility of the Clearance Technique for the Study of Diuretic Site and Mechanism of Action in Man Diuretic Effects on the Excretion of Specific Solutes Cellular and Molecular Actions of Diuretics Carbonic Anhydrase Inhibitors Loop Diuretics Thiazides Mineralcorticoid Antagonists Amiloride

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A Decade of Developments in Diuretic Drug Therapy

Martinez

1986

The Journal of Clinical Pharma

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New diuretics introduced into clinical medicine during the past decade include potent new loop diuretics such as bumetanide and piretanide, the uricosuric indanyloxyacetic acid derivative indacrinone, and a new generation of sulfamoyl diuretics such as indapamide and xipamide, which are recommended primarily for the treatment of hypertension. Pharmacokinetic studies of individual diuretics have demonstrated that the diuretic and natriuretic responses to the newer agents generally follow the plasma drug concentration-time curves and urinary drug excretion rates. Therapeutic monitoring can therefore be achieved in most patients with edema or hypertension by close clinical observation and laboratory analysis of plasma electrolyte and creatinine concentrations and urinary electrolyte excretion rates. Interest in the mechanisms involved in the renal and extrarenal vascular actions of the newer diuretics has led to a better understanding of how changes in venous compliance, peripheral vascular resistance, and renal blood flow distribution may contribute to the overall therapeutic response to these agents, especially in patients with severe congestive heart failure, renal insufficiency with low glomerular filtration rates, and hypertension with cardiorenal complications. Adverse reactions to modern diuretics, which are mainly an extension of their renal pharmacodynamic effects, have proved to be minimal, provided that the dosage is adjusted to meet but not exceed individual patient requirements. However, the long-term consequences of prolonged periods of diuretic-induced alterations in plasma potassium levels, and metabolic effects that include elevated blood lipids, are still under investigation.

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

Cited by 7 publications

References 24 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

Effects of Diuretics on Renal Function

A Decade of Developments in Diuretic Drug Therapy

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

Cited by 7 publications

References 24 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

Effects of Diuretics on Renal Function

A Decade of Developments in Diuretic Drug Therapy

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Product

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

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