Effect of prostaglandin E1 on the permeability response of the isolated collecting tubule to vasopressin, adenosine 3′,5′-monophosphate, and theophylline

Grantham, Jared J.; Orloff, Jack

doi:10.1172/jci105804

Cited by 459 publications

(158 citation statements)

References 9 publications

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“…Previous studies have established that vasopressin stimulates the formation of PGE 2 in mesangial and tubular epithelial cells and increases the urinary excretion of PGE 2 (20,44,46). PGE 2 modulates both the tubular and vascular responses to vasopressin (9,15,38). However, much less is known about the possible effect of vasopressin on the formation of EETs and 20-HETE in the kidney or whether CYP metabolites of AA contribute to the effects of AVP on renal vascular and tubular function.…”

Section: Discussionmentioning

confidence: 99%

CytochromeP-450-dependent metabolism of arachidonic acid in the kidney of rats with diabetes insipidus

Sarkis¹,

Ito²,

Mori³

et al. 2005

American Journal of Physiology-Renal Physiology

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. Cytochrome P-450-dependent metabolism of arachidonic acid in the kidney of rats with diabetes insipidus. Am J Physiol Renal Physiol 289: F1333-F1340, 2005. First published July 12, 2005 doi:10.1152/ajprenal.00188.2005.-This study compared the renal metabolism of arachidonic acid in Brattleboro (BB) (vasopressin deficient) and Long-Evans (LE) control rats and the effects of a cytochrome P-450 (CYP) inhibitor 1-aminobenzotriazole (ABT) on renal function in these animals. The production of 20-hydroxyeicosatetraenoic acid (20-HETE) by renal cortical and outer medullary microsomes was significantly greater in BB than in LE rats (155 Ϯ 16 vs. 92 Ϯ 13 and 59 Ϯ 7 vs. 33 Ϯ 3 pmol ⅐ min Ϫ1 ⅐ mg protein Ϫ1 ). Renal cortical epoxygenase activity was not different in these strains. The expression of CYP4A proteins was 58 and 78% higher in the renal cortex and outer medulla of BB than in LE rats. Chronic treatment of BB rats with a vasopressin type 2 receptor agonist for 1 wk normalized the renal production of 20-HETE. Chronic blockade of the formation of 20-HETE and EETs with ABT had little effect on renal function in LE rats. However, urine flow increased by 54% and urine osmolarity decreased by 33% in BB rats treated with ABT. Plasma levels of oxytocin fell significantly from 7.2 Ϯ 1.3 to 3.9 Ϯ 1.0 pg/ml. The effects of ABT in BB rats were attenuated by chronic infusion of oxytocin (0.7 ng ⅐ min Ϫ1 ⅐ 100 g Ϫ1 ) to maintain fixed high plasma levels of this hormone. These results indicate that the expression of CYP4A protein and the renal formation of 20-HETE are elevated in the kidney of BB rats due to a lack of vasopressin and that chronic blockade of the formation of 20-HETE and EETs with ABT promotes water excretion in vasopressin-deficient BB rats by reducing the circulating levels of oxytocin, which is a weak vasopressin agonist. Brattleboro rats; 20-hydroxyeicosatetraenoic acid; cytochrome P-450; epoxyeicosatrienoic acid; renal hemodynamics ARACHIDONIC ACID (AA) is metabolized by cytochrome P-450 (CYP) enzymes in the kidney to produce epoxyeicosatrienoic acids (EETs), 20-hydroxyeicosatetraenoic acid (20-HETE), and dihydroxyeicosatrienoic acids (DiHETEs). These compounds have been reported to play an important role in the control of both renal tubular and vascular function (26). EETs are potent endothelial-derived vasodilators in the renal circulation (17, 47). They also inhibit sodium and water reabsorption in the collecting duct (40). In contrast, 20-HETE is produced by vascular smooth muscle cells and is a potent constrictor of renal arterioles (5,19,23). Inhibition of the synthesis of 20-HETE attenuates the vasoconstrictor response of renal arterioles to elevations in transmural pressure in vitro (16, 18) and autoregulation of renal blood flow and tubuloglomerular feedback responses in vivo (8,48). At the level of the renal tubules, 20-HETE inhibits sodium reabsorption in the proximal tubule and thick ascending limb of the loop of Henle (6,32,34,39).Previous studies indicated that the renal production of EETs an...

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Section: Discussionmentioning

confidence: 99%

CytochromeP-450-dependent metabolism of arachidonic acid in the kidney of rats with diabetes insipidus

Sarkis¹,

Ito²,

Mori³

et al. 2005

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

show abstract

“…Based on the data from separate in vitro perfusion studies of Stokes et al and Iino et al (3,4), it is clear that PGE2 inhibits sodium transport in the rabbit CCD in addition to its well known modulation of vasopressin-stimulated water permeability (6,22,23). Studies examining the interaction of PGE2 with vasopressin and cyclic AMPstimulated water permeability, suggest that PGE2 interacts with at least three different signaling mechanisms in the rabbit CCD: (a) a pathway linked to stimulation ofthe hydraulic conductivity via increased cAMP accumulation; (b) a second pathway coupled through Gi by which PGE2 inhibits hydrosmotic water flow in response to vasopressin by decreasing cAMP accumulation; (c) and finally, a third pathway by which PGE2 can also release cell calcium from intracellular stores.…”

Section: Discussionmentioning

confidence: 99%

“…There is also evidence that Ca"+ inhibits apical sodium permeability indirectly through activating protein kinase C (28 (6,22,23).…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E2 inhibits sodium transport in rabbit cortical collecting duct by increasing intracellular calcium.

Hébert¹,

Jacobson²,

Breyer³

1991

J. Clin. Invest.

123

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“…Indications have arisen from in vitro studies that prostaglandin El (PGE,)1 blunts the ability of vasopressin to increase water permeability of the distal nephron (1,2). Experiments in our laboratory have recently shown that drugs that inhibit prostaglandin synthesis potentiate the in vivo hydro-osmotic action of vasopressin in the anesthetized dog (3).…”

Section: Introductionmentioning

confidence: 99%

In vivo effect of indomethacin to potentiate the renal medullary cyclic AMP response to vasopressin.

Lum¹,

Aisenbrey²,

Dünn³

et al. 1977

J. Clin. Invest.

118

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Effect of prostaglandin E1 on the permeability response of the isolated collecting tubule to vasopressin, adenosine 3′,5′-monophosphate, and theophylline

Cited by 459 publications

References 9 publications

CytochromeP-450-dependent metabolism of arachidonic acid in the kidney of rats with diabetes insipidus

CytochromeP-450-dependent metabolism of arachidonic acid in the kidney of rats with diabetes insipidus

Prostaglandin E2 inhibits sodium transport in rabbit cortical collecting duct by increasing intracellular calcium.

In vivo effect of indomethacin to potentiate the renal medullary cyclic AMP response to vasopressin.

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