Regulation of renal function by prostaglandin E receptors

Breyer, Matthew D.; Zhang, Ya-Hua; Guan, Youfei; Hao, Chuan‐Ming; Hébert, Richard; Breyer, Richard M.

doi:10.1046/j.1523-1755.1998.06718.x

Cited by 85 publications

(86 citation statements)

References 64 publications

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“…Although such a function in reproductive physiology has not previously been ascribed to these lipids, it is consistent with the diverse actions of PGs in numerous organ systems. For example, PGs have been shown to modify ion transport in a number of epithelia (27,28). It is possible that the ionic composition of the oviductal fluid is altered in the Ep2 -/-animals and that this, in turn, leads to reduced fertilization.…”

Section: Figurementioning

confidence: 99%

“…It is well established that PGs can stimulate renin release through actions on the juxtaglomerular apparatus; hormones that increase intracellular cAMP levels stimulate renin release by these specialized cells (35). Because 2 EP receptors, EP2 and EP4, are G s protein-coupled, it has been suggested that one or both of these receptors may mediate this action of PGE 2 (28,36).…”

Section: Figurementioning

confidence: 99%

See 1 more Smart Citation

Reproductive failure and reduced blood pressure in mice lacking the EP2 prostaglandin E2 receptor

Tilley

Audoly

Hicks³

et al. 1999

J. Clin. Invest.

233

134

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Section: Figurementioning

confidence: 99%

Section: Figurementioning

confidence: 99%

Reproductive failure and reduced blood pressure in mice lacking the EP2 prostaglandin E2 receptor

Tilley

Audoly

Hicks³

et al. 1999

J. Clin. Invest.

233

134

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“…Eicosanoids have been demonstrated to regulate the transepithelial NaCl transport in the mTAL (1,2,13,15,20). Moreover, a large body of evidence indicates that cytochrome P-450-dependent metabolites of arachidonic acid (AA) play an important role in regulating a variety of ion transporters in the kidney (8,23,27,29).…”

mentioning

confidence: 99%

Arachidonic acid inhibits K channels in basolateral membrane of the thick ascending limb

Wang

2002

American Journal of Physiology-Renal Physiology

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We have used the patch-clamp technique to study the effect of arachidonic acid (AA) on the basolateral K channels in the medullary thick ascending limb (mTAL) of rat kidney. An inwardly rectifying 50-pS K channel was identified in cell-attached and inside-out patches in the basolateral membrane of the mTAL. The channel open probability (Po) was 0.51 at the spontaneous cell membrane potential and decreased to 0.25 by 30 mV hyperpolarization. The addition of 5 M AA decreased channel activity, identified as NPo, from 0.58 to 0.08 in cell-attached patches. The effect of AA on the 50-pS K channel was specific because 10 M cis-11,14,17-eicosatrienoic acid had no significant effect on channel activity. To determine whether the effect of AA was mediated by AA per se or by its metabolites, we examined the effect of AA on channel activity in the presence of indomethacin, an inhibitor of cyclooxygenase, or N-methylsulfonyl-12,12-dibromododec-11-enamide (DDMS), an inhibitor of cytochrome P-450 monooxygenase. Inhibition of cyclooxygenase increased channel activity from 0.54 to 0.9. However, indomethacin did not abolish the inhibitory effect of AA on the 50-pS K channel. In contrast, inhibition of cytochrome P-450 metabolism not only increased channel activity from 0.49 to 0.83 but also completely abolished the effect of AA. Moreover, addition of DDMS can reverse the inhibitory effect of AA on channel activity. The notion that the effect of AA was mediated by cytochrome P-450-dependent metabolites of AA is also supported by the observation that addition of 100 nM of 20-hydroxyeicosatetraenoic acid, a main metabolite of AA in the mTAL, can mimic the effect of AA. We conclude that AA inhibits the 50-pS K channel in the basolateral membrane of the mTAL and that the effect of AA is mainly mediated by cytochrome P-450-dependent metabolites of AA.cyclooxygenase; cytochrome P-450 -oxidation; 20-hydroxyeicosatetraenoic acid; basolateral K channel K CHANNELS IN THE BASOLATERAL membrane of the medullary thick ascending limb (mTAL) play an important role in the regulation of epithelial transport in the loop of Henle. The basolateral K channels in the mTAL are responsible for K recycling across the basolateral membrane and participate in generating the cell membrane potential (Fig.

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“…Although studies with higher doses could help clarify this, indomethacin, nevertheless, has been shown to decrease urine output in conscious rats (13,18). This effect of indomethacin on urine flow has been attributed to its ability to inhibit prostaglandin synthesis, in particular prostaglandin E 2 (PGE 2 ), which inhibits vasopressin-stimulated water reabsorption in the collecting duct via EP3 receptor activation (19,20). Consequently there is increased tubular reabsorption of water resulting in decreased urine output.…”

Section: Discussionmentioning

confidence: 99%

Comparative Effects of Indomethacin and Nabumetone on Urine and Electrolyte Output in Conscious Rats

2005

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Abstract. The effects of indomethacin and nabumetone on urine and electrolyte excretion in conscious rats were examined. Male Sprague-Dawley rats were housed individually for a fiveweek duration, consisting of acclimatization, control, experimental, and recovery phases. During the experimental phase, rats were given either indomethacin (1.5 mg ⋅ kg −1 body weight ⋅ day −1 in 0.5 ml saline, n = 10), nabumetone (15 mg ⋅ kg −1 body weight ⋅ day −1 0.5 ml saline, n = 10), or 0.5 ml saline alone (n = 10) for a period of two weeks. Water and food intake, body weight, urine output, and electrolyte excretions were estimated. Data were analyzed using two-way ANOVA. Urine output in the indomethacin-and nabumetone-treated groups was not different from the controls, but was significantly different between the drug-treated groups (P<0.01). Sodium, potassium, calcium, and magnesium excretions were not different between nabumetone-treated and control rats. However, sodium and potassium excretion was significantly lower in rats receiving indomethacin when compared to the control rats. Calcium and magnesium outputs, although did not differ from the controls, nevertheless decreased significantly with indomethacin (P<0.01). It appears that indomethacin and nabumetone when given at maximum human therapeutic doses may affect urine and electrolyte output in conscious rats.

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Regulation of renal function by prostaglandin E receptors

Cited by 85 publications

References 64 publications

Reproductive failure and reduced blood pressure in mice lacking the EP2 prostaglandin E2 receptor

Reproductive failure and reduced blood pressure in mice lacking the EP2 prostaglandin E2 receptor

Arachidonic acid inhibits K channels in basolateral membrane of the thick ascending limb

Comparative Effects of Indomethacin and Nabumetone on Urine and Electrolyte Output in Conscious Rats

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