Effects of PGD2 on canine renal function

Bolger, P. Michael; Eisner, Gilbert M.; Shea, Phillip; Ramwell, Peter W.; Slotkoff, Lawrence M.

doi:10.1038/267628a0

Cited by 47 publications

(14 citation statements)

References 17 publications

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“…Because this effect on renin release can be blocked in vivo and in vitro by indomethacin, an inhibitor of prostaglandin synthesis (6), arachidonic acid must be converted to one of its prostaglandin (PG)l intermediates to exert its action (1,4,5). In similar studies, intrarenal infusions of PGE, and PGE2 (7)(8)(9)(10)(11), PGD2 (9, 10), PGI2 (11), and intravenous infusions of PGA, (12,13) also stimulated the release of renin; however, only the PG endoperoxides, PGG2 and PGH2, or PGI2 could increase the rate at which renin was secreted in vitro from renal cortical slices (4,5). Because the endoperoxides can be converted to PGI2 in the renal cortex (14,15), PGI2 would appear to exert a direct action on juxtaglomerular cells, and from the available evidence, would appear to be the arachidonic acid intermediate regulating the release of renin.…”

Section: Introductionmentioning

confidence: 99%

Role of Renal Prostaglandins in Sympathetically Mediated Renin Release in the Rat

Campbell¹,

Graham²,

Jackson³

1979

J. Clin. Invest.

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A B S T R A C T Renal prostaglandins (PG) appear to mediate renin release due to stimulation of the intrarenal baroreceptor, but not that due to activation of the macula densa. However, as the role of PG in sympathetically mediated renin release remains unclear, a possible interrelationship between these factors was examined in conscious rats. Hydralazine increased the serum renin levels from 3.1±0.8 to 16.7±3.0 ng/ml per h at a dose of 1 mg/kg. Indomethacin (5 mg/kg) suppressed urinary PGE2 and PGF2a excretion by 89 and 74%, respectively, arachidonate hypotension by 82%, and inhibited the elevated renin levels from hydralazine by 100% without altering the hypotensive effect of the drug. Another PG synthetase inhibitor, meclofenamate, was also effective in attenuating hydralazineinduced renin release, urinary PGE2 and PGF2c, excretion, and arachidonate hypotension. Isoproterenol, a nonselective beta-adrenergic agonist, increased heart rate, lowered blood pressure, and also stimulated the release of renin when administered intraperitoneally. However, intrarenal infusion of the drug only resulted in increased renin release. Indomethacin inhibited isoproterenol-induced renin release by 66 and 67%, respectively, without altering the hemodynamic effects associated with the intraperitoneal administration of the drug. The selective beta, agonist, H 133/22, in-creased the release of renin and heart rate in a doserelated manner without altering blood pressure. H133/ 22-induced renin release was inhibited by 80% by indomethacin pretreatment. Finally, intrarenal infusions of dibutyryl cyclic AMP (3 mg/kg per min) increased the serum activity from 4.1±0.2 to 20.4±3.9 ng/ml per h without altering mean arterial pressure. Indomethacin inhibited this renin response to dibutyryl cyclic

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Section: Introductionmentioning

confidence: 99%

Role of Renal Prostaglandins in Sympathetically Mediated Renin Release in the Rat

Campbell¹,

Graham²,

Jackson³

1979

J. Clin. Invest.

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“…This effect of PGE2 may be contrasted to that of PGD2 whose primary action is upon the renal vasculature in the absence of increased urinary Na+ loss. (Bolger et al 1977;Bolger, Eisner, Ramwell, Slotkoff & Corey, 1978). The renal actions of PGE2 and PGI2 in dogs appear to be similar (Bolger et al 1977(Bolger et al , 1978.…”

Section: Introductionmentioning

confidence: 99%

“…(Bolger et al 1977;Bolger, Eisner, Ramwell, Slotkoff & Corey, 1978). The renal actions of PGE2 and PGI2 in dogs appear to be similar (Bolger et al 1977(Bolger et al , 1978. N1S 8280 Inhibition of endogenous PG production in conscious animals is associated with reductions in urinary Na+ outputs in the absence of significant effects upon renal blood flow and glomerular filtration rates (Haylor, 1980;Haylor & Lote, 1980;Kokko, 1981).…”

Section: Introductionmentioning

confidence: 99%

Chloride secretion stimulated by prostaglandin E1 and by forskolin in a canine renal epithelial cell line.

Simmons

1991

The Journal of Physiology

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SUMMARY1. The actions of prostaglandins upon ion transport in a renal-derived cultured epithelium (MDCK) have been investigated.2. Prostaglandin E1 (PGE1) stimulates an inwards short-circuit current (SCC) in voltage-clamped epithelial layers mounted in Ussing chambers. Measurements of transepithelial Cl-fluxes, cation and anion replacement of the bathing media and the use of the Cl-channel blocker 3-nitro-2(3-phenylpropylamino)-benzoic acid (NPPB) are consistent with the PGEl-stimulated inward SCC resulting predominantly from basal to apical Cl-secretion.3. The response of MDCK epithelia is relatively specific for prostaglandins of the E series. PGE1 is most effective when applied to the basal bathing solutions, though near-maximal stimulation of SCC was possible with 1 ,M-PGE, added to the apical bathing solution.4. Forskolin addition (10 /im) stimulates an inwards SCC in MDCK epithelia which displays similar characteristics and is of a similar magnitude to that observed with PGE1. In the presence of isobutylmethylzanthine, PGE1 and forskolin are capable of elevating intracellular cyclic AMP accumulation, suggesting that stimulation of inward SCC is mediated via a cyclic AMP-dependent mechanism.

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“…Indomethacin blocks this increased renin response produced by the administration of arachidonic acid, suggesting that arachidonic acid stimulates renin release after its enzymatic conversion to one or more of its synthetic products, presumably the prostaglandins (Bolger et al, 1976;Data et al, 1978;Lin et al, 1981;Seymour and Zehr, 1979;Weber et al, 1976). Several prostaglandins derived from arachidonic acid metabolism also stimulate renin release when infused into animals (Bolger et al, 1977(Bolger et al, , 1978Echtenkamp et al, 1982;Gerber et al, 1978Gerber et al, ,1979Yun et al, 1977) or when added to in vitro systems (Franco-Saenz et al, 1980;Lin et al, 1981;Whorton et al, 1977Whorton et al, , 1980 and these include PGD 2 , PGI 2 , PGEz, and 13,14-dihydro PGE 2 . These findings are consistent with a direct stimulatory action on the JG cells of one or more prostaglandins derived from precursor arachidonic acid.…”

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confidence: 99%