Kinin-induced prostaglandin synthesis by renal papillary collecting tubule cells in culture

Grenier, Frank C.; Rollins, Thomas E.; Smith, William L.

doi:10.1152/ajprenal.1981.241.1.f94

Cited by 71 publications

(63 citation statements)

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“…Although bradykinin receptors have been detected in the lamina propria (Manning et al, 1982) there is no incontrovertible evidence that the eicosanoids are actually generated by the transporting epithelial cells themselves. Perhaps the strongest evidence to involve the epithelial cells is that cultures of collecting tubule cells can release eicosanoids when challenged with kinin (Grenier et al, 1981). Our results, for PGE2, have been confirmed in rabbit ileum and colon, where kinin was found to induce a five fold increase in release (Musch et al, 1983).…”

Section: Possible Involvement Ofcyclic Amp In the Responses To Kininssupporting

confidence: 71%

Mediators of the secretory response to kinins

Cuthbert

Halushka

Margolius

et al. 1984

British J Pharmacology

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1 The output of immunoreactive (i) 6 keto prostaglandin Fl, (i6ketoPGF1,). iPGE2 and ithromboxane B2 (iTXB2) from isolated colonic epithelium of the rat into the apical and basolateral bathing solution has been measured. In some instances tissues were also voltage clamped at 0 mV to measure short circuit current (SCC). 2 Kallidin (lysylbradykinin) stimulated the output of all three eicosanoids, specifically from the basolateral face of the tissue. The output was similar whether or not the tissues were short circuited. 3 Both the SCC response and eicosanoid output were dependent upon the concentration of kallidin, but not in a strictly proportional manner, there being relatively more eicosanoid output at submaximal kinin concentrations. 4 Indomethacin, 5 JiM, abolished the eicosanoid output, in response to kinin, while some part of the SCC response remained. 5 Calcium removal from the basolateral bathing fluid severely attenuated the SCC response, reduced the output of i6ketoPGFp, to half, but left the output of iPGE2 unchanged. In the presence or absence of calcium it is probable that sufficient PGE material is released to cause part of the SCC changes seen with kinin. 6 Kinin and PGE1 increased the cyclic AMP content of intact epithelia, provided a phosphodiesterase inhibitor was added at the same time.7 It is proposed that kinin causes an increase in calcium influx at the basolateral pole of the tissue. This calcium is necessary for the production of some eicosanoids and the subsequent generation of cyclic AMP, which then increases apical chloride permeability. In addition, calcium may facilitate entry of chloride through the basolateral face of the cells by activating a cotransport mechanism.

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Section: Possible Involvement Ofcyclic Amp In the Responses To Kininssupporting

confidence: 71%

Mediators of the secretory response to kinins

Cuthbert

Halushka

Margolius

et al. 1984

British J Pharmacology

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“…AVPinduced increases in PGE 2 were also greater in medullary slices from DR versus DS rats. Consistent with previous results, 20 AVP did not increase PGE2 in RPCT cells. Arachidonate increased PGE 2 production to the same absolute level in medullary slices from DR versus DS rats thus suggesting that altered availability of endogenous arachidonate may be the basis for the differences in medullary PGE 2 synthesis.…”

Section: Statisticssupporting

confidence: 93%

Decreased cytosolic calcium and prostaglandin synthesis in prehypertensive rats.

1990

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The capacity of cultured renal medullary interstitial cells derived from Dahl salt-sensitive and salt-resistant rats to synthesize prostaglandin E 2 (PGE 2 ) was compared. Basal and arginine vasopressin (AVP) -induced PGE 2 production by interstitial cells from salt-resistant rats was fourfold to fivefold higher than corresponding values of those from the salt-sensitive rats. Similarly, basal and AVP-responsive release of [ and further supports a role for the interstitial cell as a source of vasodepressor humoral agents. Studies in experimental genetic models of salt-induced hypertension such as the Dahl salt-sensitive (DS) and saltresistant (DR) rat model 5 suggest that inherited differences in the antihypertensive capacity of the renal medulla may explain the differences in the susceptibility of these rats to the development of high blood pressure when they are placed on a high salt diet. Received September 13,1989; accepted in revised form December 11, 1989. Among the factors that have been suggested as contributing to the antihypertensive action of the renal medulla are prostaglandin E2 (PGE2) 6 -9 and antihypertensive polar renomedullary lipid (APRL), 210 a member of a class of lipids, the l-alkyl-2-acylglyceryl-ether phosphorylcholines. The release of arachidonic acid for PGE2 synthesis as well as release of APRL follows activation of cellular lipases and may be triggered by a rise in cytosolic free calcium ([Ca 2+ ]i).u Previous studies in DS and DR rats have demonstrated lower urinary PGE2 excretion and PGE2 content of quick-frozen renal medulla obtained from prehypertensive DS compared with DR rats. 7 -9 The differences in PGE2 persist after the rats are placed on a high salt diet at which point the DS rats become hypertensive, whereas the DR rats remain normotensive. "9 The mechanisms and cell types responsible for this decrease in renal medullary PGE2 production have not been examined in detail. In the present study, we examined 1) the capacity of interstitial cells cultured from the renal medulla of DS or DR rats to synthesize PGE2 basally and in response to vasopressin (AVP), the calcium ionophore A23187, and exogenous arachidonic acid; 2) the relative contribution of

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“…Tissue was prepared by a modification of the methods of GRENIER et al (1981). In brief, male sprague-Dawley rats were anesthetized with pentobarbital (30 mg/kg BW).…”

Section: Methodsmentioning

confidence: 99%

Dual regulatory mechanisms of proton transport in rat papillary collecting duct cells in culture.

et al. 1989

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The regulation of proton transport and cytosolic pH was studied in rat papillary collecting duct (PCD) cells in culture using a pH-sensitive fluorescence probe, 2,7-bis-carboxyethyl-5,6-carboxyfluorescein (BCECF). Data were obtained from confluent monolayers grown on glass coverslips and dipped in a HC03 --free medium, pH 7.40. The resting intracellular pH (pHi) was 7.16 + 0.03 (n = 20). When PCD cells had been acidified by pretreatment with NH4C1, pHi immediately recovered toward the resting value. Two mechanisms participated in this recovery: a Na + -dependent mechanism which could be inhibited by amiloride (indicative of Na+-H+ exchanger) and a Na+-independent process (a proton ATPase). The pHi recovery from acid loading was inhibited by amiloride to about 55% of the control recovery (half maximal effect at 100 µM). The rate of pHi recovery after the readdition of Na+ to a sodium-free medium exhibited saturation kinetics (half maximal rate at 28 mM). Dicyclohexylcarbodiimide (DCCD), an inhibitor of a plasma membrane proton ATPase, and the depletion of cellular ATP induced by 2 mM potassium cyanide (KCN) also partially inhibited the rate of pHi recovery after cell acidification with a NH4C1 load. When PCD cells were treated with 1 mM DCCD, amiloride almost completely inhibited pH, recovery. Amiloride and the removal of external Na+ had induced a gradual fall in pHi to a new resting value and rapidly recovered when Na+ was added. We conclude that PCD cells grown in culture have at least two proton transport mechanisms: a Na+-H+ exchanger and a plasma membrane proton ATPase. The kinetics of these processes can be reliably assessed by the pH-sensitive fluorescent probe, BCECF. Both the Na+-H+ exchanger and the plasma membrane proton ATPase may contribute to urinary acidification.

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Kinin-induced prostaglandin synthesis by renal papillary collecting tubule cells in culture

Cited by 71 publications

References 0 publications

Mediators of the secretory response to kinins

Mediators of the secretory response to kinins

Decreased cytosolic calcium and prostaglandin synthesis in prehypertensive rats.

Dual regulatory mechanisms of proton transport in rat papillary collecting duct cells in culture.

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