Role of prostaglandin E2 in mediating the effects of pH on the hydroosmotic response to vasopressin in the toad urinary bladder.

Forrest, Jeffrey Yi‐Lin; Schneider, Carol J.; Goodman, David B. P.

doi:10.1172/jci110475

Cited by 36 publications

(19 citation statements)

References 35 publications

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“…Prostaglandins inhibit the ADH-induced increase in water permeability (29,35) by acting at pre-and post-cAMP steps (35); their synthesis can be activated by Ca2+ (29). Through the use of indomethacin, we indirectly tested the possibility that the extracellular Ca2+-dependent inhibitions may be mediated by endogenous prostaglandins.…”

Section: Effect Of Indomethacin On the Ca2+-mediated Inhibition Ofpumentioning

confidence: 99%

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Roles of Ca2+ and Na+ on the modulation of antidiuretic hormone action on urea permeability in toad urinary bladder.

Hardy¹,

Ware²

1985

J. Clin. Invest.

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The present studies probe the role of Ca2" and Na+ in the stimulation-permeability coupling sequences by which antidiuretic hormone (ADH) induces a cyclic AMP (cAMP)-mediated increase in urea permeability in toad urinary bladder. The following results were obtained: (a) Removal of mucosal Na+ or Ca2" or deletion of serosal Ca2" did not modify ADH action.(b) Reduction of the serosal Na+ concentration to <50 mM inhibited the effects of both ADH and cAMP. The minimal concentration of serosal Na+ needed for the hormone to elicit its maximal effect was reduced to -10 mM if serosal Ca2+ was concomitantly deleted. (c) The Na+ ionophore monensin produced an inhibition of ADH and cAMP actions that was dependent on the presence of Na+ and Ca2" in the serosa. (d)The Ca2+ ionophore A23187 produced a serosal Ca2+-dependent inhibition of ADH effect and did not modify cAMP action. (e) Carbachol, which increases Ca2+ uptake to the same extent that A23187 does, had no effect on ADH action. (f) Quinidine, which releases Ca2" from intracellular stores, produced a large inhibition of the action of ADH but not that of cAMP; the inhibition was greatly reduced if serosal Ca2+ was deleted. (g) Dinitrophenol and iodoacetate, which also release Ca2+ from intracellular pools, had no effect on ADH action. (h) The Ca2+ channel blocker diltiazem had no effect on ADH action and did not modify the inhibitions produced by deletion of serosal Na+ or monensin. (i) The cyclooxygenase inhibitor indomethacin partially removed the inhibition produced by deletion of serosal Na+ and almost completely impeded the inhibitions produced by either monensin or A23187. It is concluded: (a) Extracellular Ca2", Na+ transport rates, and serosal Na+, in concentrations between 10 and 110 mM, have no participation in modulating the increase in urea permeability produced by ADH. (b) Increases in cytosolic Ca2' activity, which are capable of inhibiting the effect of ADH on urea permeability at pre-and/or post-cAMP steps, seem to be highly compartmentalized. (c) Endogenous prostaglandins might play a role in the inhibitions produced by absence of serosal Na+, monensin, or A23187.

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Section: Effect Of Indomethacin On the Ca2+-mediated Inhibition Ofpumentioning

confidence: 99%

“…The indomethacin concentration (lO-1 M) and time of incubation (120 min) employed completely abolishes prostaglandin E2 production (29). Prostaglandin E2 inhibits ADH action on both water permeation and Pu, though it is much more effective on the former than on the latter (2).…”

Section: Effect Of Indomethacin On the Ca2+-mediated Inhibition Ofpumentioning

confidence: 99%

Roles of Ca2+ and Na+ on the modulation of antidiuretic hormone action on urea permeability in toad urinary bladder.

Hardy¹,

Ware²

1985

J. Clin. Invest.

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“…Indeed, a number of previously published studies suggested that acid-base changes did modify PGs synthesis (5)(6)(7)(8)(9)(10).…”

Section: Discussionmentioning

confidence: 99%

“…Many studies have demonstrated that acidification of the serosal medium of the toad bladder inhibits the action of ADH (5)(6)(7)(8)(9). Recently, Forrest et al (9) confirmed these results and demonstrated that acidification of the medium is also associated with increased prostaglandin E2 (PGE2) production. The addition of meclofenamate or indomethacin, inhibitors of PG production, to acidified bladders restored the effect of ADH.…”

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confidence: 99%

Prostaglandins inhibit renal ammoniagenesis in the rat.

Jones¹,

Beck²,

Kapoor³

et al. 1984

J. Clin. Invest.

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Abstract. We describe the inhibitory effect of prostaglandins (PGs) on in vivo rat renal ammonia synthesis. The influence of systemic pH upon urinary PG excretion and ammoniagenesis was also investigated. Finally, PG production by incubated rat renal cortical slices was suppressed to investigate the PG-ammonia interplay in the absence of changes in renal blood flow, glomerular filtration rate, ambient electrolyte concentrations or extrarenal hormonal factors.In vivo ammonia synthesis doubled and PG excretion fell by 44% in normal rats, after intravenous administration of 1 mg/kg of meclofenamate. Higher doses of meclofenamate further augmented ammonia production and further reduced PG excretion. PG depletion was also associated with an increase in fractional excretion of ammonia (FENH3) that was independent of changes in urine flow rate or pH.Acute metabolic acidosis (AMA) increased total ammonia synthesis but also stimulated PG production. Administration of meclofenamate to rats with mild AMA markedly reduced urinary PG excretion, further augmented ammonia synthesis, and significantly increased the FENH3. Inhibition of stimulated PG synthesis during severe AMA did not increase ammoniagenesis or FENH3. Acute metabolic alkalosis did not alter production of PGs or ammonia, but reduced the FENH3 by A preliminary abstract was presented at

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“…In nonosseus cells, metabolic acidosis increases the levels of prostaglandins (1,34,35,41). In both toad bladder (34,35) and rat kidney (41), PGE 2 levels have been shown to increase in response to metabolic acidosis.…”

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confidence: 99%

Metabolic, but not respiratory, acidosis increases bone PGE₂levels and calcium release

Bushinsky

Parker

Alexander

et al. 2001

American Journal of Physiology-Renal Physiology

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. Metabolic, but not respiratory, acidosis increases bone PGE2 levels and calcium release. Am J Physiol Renal Physiol 281: F1058-F1066, 2001. First published July 12, 2001; 10.1152/ajprenal.00355.2001A decrease in blood pH may be due to either a reduction in bicarbonate concentration ([HCO 3 Ϫ ]; metabolic acidosis) or to an increase in PCO2 (respiratory acidosis). In mammals, metabolic, but not respiratory, acidosis increases urine calcium excretion without altering intestinal calcium absorption, indicating that the additional urinary calcium is derived from bone. In cultured bone, chronic metabolic, but not respiratory, acidosis increases net calcium efflux (JCa), decreases osteoblastic collagen synthesis, and increases osteoclastic bone resorption. Metabolic acidosis increases bone PGE2 production, which is correlated with JCa, and inhibition of PGE2 production inhibits this acid-induced JCa. Given the marked differences in the osseous response to metabolic and respiratory acidosis, we hypothesized that incubation of neonatal mouse calvariae in medium simulating respiratory acidosis would not increase medium PGE 2 levels, as observed during metabolic acidosis. To test this hypothesis, we determined medium PGE2 levels and JCa from calvariae incubated at pH ϳ7.1 to model either metabolic (Met; [HCO 3 Ϫ ] ϳ11 mM) or respiratory (Resp; PCO2 ϳ83 Torr) acidosis, or at pH ϳ7.5 as a control (Ntl). We found that after 24-48 and 48-51 h in culture, periods when cell-mediated JCa predominates, medium PGE2 levels and JCa were increased with Met, but not Resp, compared with Ntl, and there was a direct correlation between medium PGE 2 levels and JCa. Thus metabolic, but not respiratory, acidosis induces the release of bone PGE2, which mediates JCa from bone. calvariae; osteoblasts; protons; pH IN HUMANS AND EXPERIMENTAL ANIMALS, chronic metabolic acidosis, a decrease in systemic pH induced by a decrease in serum bicarbonate concentration ([HCO 3 Ϫ ]), increases urine calcium excretion (15, 49, 51) without increasing intestinal calcium absorption (50, 51), resulting in a negative calcium balance (15,50,51). Because Ͼ98% of total body calcium is contained within the bone mineral (83), this negative calcium balance strongly implies a loss of bone calcium. Indeed, in humans dietary intake of acid precursors causes an apparent decrease in bone mineral content, which is reversed by the provision of alkali (50, 67).In contrast, chronic respiratory acidosis, a decrease in systemic pH induced by an increase in PCO 2 , appears to have little (30) or no (48, 65, 66) effect on urine calcium excretion. Clearly, any effect on urine calcium excretion is far less than that induced by metabolic acidosis (30). Serum calcium may increase slightly during respiratory acidosis (48). The lack of an appreciable change in urine calcium excretion during respiratory, compared with metabolic, acidosis suggests a marked difference in the osseous response to these two types of acidosis (10).We have extensively compared the response of cultured bone...

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Role of prostaglandin E2 in mediating the effects of pH on the hydroosmotic response to vasopressin in the toad urinary bladder.

Cited by 36 publications

References 35 publications

Roles of Ca2+ and Na+ on the modulation of antidiuretic hormone action on urea permeability in toad urinary bladder.

Roles of Ca2+ and Na+ on the modulation of antidiuretic hormone action on urea permeability in toad urinary bladder.

Prostaglandins inhibit renal ammoniagenesis in the rat.

Metabolic, but not respiratory, acidosis increases bone PGE₂levels and calcium release

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Role of prostaglandin E2 in mediating the effects of pH on the hydroosmotic response to vasopressin in the toad urinary bladder.

Cited by 36 publications

References 35 publications

Roles of Ca2+ and Na+ on the modulation of antidiuretic hormone action on urea permeability in toad urinary bladder.

Roles of Ca2+ and Na+ on the modulation of antidiuretic hormone action on urea permeability in toad urinary bladder.

Prostaglandins inhibit renal ammoniagenesis in the rat.

Metabolic, but not respiratory, acidosis increases bone PGE2levels and calcium release

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Metabolic, but not respiratory, acidosis increases bone PGE₂levels and calcium release