Vasopressin-stimulated prostaglandin E biosynthesis in the toad urinary bladder. Effect of water flow.

Zusman, Randall M.; Keiser, Harry R.; Handler, Jerome S.

doi:10.1172/jci108893

Cited by 121 publications

(54 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…PMA did increase PGE2 levels, an effect that has been described in Madin-Darby canine kidney cells (19), and would tend to block the effects of AVP (13,20). Nonetheless, inhibition ofAVP-stimulated transport persisted even when the tissues were incubated with sufficient naproxen to block prostaglandin synthesis completely.…”

Section: Resultsmentioning

confidence: 65%

“…This pattern of response would suggest that the inhibitory effect of PMA on forskolin-stimulated flow is not a direct one, but instead is secondary to increased prostaglandin production. To eliminate effects of PMA via metabolites of arachidonic acid other than prostaglandins, we performed transport experiments in the presence of mepacrine, a phospholipase inhibitor that prevents the release ofarachidonic acid from phospholipids (20). In the presence of mepacrine (0.1 mM), PMA (200 ng/ml) also decreased water flow in response to AVP (1 mU/ml) from 20±3 to 14±2 ul/min; n = 12; P < 0.05.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Inhibition of vasopressin-stimulated water flow in toad bladder by phorbol myristate acetate, dioctanoylglycerol, and RHC-80267. Evidence for modulation of action of vasopressin by protein kinase C.

Schlöndorff¹,

Levine²

1985

J. Clin. Invest.

View full text Add to dashboard Cite

The action of vasopressin (AVP) in transporting epithelia is mediated by cyclic AMP (cAMP), whereas its effects in hepatocytes are mediated by calcium and phosphoinositides. Based on our recent observation that AVP stimulates phosphoinositide turnover in toad bladder, we examined the role of calcium-phospholipid-dependent kinase (protein kinase C) as a modulator of AVP's hydroosmotic effect. Phorbol myristate acetate (PMA), which can substitute for diglyceride as an activator of protein kinase C, the diglyceride dioctanoylglycerol, and RHC-80267, a glyceride lipase inhibitor that should increase diglyceride levels, inhibited AVP-stimulated water flow, but not water flow stimulated by cAMP, suggesting inhibition ofcyclic AMP production. Both the dioctanoylglycerol and RHC-80267, but not PMA, also decreased water flow in response to 8-bromo cAMP indicating a potential inhibition at post-cAMP events as well. PMA increased prostaglandin synthesis; however, inhibition of water flow persisted even when prostaglandin synthesis was completely blocked by incubation with naproxen. Furthermore, water flow was not inhibited by incubation with the inactive diglyceride substitute phorbol didecanoate, supporting the specificity of the PMA inhibition. Consistent with the site of action at adenylate cyclase suggested by the transport experiments, PMA and RHC-80237 decreased both cell cAMP content and the cyclic AMPdependent kinase ratio (-cAMP/+cAMP), an index of intracellular cyclic AMP effect. Assay for protein kinase C activity in toad bladder epithelial cell supernatant demonstrated that the toad bladder indeed contains a kinase stimulable by phospholipid, calcium, and PMA.As an apparently independent effect, we found that addition of PMA, but not dioctanoylglycerol or RHC-80267, to the mucosal bath increased both water permeability and the frequency of granular cell luminal membrane aggregates in the absence of vasopressin, consistent with stimulation of fusion events at the luminal membrane.Our data suggest that protein kinase C can modulate AVPstimulated water flow in toad bladder by inhibiting cAMP generation, and perhaps post-cAMP steps as well, and support the hypothesis that AVP-stimulated turnover of membrane phos-A preliminary report of this work was presented at the 17th Annual

show abstract

Section: Resultsmentioning

confidence: 65%

Section: Resultsmentioning

confidence: 99%

Inhibition of vasopressin-stimulated water flow in toad bladder by phorbol myristate acetate, dioctanoylglycerol, and RHC-80267. Evidence for modulation of action of vasopressin by protein kinase C.

Schlöndorff¹,

Levine²

1985

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…In liver, PGE 2 also inhibits adenylate cyclase activity and decreases glucagon-stimulated glycogenolysis (33,34). In kidney, PGE 2 has been shown to decrease cAMP levels and vasopressin-induced water resorption by the collecting tubules (35)(36)(37). In skeletal muscle, the greater abundance of the EP1 and EP2 receptor types is consistent with the reported effects of PGE 2 to influence both contraction and relaxation of muscle fibers (14).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Interleukin-1β-Induced COX-2 and EP3 Gene Expression by Sodium Salicylate Enhances Pancreatic Islet β-Cell Function

2002

View full text Add to dashboard Cite

Previous work has suggested that functional interrelationships may exist between inhibition of insulin secretion by interleukin (IL)-1␤ and the endogenous synthesis of prostaglandin E 2 (PGE 2 ) in the pancreatic islet. These studies were performed to ascertain the relative abundance of E prostaglandin (EP) receptor mRNAs in tissues that are major targets, or major degradative sites, of insulin; to identify which EP receptor type mediates PGE 2 inhibition of insulin secretion in pancreatic islets; and to examine possible sites of action through which sodium salicylate might affect IL-1␤/PGE 2 interactions. Real-time fluorescence-based RT-PCR indicated that EP3 is the most abundant EP receptor type in islets, liver, kidney, and epididymal fat. EP3 mRNA is the least, whereas EP2 mRNA is the most, abundant type in skeletal muscle. Misoprostol, an EP3 agonist, inhibited glucose-induced insulin secretion from islets, an event that was prevented by preincubation with pertussis toxin, by decreasing cAMP. Electromobility shift assays demonstrated that sodium salicylate inhibits IL-1␤-induced nuclear factor-B (NF-B) activation. Sodium salicylate also prevented IL-1␤ from inducing EP3 and cyclooxygenase (COX)-2 gene expression in islets and thereby prevented IL-1␤ from inhibiting glucose-induced insulin secretion. These findings indicate that the sites of action through which sodium salicylate inhibits these negative effects of IL-1␤ on ␤-cell function include activation of NF-B as well as generation of PGE 2 by COX-2.

show abstract

“…PGs converted from PGH2, only PGE2 inhibited the water flow at 10-8 M, but PGD2, PGF2a, and PGI2 were incapable of this even at 10 -' M. Concerning endogenous prostaglandins in the toad bladder, the synthesis of both PGE2 and PGF2a was stimulated by vasopressin (ZUSMAN et al, 1977;BURCH et al, 1979). That PGH2 has an effect at 10-' M indicates PGE2 physiologically inhibits vasopressin action while PGF2a has merely a pharmacological effect.…”

Section: Discussionmentioning

confidence: 99%

“…They reported that 10 -5 M PGE2 increased cyclic AMP content and kinase ratio even more than vasopressin but had no effect on the rate of water flow, and that 5 mU/ml vasopressin and 10 -5 M PGE2 when added together, increased the water flow but had no effect on cyclic AMP content or the kinase ratio compared to that of PGE2 when administered alone. ZUSMAN et al (1977) were the first to report that vasopressin stimulates PGE2 biosynthesis in the toad bladder, and that 1 mU/ml vasopressin increases PGE2 synthesis from 0.5 + 0.1 pmoles/min • hemibladder to 5.0 + 0.4. In a recent study, it was found that when PGE2 biosynthesis in the toad bladder was at a basal level of 0.22 + 0.01 pmoles/min • hemibladder, it was stimulated 5 times as much as by Japanese Journal of Physiology vasopressin (BURCH et al, 1980) and when at a basal level of 0.27 + 0.05 pmoles/ min mg prot., it was stimulated by 5 mU/ml vasopressin to 0.53 + 0.09 (BURCH and HALUSHKA, 1982).…”

Section: Discussionmentioning

confidence: 99%

Role of inhibitory and stimulative effects of prostaglandins on vasopressin-stimulated osmotic water flow in the toad bladder.

Marumo

Nara

1986

Jpn.J.Physiol

View full text Add to dashboard Cite

Vasopressin-prostaglandin (PG) interaction, especially the role of the inhibitory effects of PGE2 on vasopressin action, was studied using toad urinary bladders. The PGH2, at 1 x 10 -' M, inhibited vasopressinstimulated water flow (MARUMO, 1982); PGE2 inhibited the water flow at 10-8 M, but PGD2, PGF2a, and PGI2 did not do so even at 10-' M. Thus, PGE2 has a physiological effect in contrast to other PGs converted from PGH2. Indomethacin enhanced both the vasopressin-and cyclic AMPstimulated water flow across the toad bladder. However, the half maximum activation dose for vasopressin was 2 x 10-10 M, but for cyclic AMP, as much as 3 x 10-8 M. The PGE2 inhibited both vasopressin-and cyclic AMP-stimulated water flow. However, PGE2 inhibited vasopressin action in a dose-dependent manner which was not noted as a PGE2 effect on cyclic AMP action. The W-7, which is a specific inhibitor of calmodulin, suppressed cyclic AMP-stimulated water flow in a dose-dependent manner. Thus, PGE2 may suppress vasopressin-stimulated water flow at a site of cyclic AMP generation under physiological conditions. Thromboxane B2 (TXB2) enhanced vasopressin-stimulated water flow but not cyclic AMP-stimulated one. Thus PGE2 and TXB2 may be concluded as negative or positive modulators of vasopressin action in the toad bladder on the step(s) as the site of cyclic AMP generation under physiological conditions. Key words : vasopressin, prostaglandins, toad bladder, osmotic water flow, PGE2. ORLOFF et al. (1965) were the first to report that prostaglandin E1 (PGE1) inhibits vasopressin-and theophylline-induced water flow across the toad bladder but not that induced by cyclic AMP. OMACHI et al. (1974) found PGE1 diminished the accumulation of cyclic AMP in response to vasopressin in the toad bladder, and thus concluded that PGE1 suppresses vasopressin-stimulated water flow by inhibiting adenylate cyclase activity. This is supported by other reports in which

show abstract

Vasopressin-stimulated prostaglandin E biosynthesis in the toad urinary bladder. Effect of water flow.

Cited by 121 publications

References 21 publications

Inhibition of vasopressin-stimulated water flow in toad bladder by phorbol myristate acetate, dioctanoylglycerol, and RHC-80267. Evidence for modulation of action of vasopressin by protein kinase C.

Inhibition of vasopressin-stimulated water flow in toad bladder by phorbol myristate acetate, dioctanoylglycerol, and RHC-80267. Evidence for modulation of action of vasopressin by protein kinase C.

Inhibition of Interleukin-1β-Induced COX-2 and EP3 Gene Expression by Sodium Salicylate Enhances Pancreatic Islet β-Cell Function

Role of inhibitory and stimulative effects of prostaglandins on vasopressin-stimulated osmotic water flow in the toad bladder.

Contact Info

Product

Resources

About