Effect of Prostaglandin (PGEI) on the Permeability Response of Toad Bladder to Vasopressin, Theophylline and Adenosine 3′,5′-monophosphate

Orloff, Jack; Handler, Jerome S.; Bergström, Sune

doi:10.1038/205397a0

Cited by 293 publications

(90 citation statements)

References 8 publications

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“…Where tested, the inhibitory effects of PGE1 are not observed during cyclic AMP-stimulated transport (bladder: Orloff et al 1965;kidney: Grantham & Orloff, 1968;gastric mucosa: Way & Durbin, 1969) indicating that PGE, acts by modifying adenylate cyclase activity. Indeed, adenylate cyclase preparations from a number of tissues, including gastric mucosa (Perrier & Laster, 1972) and gut (Kimberg et al 1971) are stimulated by PGE1.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin action on pancreatic blood flow and on electrolyte and enzyme secretion by exocrine pancreas in vivo and in vitro

Case¹,

Scratcherd²

1972

The Journal of Physiology

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SUMMARY1. Intra-arterial injection or infusion of prostaglandins E1 and E2 into anaesthetized cats caused a fall in arterial blood pressure, a reduction in pancreatic blood flow and an inhibition of secretin-stimulated pancreatic electrolyte secretion. In some experiments these effects were preceded by a transient increase in blood flow and secretion.2. The fall in blood pressure and reduction in blood flow, but not the inhibition of secretion, were much less marked following administration of the a-adrenergic blocking agent phenoxybenzamine. This stimulatory action was markedly potentiated by theophylline. 5. Enzyme secretion was not stimulated by any of the prostaglandins, even in the presence of theophylline.6. It is concluded that prostaglandins can stimulate electrolyte transport by exocrine pancreas, perhaps through a mechanism involving adenylate cyclase, but that in vivo this action is masked by a secondary inhibition resulting either from vasoconstriction, or from the vibration of an antisecretory agent, or both.

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Section: Discussionmentioning

confidence: 99%

Prostaglandin action on pancreatic blood flow and on electrolyte and enzyme secretion by exocrine pancreas in vivo and in vitro

Case¹,

Scratcherd²

1972

The Journal of Physiology

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“…Prostaglandins are released from the surface of the cerebral and cerebellar cortex and spinal cord (50)(51)(52), and from peripheral synaptic sites in association with the release of chemical transmitters in many tissues. Prostaglandin E have potent inhibitory actions on the re sponses to hormones in several tissues (26,27,53,54). These inhibitory actions were at tributed to suppression of increase in the intracellular level of cyclic AMP, conceivably resulting from inhibition of the activation of adenyl cyclase by hormones (28)(29)(30)(31).…”

Section: Discussionmentioning

confidence: 99%

“…In adipose tissue and toad bladder, prostaglandin E was reported to inhibit the responses to lipolytic hormones and vasopressin, and this inhibition was attributed to inhibition of the activation of adenyl cyclase by these hormones (26)(27)(28)(29)(30)(31). It is also possible that prostaglandin E may be involved in regulation of the intracellular concentration of cyclic AMP in the central nervous system.<BR> These observations suggest that cyclic AMP, histamine and prostaglandin E are all…”

mentioning

confidence: 92%

Studies on the Functional Role of Adenosine 3', 5'-Monophosphate, Histamine and Prostaglandin E1 in the Central Nervous System

Asakawa

Yoshida

1971

Jpn.J.Pharmacol

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“…MARUMO and EDELMAN (1971) previously reported that PGE1 inhibits adenylate cyclase activity in the hamster kidney, and BECK et al (1971) found the same in the rat kidney. However, SHLONDORFF et al (1981) observed that PGE2 inhibited cyclic AMP-stimulated water flow when the bladders were pretreated with prostaglandin synthesis inhibitors, but had no effect on water flow (ORLOFF et al, 1965;FLORES and SHARP, 1972;ALBERT and HANDLER, 1974). SCHLONDORFF et al (1981) suggest that PGE2 interferes with the stimulation of water flow at both "post cyclic AMP" and "pre cyclic AMP" sites, but they have not clarified at which of these two sites PGE2 exerts its effects against vasopressin under physiological conditions.…”

mentioning

confidence: 99%

“…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.…”

mentioning

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

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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

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Effect of Prostaglandin (PGEI) on the Permeability Response of Toad Bladder to Vasopressin, Theophylline and Adenosine 3′,5′-monophosphate

Cited by 293 publications

References 8 publications

Prostaglandin action on pancreatic blood flow and on electrolyte and enzyme secretion by exocrine pancreas in vivo and in vitro

Prostaglandin action on pancreatic blood flow and on electrolyte and enzyme secretion by exocrine pancreas in vivo and in vitro

Studies on the Functional Role of Adenosine 3', 5'-Monophosphate, Histamine and Prostaglandin E1 in the Central Nervous System

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

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