Distribution of prostaglandins E1, E2, F1α and F2α, in some animal tissues

Karim, S. M. M.; Hillier, Keith; Devlin, Jean

doi:10.1111/j.2042-7158.1968.tb09633.x

Cited by 75 publications

(19 citation statements)

References 27 publications

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“…We also showed the action of PGE 2 on pacemaker currents in ICC was not mediate via cAMP pathway and involved the regulation of spontaneous [Ca 2+ ] i oscillations generated by ICC. Fatty acid cyclooxygenase in the gastrointestinal tract converts eicosateraenoic acid (arachidonic acid) primarily to prostacyclin (prostaglandin I 2 ), and, to a lesser extent, to PGE 2 , PGF 2 α, and thromboxane A 2 [28][29][30][31]. Previous studies on gastrointestinal tract motility have shown that PGE 2 generally contracts the longitudinal smooth muscle layer of the small intestine and relaxes the circular muscle layer [26,27].…”

Section: Discussionmentioning

confidence: 99%

Activating of ATP-Dependent K+ Channels Comprised of Kir 6.2 and SUR 2B by PGE2 Through EP2 Receptor in Cultured Interstitial Cells of Cajal from Murine Small Intestine

Choi

Yeum

Chang

et al. 2006

Cell Physiol Biochem

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The interstitial cells of Cajal (ICC) are pacemaker cells in gastrointestinal tract and generate an electrical rhythm in gastrointestinal muscles. We investigated the possibility that PGE₂ might affect the electrical properties of cultured ICC by activating ATPdependent K⁺ channels and, the EP receptor subtypes and the subunits of ATP-dependent K⁺ channels involved in these activities were identified. In addition, the regulation of intracellular Ca²⁺ ([Ca²⁺]i) mobilization may be involved the action of PGE₂ on ICC. Treatments of ICC with PGE₂ inhibited electrical pacemaker activities in the same manner as pinacidil, an ATPdependent K⁺ channel opener and PGE₂ had only a dose-dependent effect. Using RT-PCR technique, we found that ATP-dependent K⁺ channels exist in ICC and that these are composed of K_ir 6.2 and SUR 2B subunits. To characterize the specific membrane EP receptor subtypes in ICC, EP receptor agonists and RT-PCR were used: Butaprost (an EP₂ receptor agonist) showed the actions on pacemaker currents in the same manner as PGE₂. However sulprostone (a mixed EP₁ and EP₃ agonist) had no effects. In addition, RT-PCR results indicated the presence of the EP₂ receptor in ICC. To investigate cAMP involvement in the effects of PGE₂ on ICCs, SQ-22536 (an inhibitor of adenylate cyclase) and cAMP assays were used. SQ-22536 did not affect the effect of PGE₂ on pacemaker currents, and PGE₂ did not stimulate cAMP production. Also, we found PGE₂ inhibited the spontaneous [Ca²⁺]i oscillations in cultured ICC. These observations indicate that PGE₂ alters pacemaker currents by activating the ATP-dependent K⁺ channels comprised of K_ir 6.2-SUR 2B in ICC and this action of PGE₂ are through EP₂ receptor subtype and also the activation of ATP-dependent K⁺ channels involves intracellular Ca²⁺ mobilization.

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Section: Discussionmentioning

confidence: 99%

Activating of ATP-Dependent K+ Channels Comprised of Kir 6.2 and SUR 2B by PGE2 Through EP2 Receptor in Cultured Interstitial Cells of Cajal from Murine Small Intestine

Choi

Yeum

Chang

et al. 2006

Cell Physiol Biochem

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“…Lung tissues ofall species so far investigated contain high amounts ofprostaglandins (Anggard, 1965;Karim, Hillier & Devlin, 1968), and prostaglandins are released spontaneously from perfused whole lung or lung fragments (Yen, Mathe & Dugan, 1976;Mathe, Yen, Sohn & Hedqvist, 1977). It is also known that prostaglandins are released into the incubation media from tracheal tissue (Hedqvist & Mathe, 1977), and that the prostaglandin E series of compounds relaxes tracheobronchial smooth muscle preparations from a number of species, including man (Main, 1964;Horton & Main, 1965;Sweatman & Collier, 1968).…”

Section: Methodsmentioning

confidence: 99%

Actions of indomethacin and prostaglandins on neuroeffector transmission in the dog trachea

Ito

Tajima

1981

The Journal of Physiology

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“…While all these studies make the effector cell membrane the logical candidate for PG release, the possibility should not be overlooked that PG may be formed in the nerve terminal membrane in amounts sufficient to affect neurotransmission but too small to be detected in the effluent from stimulated organs. In fact, PGs have been demonstrated in several types of reasonably pure nerve tissue (Kataoka et al, 1967;Karim et al, 1968). However, at present the effector cell membrane is the most plausible source for PG release when tissues are stimulated.…”

Section: Prostaglandin-induced Feedback Control Of Sympathetic Nementioning

confidence: 98%

Autonomic Neurotransmission

Hedqvist

1973

The Prostaglandins

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Distribution of prostaglandins E1, E2, F1α and F2α, in some animal tissues

Abstract: A survey of the distribution of prostaglandins E1, E2, F1α and F2α in fourteen tissues from the dog, cat, rat, rabbit, guinea‐pig and chicken has been made. One or more of these prostaglandins are present in varying amounts in most tissues with PGE2 PGF2α occurring most commonly.

Cited by 75 publications

References 27 publications

Activating of ATP-Dependent K<sup>+</sup> Channels Comprised of K<sub>ir</sub> 6.2 and SUR 2B by PGE<sub>2</sub> Through EP<sub>2</sub> Receptor in Cultured Interstitial Cells of Cajal from Murine Small Intestine

Activating of ATP-Dependent K<sup>+</sup> Channels Comprised of K<sub>ir</sub> 6.2 and SUR 2B by PGE<sub>2</sub> Through EP<sub>2</sub> Receptor in Cultured Interstitial Cells of Cajal from Murine Small Intestine

Actions of indomethacin and prostaglandins on neuroeffector transmission in the dog trachea

Autonomic Neurotransmission

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