Signal transduction mechanisms imohed in angiotensin-(1-7) Ant-(1-7)| stimulated arachidonic acid (AA) release and prostanoid synthesis (PC) in rabbit vascular smooth muscle cells (VSMC)

M. M. Mutlialif, I. F. Benter, M. R. Uddin, Kafait Malik

Research output: Contribution to journalArticle

Abstract

Ang-(1-7) is known to produce anti-hypert4ensive actions by stimulating production of vasodilator PGs. The purpose of this .study was to investigate the signal transduclion mechanisms of Any-(1-7) stimulated AA release fur PG production in lahhit VSMC'. In cells pre-laheled with [3H]AA. all angiolensin peplidcs (Aug-(1-7), Any II, Ang I and Ang III) enhanced tritium release. However. Anu-U-7) was the most potent; the fractional release of [3H]AA release was 70%, 46%, 30%, 23%, respectively, for Ang-(1-7). Ang II, Ang I and Ang III. Ang II, but not Ang-(1-7) induced [3H]AA. was blocked hy ATI receptor antagonist Dup 75.V whereas AT2 receptor :tntagonisl Sar inhihitetl holh Ang II and Ang-(1-7) indticed [3H] A A release. Ang-(1.7) receptor antagonist (Aspl -Arg2-Val3-Tryr4-Ilc5-His6-D-Ala7), aholisked the effect of Ang-(1-7), hut not Ang II. to increase |'H|AA release In cells transiently transfccted with cytosolie (c). secretory (s) PI.A: and MAPK and CaMK II anlisense uliuonticleotides Ang-(1-7) induced PH)AA release was atlenualed by 79%. 50%, 30%, and 67% respectively. These data suggest that Ang-(1-7) stimulates A A release lor prosiaeyclin synthesis via a distinct receptor and that Ang-(1-7) promotes activation of CaMK II and MAPK which in turn stimulate cPl.Ai ami sPLA-> lo release AA from tissue lipids. (Supporlcd hy USPHS-NIII gRant 19134-24).

Original languageEnglish (US)
JournalFASEB Journal
Volume10
Issue number3
StatePublished - Dec 1 1996

Fingerprint

Signal transduction
Ants
Vascular Smooth Muscle
Arachidonic Acid
Prostaglandins
Smooth Muscle Myocytes
Muscle
Signal Transduction
Cells
Rabbits
United States Public Health Service
Tritium
angiotensin I (1-7)
Vasodilator Agents
Chemical activation
Tissue
Lipids

All Science Journal Classification (ASJC) codes

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

Cite this

@article{697c6105b07148c2b2260124771418d8,
title = "Signal transduction mechanisms imohed in angiotensin-(1-7) Ant-(1-7)| stimulated arachidonic acid (AA) release and prostanoid synthesis (PC) in rabbit vascular smooth muscle cells (VSMC)",
abstract = "Ang-(1-7) is known to produce anti-hypert4ensive actions by stimulating production of vasodilator PGs. The purpose of this .study was to investigate the signal transduclion mechanisms of Any-(1-7) stimulated AA release fur PG production in lahhit VSMC'. In cells pre-laheled with [3H]AA. all angiolensin peplidcs (Aug-(1-7), Any II, Ang I and Ang III) enhanced tritium release. However. Anu-U-7) was the most potent; the fractional release of [3H]AA release was 70{\%}, 46{\%}, 30{\%}, 23{\%}, respectively, for Ang-(1-7). Ang II, Ang I and Ang III. Ang II, but not Ang-(1-7) induced [3H]AA. was blocked hy ATI receptor antagonist Dup 75.V whereas AT2 receptor :tntagonisl Sar inhihitetl holh Ang II and Ang-(1-7) indticed [3H] A A release. Ang-(1.7) receptor antagonist (Aspl -Arg2-Val3-Tryr4-Ilc5-His6-D-Ala7), aholisked the effect of Ang-(1-7), hut not Ang II. to increase |'H|AA release In cells transiently transfccted with cytosolie (c). secretory (s) PI.A: and MAPK and CaMK II anlisense uliuonticleotides Ang-(1-7) induced PH)AA release was atlenualed by 79{\%}. 50{\%}, 30{\%}, and 67{\%} respectively. These data suggest that Ang-(1-7) stimulates A A release lor prosiaeyclin synthesis via a distinct receptor and that Ang-(1-7) promotes activation of CaMK II and MAPK which in turn stimulate cPl.Ai ami sPLA-> lo release AA from tissue lipids. (Supporlcd hy USPHS-NIII gRant 19134-24).",
author = "Mutlialif, {M. M.} and Benter, {I. F.} and Uddin, {M. R.} and Kafait Malik",
year = "1996",
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language = "English (US)",
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journal = "FASEB Journal",
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T1 - Signal transduction mechanisms imohed in angiotensin-(1-7) Ant-(1-7)| stimulated arachidonic acid (AA) release and prostanoid synthesis (PC) in rabbit vascular smooth muscle cells (VSMC)

AU - Mutlialif, M. M.

AU - Benter, I. F.

AU - Uddin, M. R.

AU - Malik, Kafait

PY - 1996/12/1

Y1 - 1996/12/1

N2 - Ang-(1-7) is known to produce anti-hypert4ensive actions by stimulating production of vasodilator PGs. The purpose of this .study was to investigate the signal transduclion mechanisms of Any-(1-7) stimulated AA release fur PG production in lahhit VSMC'. In cells pre-laheled with [3H]AA. all angiolensin peplidcs (Aug-(1-7), Any II, Ang I and Ang III) enhanced tritium release. However. Anu-U-7) was the most potent; the fractional release of [3H]AA release was 70%, 46%, 30%, 23%, respectively, for Ang-(1-7). Ang II, Ang I and Ang III. Ang II, but not Ang-(1-7) induced [3H]AA. was blocked hy ATI receptor antagonist Dup 75.V whereas AT2 receptor :tntagonisl Sar inhihitetl holh Ang II and Ang-(1-7) indticed [3H] A A release. Ang-(1.7) receptor antagonist (Aspl -Arg2-Val3-Tryr4-Ilc5-His6-D-Ala7), aholisked the effect of Ang-(1-7), hut not Ang II. to increase |'H|AA release In cells transiently transfccted with cytosolie (c). secretory (s) PI.A: and MAPK and CaMK II anlisense uliuonticleotides Ang-(1-7) induced PH)AA release was atlenualed by 79%. 50%, 30%, and 67% respectively. These data suggest that Ang-(1-7) stimulates A A release lor prosiaeyclin synthesis via a distinct receptor and that Ang-(1-7) promotes activation of CaMK II and MAPK which in turn stimulate cPl.Ai ami sPLA-> lo release AA from tissue lipids. (Supporlcd hy USPHS-NIII gRant 19134-24).

AB - Ang-(1-7) is known to produce anti-hypert4ensive actions by stimulating production of vasodilator PGs. The purpose of this .study was to investigate the signal transduclion mechanisms of Any-(1-7) stimulated AA release fur PG production in lahhit VSMC'. In cells pre-laheled with [3H]AA. all angiolensin peplidcs (Aug-(1-7), Any II, Ang I and Ang III) enhanced tritium release. However. Anu-U-7) was the most potent; the fractional release of [3H]AA release was 70%, 46%, 30%, 23%, respectively, for Ang-(1-7). Ang II, Ang I and Ang III. Ang II, but not Ang-(1-7) induced [3H]AA. was blocked hy ATI receptor antagonist Dup 75.V whereas AT2 receptor :tntagonisl Sar inhihitetl holh Ang II and Ang-(1-7) indticed [3H] A A release. Ang-(1.7) receptor antagonist (Aspl -Arg2-Val3-Tryr4-Ilc5-His6-D-Ala7), aholisked the effect of Ang-(1-7), hut not Ang II. to increase |'H|AA release In cells transiently transfccted with cytosolie (c). secretory (s) PI.A: and MAPK and CaMK II anlisense uliuonticleotides Ang-(1-7) induced PH)AA release was atlenualed by 79%. 50%, 30%, and 67% respectively. These data suggest that Ang-(1-7) stimulates A A release lor prosiaeyclin synthesis via a distinct receptor and that Ang-(1-7) promotes activation of CaMK II and MAPK which in turn stimulate cPl.Ai ami sPLA-> lo release AA from tissue lipids. (Supporlcd hy USPHS-NIII gRant 19134-24).

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