The position of NO among endogenous vasodilators

J. Quilley, David J Fulton, J. C. McGiff

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Bradykinin stimulates phospholipases to release arachidonic acid (AA) which can be metabolized by cyclooxygenase, lipoxygenase and cytochrome P450 (P450) to yield vasoactive products that may contribute to the effect of the peptide. In the rat kidney, pharmacological evidence suggests that a substantial component of the vasodilator response is dependent on P450-AA metabolism. In the heart, the vasodilator response to bradykinin is independent of NO and prostaglandins but reduced by inhibitors of P450, including 17-ODYA, an inhibitor of fatty acid metabolism, also suggesting a role of P450-AA. Moreover, the renal and coronary vasodilator responses to bradykinin are associated with release of P450-AA products measured by gas chromatography-mass spectrometry (GC-MS). The coronary vasodilator response to bradykinin is also dependent on activation of K+ channels linking P450-AA and hyperpolarization. Formation of vasodilator eicosanoids derived via the P450 pathway may make important contributions to the control of vascular tone, local blood flow and, thereby, blood pressure.

Original languageEnglish (US)
Pages (from-to)523-530
Number of pages8
JournalPolish Journal of Pharmacology
Volume46
Issue number6
StatePublished - Dec 1 1994

Fingerprint

Vasodilator Agents
Arachidonic Acid
Bradykinin
Kidney
Prostaglandin Antagonists
Lipoxygenase
Eicosanoids
Phospholipases
Prostaglandin-Endoperoxide Synthases
Gas Chromatography-Mass Spectrometry
Cytochrome P-450 Enzyme System
Blood Vessels
Fatty Acids
Pharmacology
Blood Pressure
Peptides

Keywords

  • arachidonate metabolism
  • bradykinin
  • cytochrome P450
  • potassium channels
  • review
  • vascular mechanisms

ASJC Scopus subject areas

  • Pharmacology

Cite this

The position of NO among endogenous vasodilators. / Quilley, J.; Fulton, David J; McGiff, J. C.

In: Polish Journal of Pharmacology, Vol. 46, No. 6, 01.12.1994, p. 523-530.

Research output: Contribution to journalArticle

Quilley, J, Fulton, DJ & McGiff, JC 1994, 'The position of NO among endogenous vasodilators', Polish Journal of Pharmacology, vol. 46, no. 6, pp. 523-530.
Quilley, J. ; Fulton, David J ; McGiff, J. C. / The position of NO among endogenous vasodilators. In: Polish Journal of Pharmacology. 1994 ; Vol. 46, No. 6. pp. 523-530.
@article{9d47f12d71894fd188100e5c392a0821,
title = "The position of NO among endogenous vasodilators",
abstract = "Bradykinin stimulates phospholipases to release arachidonic acid (AA) which can be metabolized by cyclooxygenase, lipoxygenase and cytochrome P450 (P450) to yield vasoactive products that may contribute to the effect of the peptide. In the rat kidney, pharmacological evidence suggests that a substantial component of the vasodilator response is dependent on P450-AA metabolism. In the heart, the vasodilator response to bradykinin is independent of NO and prostaglandins but reduced by inhibitors of P450, including 17-ODYA, an inhibitor of fatty acid metabolism, also suggesting a role of P450-AA. Moreover, the renal and coronary vasodilator responses to bradykinin are associated with release of P450-AA products measured by gas chromatography-mass spectrometry (GC-MS). The coronary vasodilator response to bradykinin is also dependent on activation of K+ channels linking P450-AA and hyperpolarization. Formation of vasodilator eicosanoids derived via the P450 pathway may make important contributions to the control of vascular tone, local blood flow and, thereby, blood pressure.",
keywords = "arachidonate metabolism, bradykinin, cytochrome P450, potassium channels, review, vascular mechanisms",
author = "J. Quilley and Fulton, {David J} and McGiff, {J. C.}",
year = "1994",
month = "12",
day = "1",
language = "English (US)",
volume = "46",
pages = "523--530",
journal = "Pharmacological Reports",
issn = "1734-1140",
publisher = "Polish Academy of Sciences Publishing House",
number = "6",

}

TY - JOUR

T1 - The position of NO among endogenous vasodilators

AU - Quilley, J.

AU - Fulton, David J

AU - McGiff, J. C.

PY - 1994/12/1

Y1 - 1994/12/1

N2 - Bradykinin stimulates phospholipases to release arachidonic acid (AA) which can be metabolized by cyclooxygenase, lipoxygenase and cytochrome P450 (P450) to yield vasoactive products that may contribute to the effect of the peptide. In the rat kidney, pharmacological evidence suggests that a substantial component of the vasodilator response is dependent on P450-AA metabolism. In the heart, the vasodilator response to bradykinin is independent of NO and prostaglandins but reduced by inhibitors of P450, including 17-ODYA, an inhibitor of fatty acid metabolism, also suggesting a role of P450-AA. Moreover, the renal and coronary vasodilator responses to bradykinin are associated with release of P450-AA products measured by gas chromatography-mass spectrometry (GC-MS). The coronary vasodilator response to bradykinin is also dependent on activation of K+ channels linking P450-AA and hyperpolarization. Formation of vasodilator eicosanoids derived via the P450 pathway may make important contributions to the control of vascular tone, local blood flow and, thereby, blood pressure.

AB - Bradykinin stimulates phospholipases to release arachidonic acid (AA) which can be metabolized by cyclooxygenase, lipoxygenase and cytochrome P450 (P450) to yield vasoactive products that may contribute to the effect of the peptide. In the rat kidney, pharmacological evidence suggests that a substantial component of the vasodilator response is dependent on P450-AA metabolism. In the heart, the vasodilator response to bradykinin is independent of NO and prostaglandins but reduced by inhibitors of P450, including 17-ODYA, an inhibitor of fatty acid metabolism, also suggesting a role of P450-AA. Moreover, the renal and coronary vasodilator responses to bradykinin are associated with release of P450-AA products measured by gas chromatography-mass spectrometry (GC-MS). The coronary vasodilator response to bradykinin is also dependent on activation of K+ channels linking P450-AA and hyperpolarization. Formation of vasodilator eicosanoids derived via the P450 pathway may make important contributions to the control of vascular tone, local blood flow and, thereby, blood pressure.

KW - arachidonate metabolism

KW - bradykinin

KW - cytochrome P450

KW - potassium channels

KW - review

KW - vascular mechanisms

UR - http://www.scopus.com/inward/record.url?scp=0028566411&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028566411&partnerID=8YFLogxK

M3 - Article

C2 - 7620514

AN - SCOPUS:0028566411

VL - 46

SP - 523

EP - 530

JO - Pharmacological Reports

JF - Pharmacological Reports

SN - 1734-1140

IS - 6

ER -