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January 1, 2008Journal of Pharmacological SciencesOpen Access

Characterization of the Inhibitory Effect of Vascular Endothelium on Agonist-Induced Vasoconstriction in Rat Mesenteric Resistance Arteries

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Population

Rat mesenteric resistance arteries/vascular beds

Comparison

Continuous perfusion of methoxamine or high KCl… vs Endothelium-denuded preparations or baseline…

Design

Preclinical

Follow-up

180 min

Authors

XJXin JinNankai UniversityYSYukiko Satoh-OtonashiOkayama UniversityYZYoshito ZamamiOkayama University of Science

Discussion

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Implication

No immediate clinical translation; leaves open EDHF-gap junction targeting in human resistance vessels.

Key Points

  • To characterize the inhibitory mechanisms by which the vascular endothelium counteracts agonist-induced vasoconstriction in rat mesenteric resistance arteries.
  • Measured perfusion pressure in isolated rat mesenteric vascular beds during 180-minute continuous perfusion with methoxamine or high potassium chloride.
  • Tested vascular responses following mechanical endothelial denudation and exposure to inhibitors of nitric oxide synthase, cyclooxygenase, potassium channels, and gap junctions.
  • Methoxamine-induced vasoconstriction exhibited a time-dependent 60% to 80% reduction from initial levels in intact vessels, whereas high-potassium-induced constriction showed no reduction.
  • Endothelial denudation, potassium channel blockers, and the gap junction inhibitor 18alpha-glycyrrhetinic acid blunted this reduction, while nitric oxide and cyclooxygenase inhibitors had no effect.

Structured PICO

P
Population
Rat mesenteric resistance arteries/vascular beds
I
Intervention
Continuous perfusion of methoxamine or high KCl, with or without various inhibitors (L-NAME, indomethacin, tetraethylammonium, apamin, charybdotoxin, 18alpha-GA) and vasodilators (acetylcholine, A23187)
C
Comparator
Endothelium-denuded preparations or baseline conditions
O
Outcome
Changes in perfusion pressure (vasoconstriction/vasodilation) over 180 minsurrogate

Endothelium-derived hyperpolarizing factor (EDHF) acting via gap junctions is the primary mechanism counteracting alpha-1-adrenoceptor-induced vasoconstriction in rat mesenteric resistance arteries.

Cite This Study

Jin et al. (2008) studied this question.

synapsesocial.com/papers/6a75978920ccc22d0a67a662https://doi.org/10.1254/jphs.08115fp
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Endothelium‐dependent hyperpolarization and intercellular electrical coupling in guinea‐pig mesenteric arterioles1999 · 198 citations
  2. 2Structure and function of small arteries1990 · 917 citations
  3. 3Characterization of the potassium channels involved in EDHF‐mediated relaxation in cerebral arteries1997 · 131 citations
  4. 4Acetylcholine releases endothelium‐derived hyperpolarizing factor and EDRF from rat blood vessels1988 · 691 citations
  5. 5Endogenous calcitonin gene‐related peptide (CGRP) mediates adrenergic‐dependent vasodilation induced by nicotine in mesenteric resistance arteries of the rat2000 · 48 citations