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June 1, 2000Cardiovascular Research

Endothelium-dependent hyperpolarization and relaxation resistance to NG-nitro-?-arginine and indomethacin in coronary circulation

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Key result

Bradykinin relaxes coronary arteries via EDHF and NO through large-conductance calcium-activated potassium channels.

Why the study?

It is controversial whether endothelium-dependent relaxation resistance to nitric oxide and prostacyclin synthase inhibitors is fully attributed to endothelium-derived hyperpolarizing factor in coronary arteries.

Does bradykinin induce endothelium-dependent relaxation and hyperpolarization in porcine coronary arteries resistant to L-NNA and indomethacin?

Population

Porcine coronary arteries including large arteries and microarteries

Comparison

Bradykinin-induced relaxation with and without inhibitors L-NNA, indomethacin, K+ channel blockers, and oxyhemoglobin

Design

Preclinical experimental study measuring NO release, isometric force, and membrane potential

Authors

ZGZhen GeDalian Medical University

Discussion

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Implication

Does not support clinical translation; leaves open human in vivo validation of BKCa-mediated coronary relaxation.

Structured PICO

Does bradykinin induce endothelium-dependent relaxation and hyperpolarization in porcine coronary arteries resistant to L-NNA and indomethacin?

P
Population
Porcine coronary arteries (large arteries and microarteries)
I
Intervention
Bradykinin (BK) administration in the presence of indomethacin and N(G)-nitro-L-arginine (L-NNA), with or without K+ channel blockers (tetraethylammonium, charybdotoxin, iberiotoxin, apamin) and oxyhemoglobin
O
Outcome
Nitric oxide (NO) release, isometric force (relaxation), and membrane potential (hyperpolarization)surrogate

Both EDHF and NO contribute to bradykinin-induced relaxation resistance to indomethacin and L-NNA in porcine coronary arteries, mediated primarily by large conductance Ca2+-activated K+ channels.

Cite This Study

Zhen Ge (2000) studied this question. Bradykinin was evaluated on NO release, isometric force, and membrane potential. In porcine coronary arteries, both EDHF and NO contribute to bradykinin-induced relaxation resistance to indomethacin and L-NNA, with large conductance Ca2+-activated K+ channels playing a key role.

synapsesocial.com/papers/6ab6451e008d5ec36e739239https://doi.org/10.1016/s0008-6363(00)00040-7
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Also Consider

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

  1. 1NO/PGI<sub>2</sub>‐independent vasorelaxation and the cytochrome P450 pathway in rabbit carotid artery1997 · 82 citations
  2. 2Lysophosphatidylcholine Inhibits Endothelium-Dependent Hyperpolarization andNω-Nitro- l -Arginine/IndomethacinResistant Endothelium-Dependent Relaxation in the Porcine Coronary Artery1995 · 56 citations
  3. 3Nitric oxide is the mediator of both endothelium-dependent relaxation and hyperpolarization of the rabbit carotid artery1997 · 214 citations
  4. 4Endothelium‐dependent hyperpolarization of canine coronary smooth muscle1988 · 776 citations
  5. 5Identification of Epoxyeicosatrienoic Acids as Endothelium-Derived Hyperpolarizing Factors1996 · 1,223 citations