October 26, 2004HypertensionOpen Access

cGMP-Dependent Protein Kinase Mediates NO- but not Acetylcholine-Induced Dilations in Resistance Vessels In Vivo

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Population

cGKI-deficient (cGKI-/-) or endothelial NO synthase-deficient (eNOS-/-) mice, and wild-type mice

Comparison

Intracarotid bolus application of NO donor… vs Wild-type mice

Design

Preclinical

Authors

MKMichael KoeppenIntensive Care Society RFRobert FeilVascular / Pulmonary Vascular DSDaniel SieglLiebherr (Austria)

Discussion

Member takes

Implication

These murine findings should not alter vasodilator use in patients; they leave open cGKI necessity for NO signaling in human resistance vessels.

Structured PICO

Population

cGKI-deficient (cGKI-/-) or endothelial NO synthase-deficient (eNOS-/-) mice, and wild-type mice

Intervention

Intracarotid bolus application of NO donor sodium nitroprusside (SNP) or acetylcholine (ACh)

Comparator

Wild-type mice

Outcome

Arterial pressure changes and arteriole dilations in the cremaster musclesurrogate

cGMP and cGKI are major effectors for NO-induced acute dilations in murine resistance vessels, but are not essential for ACh-induced dilation or basal blood pressure regulation.

Cite This Study

Koeppen et al. (2004) studied this question.

synapsesocial.com/papers/6a843c2dbaf48c4c4c8d687e https://doi.org/10.1161/01.hyp.0000147661.80059.ca

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Implication

These murine findings should not alter vasodilator use in patients; they leave open cGKI necessity for NO signaling in human resistance vessels.

cGMP-Dependent Protein Kinase Mediates NO- but not Acetylcholine-Induced Dilations in Resistance Vessels In Vivo

Discussion

Member takes

Implication

Structured PICO

Cite This Study

cGMP-Dependent Protein Kinase Mediates NO- but not Acetylcholine-Induced Dilations in Resistance Vessels In Vivo

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider