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October 27, 2000Circulation ResearchOpen Access

Mechanisms of NO/cGMP-Dependent Vasorelaxation

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Population

Pressurized small arteries, aortic rings, and vascular smooth muscle cells from wild-type and cGMP kinase…

Comparison

Acetylcholine and NO donor at varying… vs Wild-type vs cGKI vessels; presence vs absence…

Design

Preclinical

Authors

MSMatthias SausbierRSRudolf SchubertVVViktor Voigt

Discussion

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Overview

Animal data reveal concentration-dependent NO mechanisms; leaves open translation to human vascular therapies.

Structured PICO

P
Population
Pressurized small arteries, aortic rings, and vascular smooth muscle cells from wild-type (wt) and cGMP kinase I-deficient (cGKI(-/-)) mice
I
Intervention
Acetylcholine (ACh) and NO donor (DEA-NO) at varying concentrations
C
Comparator
Wild-type vs cGKI(-/-) vessels; presence vs absence of specific blockers (Iberiotoxin, soluble guanylyl cyclase inhibitor, cAK inhibitor)
O
Outcome
Vasorelaxation (vascular tone) and BK(Ca) channel activitysurrogate

This study demonstrates that NO mediates vasorelaxation through dual mechanisms: cGKI-dependent pathways at low physiological concentrations and cGKI-independent, cAK-dependent pathways at high concentrations.

Cite This Study

Sausbier et al. (2000) studied this question.

synapsesocial.com/papers/69d9a34d7f18ff2fefa3c1c1https://doi.org/10.1161/01.res.87.9.825
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