Key result
Hypoxia-induced vasocontraction in rat aorta and canine coronary arteries was abolished by L-NAME, suggesting the contraction is due to continuous inhibition of basal nitric oxide synthesis.
Why the study?
Does hypoxia induce vasocontraction via the removal of endothelium-derived nitric oxide rather than the release of a contracting factor in vascular rings?
Population
Vascular rings isolated from spontaneously hypertensive rat (SHR) aorta and canine coronary artery
Comparison
Hypoxia and inhibition of nitric oxide… vs Normoxia and baseline precontraction states
Design
Preclinical
Authors
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Challenges endothelium-derived contracting factor hypothesis in hypoxia; leaves open relevance to human vessels.
Does hypoxia induce vasocontraction via the removal of endothelium-derived nitric oxide rather than the release of a contracting factor in vascular rings?
Hypoxia-induced vasocontraction is likely a phenomenon derived from the continuous inhibition of basal nitric oxide synthesis rather than the release of a specific endothelium-derived contracting factor.
Muramatsu et al. (1992) studied this question. Hypoxia and L-NAME vs. Normoxia was evaluated on Vascular tension. Hypoxia-induced vasocontraction in rat aorta and canine coronary arteries was abolished by L-NAME, suggesting the contraction is due to continuous inhibition of basal nitric oxide synthesis.
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