What question did this study set out to answer?

To examine the contribution of nitric oxide synthase to endothelium-dependent reductions in vasocontractile responsiveness following sustained alpha1-adrenergic receptor activation.

March 7, 2005British Journal of PharmacologyOpen Access

The role of nitric oxide synthase in reduced vasocontractile responsiveness induced by prolonged α1‐adrenergic receptor stimulation in rat thoracic aorta

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Why the study?

Does prolonged exposure to phenylephrine alter vasocontractile responsiveness and NOS activity in rat thoracic aorta?

Population

Rat thoracic aorta and isolated endothelial cells from rat aorta

Comparison

Prolonged exposure to alpha1-adrenergic receptor… vs Vehicle-exposed control aortas/rings

Design

Preclinical

Follow-up

6-12 hours

Authors

HGHakan GürdalAnkara University ACAlp CanAnkara University MUMehmet UğurIzmir University

Discussion

Member takes

Implication

Hypothesis-generating for alpha-agonist tachyphylaxis via eNOS; human studies required before any clinical consideration.

Key Points

To examine the contribution of nitric oxide synthase to endothelium-dependent reductions in vasocontractile responsiveness following sustained alpha1-adrenergic receptor activation.
Exposed rat thoracic aortic rings to the alpha1-adrenergic receptor agonist phenylephrine for 6 to 12 hours with or without the receptor antagonist prazosin.
Assessed nitric oxide synthase activity by quantifying the conversion of [3H]L-arginine to [3H]L-citrulline in intact aortic tissue and isolated endothelial cells.
Evaluated endothelial (eNOS) and inducible (iNOS) nitric oxide synthase expression via immunoblotting, RT-PCR, and immunohistochemical staining.
Prolonged phenylephrine exposure elevated basal nitric oxide synthase activity and enhanced acetylcholine-mediated vasorelaxation in intact rat aorta.
Exposure to phenylephrine increased eNOS mRNA and protein expression in endothelial cells without altering iNOS expression, an effect prevented by prazosin co-treatment.
Phenylephrine failed to increase nitric oxide synthase activity or intracellular calcium in isolated endothelial cells, demonstrating that the endothelial response requires mediation by adjacent vascular smooth muscle cells.

Structured PICO

Does prolonged exposure to phenylephrine alter vasocontractile responsiveness and NOS activity in rat thoracic aorta?

Population

Rat thoracic aorta and isolated endothelial cells from rat aorta

Intervention

Prolonged exposure (6-12 h) to alpha1-adrenergic receptor agonist phenylephrine (Phe)

Comparator

Vehicle-exposed control aortas/rings

Outcome

Vasocontractile responsiveness, nitric oxide synthase (NOS) activity, and eNOS expressionsurrogate

Prolonged alpha1-adrenergic stimulation in rat aorta induces functional antagonism of vasocontraction by enhancing endothelial eNOS expression and basal NOS activity.

Cite This Study

Gürdal et al. (2005) studied this question.

synapsesocial.com/papers/6a882515010a27dee476fc18 https://doi.org/10.1038/sj.bjp.0706177

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The role of nitric oxide synthase in reduced vasocontractile responsiveness induced by prolonged α1‐adrenergic receptor stimulation in rat thoracic aorta

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

The role of nitric oxide synthase in reduced vasocontractile responsiveness induced by prolonged α1‐adrenergic receptor stimulation in rat thoracic aorta

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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