What question did this study set out to answer?

This research investigates how the loss of the endothelial nitric oxide synthase (eNOS) gene affects vascular reactivity and blood pressure in mice.

April 1, 1999Cardiovascular ResearchOpen Access

Protein expression, vascular reactivity and soluble guanylate cyclase activity in mice lacking the endothelial cell nitric oxide synthase: contributions of NOS isoforms to blood pressure and heart rate control

View Full Paper

Ask AI

Bookmark

This research investigates how the loss of the endothelial nitric oxide synthase (eNOS) gene affects vascular reactivity and blood pressure in mice.
Examined protein expression, vascular reactivity, soluble guanylate cyclase activity, blood pressure, and heart rate in eNOS-/- and eNOS+/- mice, as well as wild-type controls.
Administered L-NAME (100 mg/kg/day for 21 days) to evaluate its effects on hypertensive responses.
Utilized aortic ring assays to assess endothelium-dependent vascular relaxation.
eNOS-/- mice displayed mild hypertension and bradycardia, while eNOS+/- mice maintained normal blood pressure.
L-NAME treatment failed to increase blood pressure in eNOS-/- mice, suggesting minimal contribution from other NOS isoforms.
Aortic rings from eNOS-/- mice showed a complete lack of relaxation in response to acetylcholine, indicating significant vascular impairment.

Structured PICO

Population

Mice completely lacking the eNOS gene (eNOS-/-), wild-type mice (eNOS+/+), and mice heterozygotic for the eNOS gene (eNOS+/-)

Intervention

Oral administration of L-NAME (approximately 100 mg/kg/day x 21 days) and genetic knockout/heterozygosity of eNOS

Comparator

Wild-type mice (eNOS+/+) and untreated baseline

Outcome

Protein expression, vascular reactivity, activity of soluble guanylate cyclase, blood pressure and heart ratesurrogate

Heterozygosity for eNOS does not impair vascular reactivity or blood pressure, and non-eNOS isoforms do not appear to regulate blood pressure but may influence heart rate.

Discussion

No takes yet. Share an insight, caveat, or question.

Implication

Findings in eNOS-deficient mice should not yet inform hypertension care; extends evidence that non-eNOS isoforms minimally regulate blood pressure.

Cite This Study

Georg Kojda (1999) studied this question.

synapsesocial.com/papers/6a7213e235aa2c282ce31387 https://doi.org/10.1016/s0008-6363(98)00315-0

Topics

Hypertension management

View Full Paper

Ask AI

Bookmark

Implication

Findings in eNOS-deficient mice should not yet inform hypertension care; extends evidence that non-eNOS isoforms minimally regulate blood pressure.

Protein expression, vascular reactivity and soluble guanylate cyclase activity in mice lacking the endothelial cell nitric oxide synthase: contributions of NOS isoforms to blood pressure and heart rate control

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Topics

Protein expression, vascular reactivity and soluble guanylate cyclase activity in mice lacking the endothelial cell nitric oxide synthase: contributions of NOS isoforms to blood pressure and heart rate control

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Topics

Also Consider