What question did this study set out to answer?

To determine whether homozygous deletion of the AT1A receptor prevents blood pressure elevation and vascular dysfunction caused by chronic angiotensin II exposure.

March 9, 2004HypertensionOpen Access

Angiotensin II–Induced Vascular Dysfunction Is Mediated by the AT 1A Receptor in Mice

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Why the study?

Does AT1A receptor deletion prevent Angiotensin II-induced vascular dysfunction in mice?

Population

AT1A homozygous deletion (AT1A-/-) mice and control littermates (AT1A+/+)

Comparison

Angiotensin II infusion (1000 ng x kg x min) for… vs Vehicle infusion for 7 days by osmotic pumps

Design

Preclinical

Follow-up

7 days

Authors

MRMichael J. RyanUniversity of South Carolina SDSean P. DidionUniversity of Mississippi Medical Center SMSatya N. MathurUniversity of Iowa Hospitals and Clinics

Discussion

Member takes

Implication

AT1A mediates Ang II effects in mice; leaves open translation to human hypertension therapies.

Key Points

To determine whether homozygous deletion of the AT1A receptor prevents blood pressure elevation and vascular dysfunction caused by chronic angiotensin II exposure.
Infused AT1A knockout (AT1A-/-) and wild-type control (AT1A+/+) mice with vehicle or angiotensin II (1000 ng/kg/min) for 7 days using osmotic pumps.
Evaluated systolic blood pressure, ex vivo carotid artery responses to vasodilators and vasoconstrictors, superoxide generation, and Rho-kinase pathway activity.
Angiotensin II significantly increased systolic blood pressure in wild-type mice (Δ45±8 mm Hg, P<0.0001) but not in AT1A-/- mice (Δ5±3 mm Hg, P>0.13).
Angiotensin II impaired acetylcholine relaxation and increased 5-hydroxytryptamine contraction in wild-type carotids, whereas carotid responses in AT1A-/- mice were completely unaffected.
Superoxide levels and RhoA protein expression did not differ between wild-type and knockout mice under vehicle or angiotensin II conditions.

Structured PICO

Does AT1A receptor deletion prevent Angiotensin II-induced vascular dysfunction in mice?

Population

AT1A homozygous deletion (AT1A-/-) mice and control littermates (AT1A+/+)

Intervention

Angiotensin II infusion (1000 ng x kg(-1) x min(-1)) for 7 days by osmotic pumps

Comparator

Vehicle (saline) infusion for 7 days by osmotic pumps

Outcome

Vascular reactivity (systolic pressure and carotid artery response to vasodilators and vasoconstrictors)surrogate

The AT1A receptor is essential for mediating Angiotensin II-induced increases in systolic blood pressure and vascular dysfunction in mice.

Cite This Study

Ryan et al. (2004) studied this question.

synapsesocial.com/papers/6a84019d121b098de683d1d6 https://doi.org/10.1161/01.hyp.0000123074.89717.3d

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Angiotensin II–Induced Vascular Dysfunction Is Mediated by the AT 1A Receptor in Mice

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Angiotensin II–Induced Vascular Dysfunction Is Mediated by the AT 1A Receptor in Mice

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Also Consider