What question did this study set out to answer?

To determine how chronic captopril administration alters in vivo vascular pressor responses and in vitro vascular smooth muscle reactivity in spontaneously hypertensive rats.

November 1, 1981Hypertension

Effects of captopril on vascular reactivity of SHR in vivo and in vitro.

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Why the study?

Does captopril affect vascular reactivity to norepinephrine and angiotensin II in spontaneously hypertensive rats?

Population

Spontaneously hypertensive rats (SHR) and untreated Sprague-Dawley rats

Comparison

Captopril vs Untreated age-matched controls and ethacrynic acid

Design

Preclinical

Follow-up

up to 6 months

Authors

MAMichael J. AntonaccioUniversity of Dundee BRBernard RubinOklahoma City University DKD G Kotler

Discussion

Member takes

Implication

Captopril's indirect pressor effects in hypertensive rats are hypothesis-generating; leaves open translation to human vascular reactivity.

Key Points

To determine how chronic captopril administration alters in vivo vascular pressor responses and in vitro vascular smooth muscle reactivity in spontaneously hypertensive rats.
Spontaneously hypertensive rats received daily oral captopril (100 mg/kg) for up to 6 months to measure in vivo pressor responses to norepinephrine and angiotensin II.
Isolated aortic helical strips from treated spontaneously hypertensive rats and untreated control rats were suspended in modified Krebs' solution for isometric tension analysis.
Untreated aortic tissue was directly incubated with 30 µg/mL captopril to assess contractile and relaxation responses to norepinephrine, potassium chloride, and nitroglycerin.
In vivo pressor responses to both norepinephrine and angiotensin II were inhibited across all treatment periods, with norepinephrine responses inhibited more consistently.
Aortic strips from captopril-treated rats exhibited equivalent or greater contractile responses to potassium chloride and norepinephrine compared to untreated age-matched controls.
Direct incubation of naive aortic strips with captopril (30 µg/mL) showed no significant effect on norepinephrine-induced contraction or nitroglycerin-induced relaxation.

Structured PICO

Does captopril affect vascular reactivity to norepinephrine and angiotensin II in spontaneously hypertensive rats?

Population

Spontaneously hypertensive rats (SHR) and untreated Sprague-Dawley rats

Intervention

Captopril (100 mg/kg by mouth daily for up to 6 months in vivo; 30 µg/ml for 1 hour in vitro)

Comparator

Untreated age-matched controls (for ex vivo aortic strips) and ethacrynic acid (for in vitro)

Outcome

Pressor responses to norepinephrine (NE) and angiotensin II (AII) in vivo, and contractile/relaxation responses of aortic strips in vitrosurrogate

Captopril inhibits in vivo pressor responses to norepinephrine and angiotensin II in spontaneously hypertensive rats without directly affecting isolated vascular smooth muscle contractility.

Cite This Study

Antonaccio et al. (1981) studied this question.

synapsesocial.com/papers/6a8299a40f52607ca18adb51 https://doi.org/10.1161/01.hyp.3.6_pt_2.ii-211

Topics

Hypertension management

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Implication

Captopril's indirect pressor effects in hypertensive rats are hypothesis-generating; leaves open translation to human vascular reactivity.

Effects of captopril on vascular reactivity of SHR in vivo and in vitro.

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Topics

Effects of captopril on vascular reactivity of SHR in vivo and in vitro.

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Topics

Also Consider