What question did this study set out to answer?

To examine blood pressure variability changes caused by nitric oxide synthesis inhibition in conscious rats and assess the contribution of the renin-angiotensin system using the AT1-receptor antagonist losartan.

November 1, 1996British Journal of PharmacologyOpen Access

Contribution of the renin‐angiotensin system to short‐term blood pressure variability during blockade of nitric oxide synthesis in the rat

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Why the study?

Does losartan prevent blood pressure variability changes induced by L-NAME in conscious rats?

Population

Conscious rats (n=40)

Comparison

L-NAME with or without losartan vs L-NAME alone vs L-NAME + losartan

Design

Preclinical

Follow-up

1 hour

Authors

OGOlivier GouédardBristol-Myers Squibb (Switzerland)JBJocelyne BlancCentre National de la Recherche Scientifique EGE GaudetBaker Heart and Diabetes Institute

Discussion

Member takes

Implication

Implicates RAS in L-NAME-induced BP variability in rats; hypothesis-generating with no clinical implications yet.

Key Points

To examine blood pressure variability changes caused by nitric oxide synthesis inhibition in conscious rats and assess the contribution of the renin-angiotensin system using the AT1-receptor antagonist losartan.
Conscious rats received a 1-hour intravenous infusion of low-dose (10 µg/kg/min, n=10) or high-dose (100 µg/kg/min, n=10) L-NAME.
Two additional groups (2 x n=10) were pretreated with an intravenous bolus of losartan (10 mg/kg) prior to identical L-NAME infusions.
Blood pressure variability was evaluated across low-frequency (0.02–0.2 Hz) and mid-frequency (0.2–0.6 Hz) spectra using spectral analysis.
Low-dose L-NAME increased systolic blood pressure (+10 ± 3 mmHg at 30 min, P < 0.01; +20 ± 4 mmHg at +5 min post-infusion, P < 0.001) and elevated low-frequency variability (6.7 ± 1.7 vs 3.4 ± 0.5 mmHg², P < 0.05).
High-dose L-NAME rapidly increased systolic blood pressure (+53 ± 4 mmHg at 40 min, P < 0.001), caused bradycardia (-44 ± 13 beats/min at 60 min, P < 0.01), raised low-frequency variability (11.7 ± 2 vs 2.7 ± 0.5 mmHg², P < 0.001), and reduced mid-frequency variability (1.14 ± 0.3 vs 1.7 ± 0.1 mmHg², P < 0.05).
Pretreatment with losartan increased baseline mid-frequency oscillations (4.26 ± 0.49 vs 2.43 ± 0.25 mmHg², P < 0.001), prevented blood pressure elevation during low-dose L-NAME, and abolished L-NAME-induced amplification of low-frequency oscillations.

Structured PICO

Does losartan prevent blood pressure variability changes induced by L-NAME in conscious rats?

Population

Conscious rats (n=40)

Intervention

L-NAME (low-dose 10 micrograms kg-1 min-1 or high-dose 100 micrograms kg-1 min-1, i.v. infusion for 1 h) with or without losartan (10 mg kg-1, i.v. bolus)

Comparator

L-NAME alone vs L-NAME + losartan

Outcome

Blood pressure variability changes measured by spectral analysissurrogate

The renin-angiotensin system mediates the increase in low-frequency systolic blood pressure variability following nitric oxide synthesis blockade in rats.

Cite This Study

Gouédard et al. (1996) studied this question.

synapsesocial.com/papers/6a720e56b5c1fe5ca9dff021 https://doi.org/10.1111/j.1476-5381.1996.tb16008.x

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Contribution of the renin‐angiotensin system to short‐term blood pressure variability during blockade of nitric oxide synthesis in the rat

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Contribution of the renin‐angiotensin system to short‐term blood pressure variability during blockade of nitric oxide synthesis in the rat

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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