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January 1, 1999AJP Renal Physiology

Suppressed impact of nitric oxide on renal arteriolar function in rats with chronic heart failure

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Key result

In rats with chronic heart failure, NO synthase inhibition with L-NNA did not alter afferent arteriolar baseline diameter or ANG II responsiveness, unlike in sham-operated rats.

Population

Rats with experimental heart failure induced by coronary artery ligation 8-10 weeks prior

Comparison

NO synthase inhibition and ANG II in the… vs Kidneys from sham-operated rats

Design

Preclinical

Follow-up

8-10 weeks

Authors

HIHideki IkenagaNINaohito IshiiSDSean P. Didion

Discussion

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Overview

Animal data link HF to impaired NO modulation of renal ANG II responses; leaves open clinical translation.

Structured PICO

P
Population
Rats with experimental heart failure induced by coronary artery ligation, evaluated 8 to 10 weeks post-induction.
I
Intervention
NO synthase inhibition (100 microM Nomega-nitro-L-arginine [L-NNA]) and ANG II (10 nM) in the presence of enalaprilat
C
Comparator
Kidneys from sham-operated rats
O
Outcome
Renal arteriolar function (afferent and efferent arteriolar diameter changes)surrogate

Main Result

p-value: p=<0.05

Experimental heart failure in rats leads to a loss of NO-dependent modulation of ANG II-induced renal vasoconstriction due to diminished NO synthesis and augmented degradation.

Cite This Study

Ikenaga et al. (1999) studied chronic heart failure. NO synthase inhibition (L-NNA) vs. Sham-operated rats was evaluated on Afferent arteriolar diameter and ANG II responsiveness (p=<0.05). In rats with chronic heart failure, NO synthase inhibition with L-NNA did not alter afferent arteriolar baseline diameter or ANG II responsiveness, unlike in sham-operated rats.

synapsesocial.com/papers/6a6c48bf34b735385cb3eee6https://doi.org/10.1152/ajprenal.1999.276.1.f79
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Also Consider

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