Key result
In female rats with aortocaval fistula-induced heart failure, intrarenal administration of angiotensin II and norepinephrine decreased renal blood flow more than in healthy sham-operated animals.
Why the study?
Aortocaval fistula-induced heart failure results in higher mortality in female than male rats, possibly related to altered renal vascular responsiveness to angiotensin II.
Female rats with ACF-induced heart failure exhibit enhanced renal vascular responsiveness to ANG II and NE, which may contribute to accelerated renal dysfunction and HF decompensation compared to males.
Hypothesis-generating for sex-specific renal ANG II targeting in HF; prospective human studies needed before clinical adoption.
BACKGROUND/AIMS: We found recently that the aortocaval fistula (ACF)-induced heart failure (HF) results in higher mortality in female than in male rats. Possibly, the development of renal dysfunction in the females, unlike in males, is associated with altered renal vascular responsiveness to angiotensin II (ANG II). METHODS: Five or 20 weeks after ACF creation (compensated and decompensated HF, respectively), we assessed renal blood flow (RBF) responses to intrarenal administration of ANG II, norepinephrine (NE), and acetylcholine (Ach) in female ACF and sham-operated rats. RESULTS: In ACF females, ANG II decreased RBF more than in healthy animals, unlike with earlier published data in male ACF rats that responded similarly. Also, NE decreased RBF more in female ACF rats, whereas Ach increased RBF to the same extent in female ACF and sham-operated rats. RBF responses to intravenous administration of NE and Ach were almost identical in female and male ACF rats. CONCLUSION: Female ACF rats studied at the onset of HF decompensation reveal, in contrast to male rats, enhanced renal vascular responsiveness to both NE and ANG II. When associated with the demonstrated increased intrarenal ANG II and NE concentrations, such hyperresponsiveness might promote the development of renal dysfunction and accelerate HF decompensation.
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Krátký et al. (2019) studied Congestive heart failure. Intrarenal administration of angiotensin II, norepinephrine, and acetylcholine vs. Sham-operated rats was evaluated on Renal blood flow (RBF) responses. In female rats with aortocaval fistula-induced heart failure, intrarenal administration of angiotensin II and norepinephrine decreased renal blood flow more than in healthy sham-operated animals.
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