Enhanced Renal Vascular Responsiveness to Angiotensin II and Norepinephrine: A Unique Feature of Female Rats with Congestive Heart Failure
Language English Country Switzerland Media print-electronic
Document type Journal Article
PubMed
31505499
DOI
10.1159/000502379
PII: 000502379
Knihovny.cz E-resources
- Keywords
- Angiotensin II, Aortocaval fistula, Female, Heart failure, Norepinephrine,
- MeSH
- Angiotensin II pharmacology therapeutic use MeSH
- Rats MeSH
- Norepinephrine pharmacology therapeutic use MeSH
- Rats, Sprague-Dawley MeSH
- Heart Failure drug therapy MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Angiotensin II MeSH
- Norepinephrine MeSH
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.
Center for Experimental Medicine Institute for Clinical and Experimental Medicine Prague Czechia
Department of Pathophysiology 2nd Faculty of Medicine Charles University Prague Czechia
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