AT II Receptor Blockade and Renal Denervation: Different Interventions with Comparable Renal Effects?
Angiotensin II
/ metabolism
Angiotensin II Type 1 Receptor Blockers
/ pharmacology
Animals
Arterial Pressure
/ drug effects
Benzimidazoles
/ pharmacology
Biphenyl Compounds
/ pharmacology
Denervation
Glomerular Filtration Rate
/ drug effects
Heart Rate
/ drug effects
Kidney
/ drug effects
Male
Rats, Sprague-Dawley
Sodium
/ metabolism
Tetrazoles
/ pharmacology
Water
/ metabolism
Angiotensin II
Congestive heart failure
Renal function
Renal nerve ablation
Renal sympathetic innervation
Journal
Kidney & blood pressure research
ISSN: 1423-0143
Titre abrégé: Kidney Blood Press Res
Pays: Switzerland
ID NLM: 9610505
Informations de publication
Date de publication:
2021
2021
Historique:
received:
18
11
2020
accepted:
02
03
2021
pubmed:
26
5
2021
medline:
17
7
2021
entrez:
25
5
2021
Statut:
ppublish
Résumé
Angiotensin II (Ang II) and the renal sympathetic nervous system exert a strong influence on renal sodium and water excretion. We tested the hypothesis that already low doses of an Ang II inhibitor (candesartan) will result in similar effects on tubular sodium and water reabsorption in congestive heart failure (CHF) as seen after renal denervation (DNX). Measurement of arterial blood pressure, heart rate (HR), renal sympathetic nerve activity (RSNA), glomerular filtration rate (GFR), renal plasma flow (RPF), urine volume, and urinary sodium. To assess neural control of volume homeostasis, 21 days after the induction of CHF via myocardial infarction rats underwent volume expansion (0.9% NaCL; 10% body weight) to decrease RSNA. CHF rat and controls with or without DNX or pretreated with the Ang II type-1 receptor antagonist candesartan (0.5 ug i.v.) were studied. CHF rats excreted only 68 + 10.2% of the volume load (10% body weight) in 90 min. CHF rats pretreated with candesartan or after DNX excreted from 92 to 103% like controls. Decreases of RSNA induced by volume expansion were impaired in CHF rats but unaffected by candesartan pointing to an intrarenal drug effect. GFR and RPF were not significantly different in controls or CHF. The prominent function of increased RSNA - retaining salt and water - could no longer be observed after renal Ang II receptor blockade in CHF rats.
Sections du résumé
BACKGROUND
BACKGROUND
Angiotensin II (Ang II) and the renal sympathetic nervous system exert a strong influence on renal sodium and water excretion. We tested the hypothesis that already low doses of an Ang II inhibitor (candesartan) will result in similar effects on tubular sodium and water reabsorption in congestive heart failure (CHF) as seen after renal denervation (DNX).
METHODS
METHODS
Measurement of arterial blood pressure, heart rate (HR), renal sympathetic nerve activity (RSNA), glomerular filtration rate (GFR), renal plasma flow (RPF), urine volume, and urinary sodium. To assess neural control of volume homeostasis, 21 days after the induction of CHF via myocardial infarction rats underwent volume expansion (0.9% NaCL; 10% body weight) to decrease RSNA. CHF rat and controls with or without DNX or pretreated with the Ang II type-1 receptor antagonist candesartan (0.5 ug i.v.) were studied.
RESULTS
RESULTS
CHF rats excreted only 68 + 10.2% of the volume load (10% body weight) in 90 min. CHF rats pretreated with candesartan or after DNX excreted from 92 to 103% like controls. Decreases of RSNA induced by volume expansion were impaired in CHF rats but unaffected by candesartan pointing to an intrarenal drug effect. GFR and RPF were not significantly different in controls or CHF.
CONCLUSION
CONCLUSIONS
The prominent function of increased RSNA - retaining salt and water - could no longer be observed after renal Ang II receptor blockade in CHF rats.
Identifiants
pubmed: 34034251
pii: 000515616
doi: 10.1159/000515616
doi:
Substances chimiques
Angiotensin II Type 1 Receptor Blockers
0
Benzimidazoles
0
Biphenyl Compounds
0
Tetrazoles
0
Water
059QF0KO0R
Angiotensin II
11128-99-7
Sodium
9NEZ333N27
candesartan
S8Q36MD2XX
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
331-341Informations de copyright
© 2021 The Author(s) Published by S. Karger AG, Basel.