Journal Article

Modulating Role of Ang1-7 in Control of Blood Pressure and Renal Function in AngII-infused Hypertensive Rats

Marta Kuczeriszka, Elżbieta Kompanowska-Jezierska, Janusz Sadowski, Minolfa C Prieto and L Gabriel Navar

in American Journal of Hypertension

Volume 31, issue 4, pages 504-511
Published in print March 2018 | ISSN: 0895-7061
Published online October 2017 | e-ISSN: 1941-7225 | DOI: https://dx.doi.org/10.1093/ajh/hpy006
Modulating Role of Ang1-7 in Control of Blood Pressure and Renal Function in AngII-infused Hypertensive Rats

More Like This

Show all results sharing these subjects:

  • Anatomy
  • Nephrology
  • Biochemistry
  • Neuroendocrinology and Autonomic Nervous System
  • Endocrinology and Diabetes

GO

Show Summary Details

Preview

Abstract

BACKGROUND

Indirect evidence suggests that angiotensin 1-7 (Ang1-7) may counterbalance prohypertensive actions of angiotensin II (AngII), via activation of vascular and/or renal tubular receptors to cause vasodilation and natriuresis/diuresis. We examined if Ang1-7 would attenuate the development of hypertension, renal vasoconstriction, and decreased natriuresis in AngII-infused rats and evaluated the mechanisms involved.

METHODS

AngII, alone or with Ang1-7, was infused to conscious Sprague-Dawley rats for 13 days and systolic blood pressure (SBP) and renal excretion were repeatedly determined. In anesthetized rats, acute actions of Ang1-7 and effects of blockade of angiotensin AT1 or Mas receptors (candesartan or A-779) were studied.

RESULTS

Chronic AngII infusion increased SBP from 143 ± 4 to 195 ± 6 mm Hg. With Ang1-7 co-infused, SBP increased from 133 ± 5 to 161 ± 5 mm Hg (increase reduced, P < 0.002); concurrent increases in urine flow (V) and sodium excretion (UNaV) were greater. In anesthetized normotensive or AngII-induced hypertensive rats, Ang1-7 infusion transiently increased mean arterial pressure (MABP), transiently decreased renal blood flow (RBF), and caused increases in UNaV and V. In normotensive rats, candesartan prevented the Ang1-7-induced increases in MABP and UNaV and the decrease in RBF. In anesthetized normotensive, rats intravenous A-779 increased MABP (114 ± 5 to 120 ± 5 mm Hg, P < 0.03) and urine flow. Surprisingly, these changes were not observed with A-779 applied during background Ang1-7 infusion.

CONCLUSIONS

The results suggest that in AngII-dependent hypertension, Ang1-7 deficit contributes to sodium and fluid retention and thereby to BP elevation; a correction by Ang1-7 infusion seems mediated by AT1 and not Mas receptors.

Keywords: angiotensin 1-7; AngII-dependent hypertension; blood pressure; hypertension; renal blood flow; sodium excretion

Journal Article.  4873 words.  Illustrated.

Subjects: Anatomy ; Nephrology ; Biochemistry ; Neuroendocrinology and Autonomic Nervous System ; Endocrinology and Diabetes

Full text: subscription required

How to subscribe Recommend to my Librarian

Users without a subscription are not able to see the full content. Please, subscribe or login to access all content. subscribe or purchase to access all content.