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Altered pressure natriuresis in chronic angiotensin II hypertension in rats.
Altered pressure natriuresis in chronic angiotensin II hypertension in rats.
- Source :
-
The American journal of physiology [Am J Physiol] 1994 Mar; Vol. 266 (3 Pt 2), pp. R739-48. - Publication Year :
- 1994
-
Abstract
- Angiotensin II (ANG II; 10 or 30 ng/min iv) was infused for 7-10 days in unilaterally adrenalectomized and nephrectomized Sprague-Dawley rats drinking 1% NaCl. The acute pressure-natriuresis relationship was studied under Inactin anesthesia in volume-expanded rats with fixed neurohumoral influences on the remaining kidney. Renal interstitial hydrostatic pressure (RIHP) was measured using a catheter implanted into the renal cortex. Arterial blood pressure before laparotomy was 149 +/- 3 (SE) mmHg (n = 6) and 152 +/- 6 mmHg (n = 16) for ANG II-infused rats (10 and 30 ng/min, respectively) and 123 +/- 5 mmHg (n = 6) and 123 +/- 7 mmHg (n = 16) for the respective control rats. Compared with values in control rats, ANG II-infused rats had significantly (P < 0.05) lower urine flow and absolute and fractional sodium excretion at renal artery pressures of 115-150 mmHg. There were no significant differences between RIHP measured in control and ANG II-hypertensive rats. The shift in the pressure-diuresis, pressure-natriuresis, and pressure-fractional sodium excretion relationships was similar with both doses of ANG II and was reversed by the acute administration of losartan (10 mg/kg iv). In all groups of rats, renal blood flow was autoregulated, whereas glomerular filtration rate was not autoregulated in ANG II-infused rats and was significantly lower than that in control rats at the lower level of renal artery pressure. The data indicate that rats with ANG II-induced hypertension have a rightward shift of the pressure-natriuresis curve caused primarily by a decrease in fractional excretion of sodium. The lack of effect of chronic ANG II infusion on filtration fraction and RIHP suggests that the increased tubular reabsorption was due to a direct action of ANG II on renal tubules. The reversal of these effects by losartan suggests that the shift in the pressure-natriuresis curve in ANG II-induced hypertension is mediated by the AT1-receptor subtype.
- Subjects :
- Angiotensin Receptor Antagonists
Animals
Biphenyl Compounds pharmacology
Chronic Disease
Imidazoles pharmacology
Losartan
Male
Rats
Rats, Sprague-Dawley
Reference Values
Tetrazoles pharmacology
Angiotensin II
Blood Pressure
Hypertension chemically induced
Hypertension physiopathology
Natriuresis
Subjects
Details
- Language :
- English
- ISSN :
- 0002-9513
- Volume :
- 266
- Issue :
- 3 Pt 2
- Database :
- MEDLINE
- Journal :
- The American journal of physiology
- Publication Type :
- Academic Journal
- Accession number :
- 8160866
- Full Text :
- https://doi.org/10.1152/ajpregu.1994.266.3.R739