title: Altered pressure natriuresis in chronic angiotensin II hypertension in rats.
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.
authors.affiliation: Department of Physiology, University of Western Ontario, London, Canada.
authors.forename: J
authors.initials: J
authors.lastname: van der Mark
authors.forename: R L
authors.initials: RL
authors.lastname: Kline
mesh_terms: D000804:Angiotensin II; D057911:Angiotensin Receptor Antagonists; D000818:Animals; D001713:Biphenyl Compounds / Q000494:pharmacology; D001794:Blood Pressure; D002908:Chronic Disease; D006973:Hypertension / Q000139:chemically induced* / Q000503:physiopathology*; D007093:Imidazoles / Q000494:pharmacology; D019808:Losartan; D008297:Male; D009318:Natriuresis; D051381:Rats; D017207:Rats, Sprague-Dawley; D012016:Reference Values; D013777:Tetrazoles / Q000494:pharmacology
chemical_list: D057911:Angiotensin Receptor Antagonists; D001713:Biphenyl Compounds; D007093:Imidazoles; D013777:Tetrazoles; D000804:Angiotensin II; D019808:Losartan