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Abstract

Angiotensin (1-7), a metabolite of All and/or Al was infused into the renal artery (I.r.a.) of anesthetized dogs in order to investigate its renal action. Renal blood flow (RBF) was measured by electromagnetic flowmeter, glomerular filtration rate (GFR) by creatinine clearance. In group 1 animals A (1-7) at a dose of 15 μ/min/kg body weight did not affect systemic arterial blood pressure (BP) or water and sodium excretion from the contralateral non-infused kidney. Group 2 animals received EXP 3174, the active metabolite of the AT1 receptor antagonist losartan (30 μ/min/kg), with A (1-7). In group 3 the AT2 receptor antagonist PD 123319, 10 μg/min/kg), was added to the infusion of A (1-7). A small significant decrease in RBF from 4.51 ± 0.32 to 3.80 ± 0.20 ml/min/g kidney weight occurred with A (1-7); a similar decrease was observed when PD 123319 was added. In contrast, an increase to 4.98 ± 0.34 ml/min/g k.w. was seen after the addition of EXP 3174 to the i.r.a. infusion of A (1-7). This increase was similar to the increase observed with EXP 3174 alone (5.21 ± 0.33 ml/min/g; p < 0.02). A similar significant increase in GFR was seen with A (1-7) or EXP 3174 alone, but only the rise in sodium excretion was statistically significant. Potassium excretion was increased with A (1-7) alone to the same degree as with EXP 3174 alone. In summary, I.r.a. infusion of A (1-7) in the dog was followed by an increase in water, sodium and urea excretion, probably due to its tubular action. This effect was partially blocked by AT1 receptor antagonist and was not affected by AT2 receptor antagonist. These data suggest indirectly that another receptor could play a role in the tubular action of A (1-7). Moreover, the decrease in RBF that disappeared after EXP 3174, suggests an additional role of the AT1 receptor in the action of A (1-7).

Angiotensin(1-7), Renal Action, Dog Kidney
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© American Journal of Hypertension, Ltd. 2001
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