Abstract
Anti‐natriuretic properties of Angiotensin II in the kidney are counterbalanced by the opposing actions of Angiotensin 1‐7 (Ang 1‐7) in normal animals. This study investigated whether the response to Ang 1‐7 was altered in models of hypertension where the renin‐angiotensin system (RAS) was either suppressed (Deoxycorticosterone (DOCA) salt hypertensive) or enhanced (2‐Kidney‐1‐clip (2K1C) hypertensive). Hypertensive groups derived from male Wistar rats (n=4) were anaesthetised and prepared for renal interstitial infusion of Ang 1‐7 (3x10‐³ M) at 1ml/h into the left kidney and cannulation of its ureter. Data±SEM were subject to one‐way ANOVA. Ang 1‐7 had no effect on blood pressure, at 139mmHg for 2K1C rats and 154mmHg for DOCA Hypertensive rats. In 2K1C rats, sodium excretion (UVNa) increased from 6.1±1.4 to 8.7±2.2µmol/min and fractional sodium excretion (FENa) from 1.2±0.2 to 1.5±0.2%, similar to normal rats. Intra‐renal infusion of the same dose of Ang 1‐7 in the DOCA model has no effect on the excretory variables showing a statistically significant difference in the response of these two models. These data suggest that the action of Ang(1‐7) correlates with the level of RAS activation.Grant Funding Source: Supported by Science Foundation Ireland (SFI)
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