Key result
Co-infusion of Ang1-7 significantly attenuated the increase in systolic blood pressure in AngII-infused rats compared to AngII alone (161 vs 195 mm Hg; P<0.002).
In a rat model of AngII-dependent hypertension, Ang1-7 co-infusion attenuates blood pressure elevation and promotes sodium and fluid excretion, an effect that appears to be mediated via AT1 rather than Mas receptors.
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Hypothesis-generating in AngII rat hypertension; clinical translation of Ang1-7 remains untested.
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.
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Kuczeriszka et al. (2017) studied AngII-dependent hypertension. Ang1-7 vs. AngII alone was evaluated on Systolic blood pressure (SBP) (p=< 0.002). Co-infusion of Ang1-7 significantly attenuated the increase in systolic blood pressure in AngII-infused rats compared to AngII alone (161 vs 195 mm Hg; P<0.002).
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