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Ns [26,32,42-45]. However, the deleterious effects of AT1R antagonists in pregnancy [46,47] preclude their use for identifying the main receptor stimulated by excess angiotensin. The acute effect of angiotensin II plus a B2R blocker provoked an increase of systolic blood pressure in a subset of the group (responders) to values that were not attained with single interventions and in non-pregnant fe
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