Key result
Intrarenal administration of Angiotensin III, but not Angiotensin II, induced natriuresis via activation of angiotensin type 2 receptors in the proximal tubule.
Why the study?
Does intrarenal Angiotensin III induce natriuresis via angiotensin type 2 receptors in Sprague-Dawley rats?
Population
Sprague-Dawley rats (with or without systemic angiotensin type 1 receptor blockade with candesartan)
Comparison
Renal interstitial administration of Angiotensin… vs RI angiotensin II, RI angiotensin, or baseline…
Design
Preclinical
Authors
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Hypothesis-generating for AT2-mediated natriuresis; leaves open any therapeutic role for aminopeptidase N inhibition in humans.
Does intrarenal Angiotensin III induce natriuresis via angiotensin type 2 receptors in Sprague-Dawley rats?
Intrarenal Angiotensin III is the primary agonist for proximal tubule AT2 receptors inducing natriuresis, suggesting aminopeptidase N inhibition as a potential therapeutic target for hypertension.
Kemp et al. (2012) studied this question. Renal interstitial administration of Angiotensin III vs. Angiotensin II or Angiotensin (1-7) was evaluated on Urine sodium excretion (natriuresis). Intrarenal administration of Angiotensin III, but not Angiotensin II, induced natriuresis via activation of angiotensin type 2 receptors in the proximal tubule.
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