Key result
Pretreatment with the ACE inhibitor lisinopril prevented the pressor response to ANG-(1-12) and suppressed ANG II formation in both normotensive and hypertensive rats, whereas chymase inhibition had no effect.
Why the study?
Does ACE or chymase inhibition alter angiotensin peptide formation during ANG-(1-12) infusion in WKY and SHR rats?
Population
Normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR)
Comparison
Continuous 15-min ANG- infusion (2 nmol·kg·min)… vs Continuous 15-min ANG- infusion with…
Design
Preclinical
Follow-up
up to 60 minutes
Authors
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ACE inhibition blocks ANG-(1-12) effects in rats; confirms pathway primacy but leaves open human translation.
Does ACE or chymase inhibition alter angiotensin peptide formation during ANG-(1-12) infusion in WKY and SHR rats?
ACE acts as the primary enzyme for the conversion of ANG-(1-12) to smaller angiotensin peptides in the circulation of WKY and SHR rats.
Moniwa et al. (2013) studied Hypertension (n=91). Lisinopril or Chymostatin vs. Saline was evaluated on Plasma angiotensin peptide concentrations and mean arterial pressure response to ANG-(1-12) infusion. Pretreatment with the ACE inhibitor lisinopril prevented the pressor response to ANG-(1-12) and suppressed ANG II formation in both normotensive and hypertensive rats, whereas chymase inhibition had no effect.
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