Similarity and dissimilarity between angiotensin A and angiotensin II in cardiovascular functions in a rat model

•Ang A deteriorated the postischemic heart function via AT1R, which was similar to that by Ang II.•Ang A increased ANP level in coronary effluent and in atrial perfusate but Ang II did not increase it.•Ang A increased blood pressure, which was 10 times less potent than Ang II.•Our results suggest that the first amino acid of Ang II is important to show various physiological functions. Angiotensin (Ang) A differs from Ang II in a single N-terminal alanine residue. The aim of this study was to investigate whether the effects of Ang A on postischemic cardiac injury and hemodynamics differ from Ang II. After euthanizing Sprague–Dawley rats, hearts were perfused with Krebs–Henseleit buffer for a 20 min preischemic period with or without Ang A or Ang II, followed by 20 min global ischemia and 50 min reperfusion. The blood pressure was measured in anesthetized rats. Ang A (0.1, 1.0, 10 μg/kg) deteriorated the postischemic left ventricular hemodynamics in a dose-dependent manner, which was similar to that by Ang II. Ang A (10 μg/kg) increased the infarct size and the lactate dehydrogenase level, and decreased the coronary flow, which were attenuated by the pretreatment with Ang type 1 receptor (AT1R) antagonist (losartan) but not by AT2R antagonist (PD123319). Ang A increased the expression of apoptotic proteins and decreased the expression of antioxidative proteins. Interestingly, Ang A increased the atrial natriuretic peptide (ANP) level in coronary effluent and in atrial perfusate but Ang II did not increase it. Ang A increased mean arterial blood pressure, which was less potent than Ang II. These results suggest that Ang A has a similar effect on postischemic injury via AT1R and less potent vasopressor effect but opposite effect on ANP secretion as compared to Ang II.