|| Checking for direct PDF access through Ovid
Objective The aim of this study was to investigate the role of angiotensin ll-induced potentiation of the α1-adrenergic contractile response in the aetiology of low-dose angiotensin ll-induced hypertension.Methods Wistar rats (250 g) received angiotensin II (120ng/kg per min) from subcutaneous minipumps for 21 days. The responses of vaso-active properties of second-order mesenteric arteries (200 µm) to potassium, phenylephrine, angiotensin II and acetylcholine were assessed. The acute amplification effects of angiotensin II on the response to phenylephrine were examined.Results Angiotensin II induced a progressive hypertension, which reached a plateau after approximately 5 days. The responses to potassium, angiotensin II and acetylcholine were not significantly modified in rats treated chronically with angiotensin II. The major finding of this study is that the response to phenylephrine (1-3 µmol/l) was potentiated (sevenfold at 1.75µmol/l) after chronic treatment with angiotensin II. In control vessels acute addition of angiotensin II (10-10mol/l) produced no contraction but induced potentiation of the phenylephrine response (1-3 µmol/l). No further potentiation of the phenylephrine response was observed in the rats treated chronically with angiotensin II.Conclusions Thus, although the direct contractile responses to potassium and angiotensin II remain unaffected following chronic angiotensin II treatment, the α1-adrenergic contractile response to phenylephrine is significantly potentiated by angiotensin II in this model of hypertension. We suggest that this potentiation contributes to the hypertension observed in response to infusion of low-dose angiotensin II.