On the central hypertensive effect of angiotensin II |
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Authors: | W B Severs A E Daniels J P Buckley |
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Affiliation: | 1. Agriculture Victoria Research, Department of Energy, Environment and Climate Action, Ellinbank, Victoria 3821, Australia;2. Centre for Agricultural Innovation, School of Agriculture and Food, Faculty of Science, The University of Melbourne, Victoria 3010, Australia;3. FutureFeed Pty Ltd, Townsville, Queensland, Australia;4. Agriculture Victoria Research, Department of Energy, Environment and Climate Action, Ferguson Road, Tatura, Victoria 3616, Australia;1. Department of Theriogenology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran;2. World Pure Heifers, Varamin, Iran |
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Abstract: | It was the purpose of this study to investigate further the mechanism by which angiotensin II produces central hypertensive effects. When administered into the perfused lateral ventricle of the cat, the peptide consistently produced neural presser effects which were essentially abolished by lesions at high midbrain levels. Presser activity was apparently not generated by bulbar efferent or afferent mechanisms, as topical application of the peptide at the termination of the cerebral aqueduct during perfusion produced little or no change in femoral blood pressure when compared with the intraventricular responses in the same animals. Similar pressor activity was observed in perfused dog lateral ventricle experiments but was not detected in experiments in which only subarachnoid structures of the dog brain were perfused. |
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