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|Title:||Angiotensins in plasma of hypertensive rats and human|
|Authors:||Sim, M.K. |
Spontaneously hypertensive rats
|Source:||Sim, M.K., Qui, X.S. (2003). Angiotensins in plasma of hypertensive rats and human. Regulatory Peptides 111 (1-3) : 179-182. ScholarBank@NUS Repository. https://doi.org/10.1016/S0167-0115(02)00289-6|
|Abstract:||The plasma levels of des-aspartate-angiotensin I (DAA-I) in three models of hypertensive rats and hypertensive subjects were determined and compared with their normotensive controls. The rationale for the study was based on our earlier findings showing that DAA-I is a physiological angiotensin peptide that is involved in the pathophysiology of the cardiovascular system. The determination was carried out by the technique of capillary electrophoresis. Plasma level of angiotensin I, angiotensin II, and angiotensin III was also determined as a measurement of the status of the renin-angiotensin system in the different models of hypertension. DAA-I was found to be significantly lower in the spontaneously hypertensive rats (SHR) (46.6±2.5 pmol/l compared to 66.1±3.4 pmol/l for the normotensive control Wistar Kyoto rats), renal hypertensive rats (54.2±5.1 pmol/l compared to 72±2.5 pmol/l for the normotensive control Sprague-Dawley rats), and essential human hypertensive subjects (15.2±0.9 pmol/l compared to 19.5±2.5 pmol/l for the normotensive adult), whilst plasma concentration of angiotensin I and angiotensin II is reflective of the state of the renin-angiotensin system in the particular model of hypertension. When the SHR and human hypertensive subjects were treated with an angiotensin converting enzyme (ACE) inhibitor, the plasma level of DAA-I increased significantly. These findings suggest that the low plasma level of DAA-I could be a characteristic defect of the renin-angiotensin system in the two genetic models of hypertension (SHR and human essential hypertensive subjects). The increase of the nonapeptide following ACE inhibitor treatment could be an important hitherto unrecorded contributory factor to the effectiveness of ACE inhibitors in combating heart pathology. © 2002 Elsevier Science B.V. All rights reserved.|
|Source Title:||Regulatory Peptides|
|Appears in Collections:||Staff Publications|
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