Sharifi A M, Heshmatian B, Karimiam S M, Akbarloo N. Mesenteric Responsiveness To Angiotensin I, II And Captopril During Renovascular Hypertension Induction. Tehran Univ Med J 2003; 61 (3) :245-253
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http://tumj.tums.ac.ir/article-1-1192-en.html
Abstract: (25111 Views)
Essential hypertension is one of the risk factors of cardiovascular diseases. Hypertension etiology is not completely known, it seems that rennin-Angiotensin system has an important role in its etiology, Thus better recognition of this system and its activity changes or vascular reaction changes to different parts of this system during progressive hypertension can be more effective in better recognition of the disease progress and treatment.
Materials and Methods: In this study responsiveness of mesenteric vessels of Goldblatt two kidney- one clip (2k-lc) renovascular hypertensive rats to angiotensin / and II with and with out captopril during a time of two , four , six and eight weeks after hypertension induction was investigated and compared with control and surgical sham groups.
Results: This study shows that vascular responsiveness to angiotensin // in animals that passed four weeks of their hypertension , (p< 0.05) and in the sixth and eight week of post induction hypertension (p< 0.01 and p< 0.001) has a significant different with both sham and control groups. Also it has been observed that an increased reaction to angiotensin II with an increased significant rate of arterial hypertension in hypertensive group. In the other hand in spite of inhibition of angiotensin converting enzyme by captopril in animals that have been eight weeks hypertension , on the contrary to other groups reactive to angiotensin /.
Conclusion: Results of this study show that vessels reaction to angiotensin /and II increased due to six to eight weeks post induction renal hypertension. Captopril does not inhibite mesenteric vessels reaction to Angiotensin / in hypertensive Rats after eight weeks. Try to completely inhibit production of angiotensin II maybe a hopful way in controlling essential hypertension.