PubMed1996
PURPOSE: Although the enhanced renin-angiotensin (R-A) system responsible for two-kidney, one-clip (2K-1C) hypertension is well known, there may be a shift with time so that this, hemodynamic factor plays a less important role and increased vascular resistance is predominant in sustaining hypertension. While increased vascular protein synthesis has been demonstrated in genetically hypertensive rats, we evaluated the possible relationship between vascular protein synthesis and 2K-1C hypertension with special reference to the R-A system. MATERIALS AND METHODS: Two-kidney one-clip rats were treated with splanchnicotomy, beta-aminopropionitrile (collagen inhibitor), or captopril (angiotensin converting enzyme inhibitor) in the acute or chronic hypertensive phase. 3H-proline was injected into rats, and incorporation rates of 3H-proline into vascular collagen, noncollagenous protein and elastin were counted. The plasma level of the R-A system was assayed. RESULTS: In the acute phase of 2K-1C hypertensive rats whose R-A system was enhanced, captopril treatment further enhanced plasma renin activity and plasma angiotensin I and suppressed plasma angiotensin II while reducing blood pressure. Synthesis of the vascular proteins was almost identical. In the chronic phase of 2K-1C hypertensive rats whose R-A system was within normal limits, increased incorporation rates of 3H-proline into noncollagenous protein or collagen of mesenteric arteries were decreased by splanchnicotomy or beta-aminopropionitrile and hypertension was lowered. Captopril failed to reduce protein synthesis. CONCLUSIONS: An enhanced R-A system participates in the pathogenesis of the acute phase of 2K-1C hypertension while increased noncollagenous protein and collagen syntheses of small arteries appear to play some role in the etiology of the chronic phase of hypertension.