Ramipril and vascular hypertrophy in spontaneously hypertensive rats

M. J. Jamieson, W. F. Romano, T. I. Jackson, S. M. Koerth, A. M.M. Shepherd

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Ramipril (RAM), an ACE inhibitor (ACEI) with high affinity for tissue ACE, appears to prevent hypertensive vascular smooth muscle and left ventricular hypertrophy (VSMH, LVH) at subantihypertensive doses. Our aim was to test whether RAM at modest and sub-antihypertensive doses could reverse LVH and VSMH of resistance arteries of mature SHRs. 16 week male SHR received RAM 1mg/kg/day in drinking water, or no drug, for 12 weeks. Wall:lumen ratios of isolated small mesenteric arteries (W:L, as %) were measured at 70-130 mmHg , in an arteriograph. Results are shown in the table: p are for unpaired t-tests. In the controls, tail cuff BFs averaged 229/199 mmHg at entry and 213/185 at the end. Diameters at 70-130 mmHg were 200-217 μn (control) and 193-207 (treated): p values for differences 0.50-0.64. control ramipril n mean sd n mean sd p(diff ) BP ↓ sys 13 16 23 14 38 31 .049 dia 13 15 23 14 48 24 .0015 heart wt (% body) 10 3.5 0.4 10 3.1 0.2 .06 W:L @ 70mmHg 23 11.6 2.9 25 12.2 2.9 0.56 W:L @ 130mmHg 23 9.3 2.3 25 10.2 2.3 0.26 Despite the reductions in BP, and LVH, RAM at this dose did not reverse VSMH. Subantihypertensive dosing was not pursued. Further studies with higher doses, with the active metabolite ramiprilat and in other (e.g. high renin) models may be justified.

Original languageEnglish (US)
Pages (from-to)54A
JournalJournal of Investigative Medicine
Issue number1
StatePublished - 1996

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology


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