Hypertension and menopause: Vascular effects of the angiotensin converting enzyme in spontaneously hypertensive rats.

JUDITH ZILBERMAN; PINEDA GONZALO; PEREYRA SILVIA; ELESGARAY ROSANA; COSTA MARÍA ÁNGELES; ARRANZ CRISTINA

Congreso; XXIII European Meeting on Hypertension; 2013

Cardiovascular disease risks in women increase after menopause. The responsiblemechanisms for the blood pressure increase in menopausal women are not known.There are multiple factors related to the development of hypertension: an increase inthe activity of the angiotensin I and II (Ang II) converting enzymes (ACE), changesin expression and activity of Ang II receptors type 1 (AT1) receptors. The activationof such receptor leads to vasoconstriction and increases the concentration of freeradicals at vascular level, increasing oxidative stress and vascular lesions. All thesechanges promote BP increase. The estrogen vascular protection effect is attributed todifferent mechanisms, such as renin-angiotensin system (RAS) components control,oxidative stress decrease and nitric oxide (NO) system activation.Aims: To evaluate the effects of enalapril, an ACE inhibitor (ACEI), on vascularmorphology and nitric oxide synthase (NOS) activity in spontaneous hypertensivemenopausal rats (SHR).Methods: The 14-month old SHR female rats were divided in two groups:1) a group treated with enalapril for 30 days (15 mg /kg/day) and 2) controlgroup using ad libitum water. We measured systolic blood pressure (SBP)(indirect method, tail-cuff). In thoracic aorta, NOS activity (pmol 14C Lcitrulline/g.tissue. min) and media thickness (μm/mm) hematoxiline eosin)were measured. Perivascular collagen area (collagen area/lumen area)in renal and coronary arteries was determined in heart and kidney slicesstained with Sirius Red.Results: Enalapril treatment decreased SBP, increased vascular NOS activityand decreased perivascular collagen area in coronary and renal arteries, as wellas, diminished media thickness in the thoracic aorta.Conclusions: RAS inhibition in menopausal SHR rats increases the aortaNO system activity and it may be related to the beneficial effects observedin its structure. On the other hand, the decrease in coronary and renalperivascular fibrosis may reveal an improvement of the cardiac and renalvascular function.