Abstract
Hypertension is a major risk factor for cardiovascular disorders. As flow-mediated outward remodeling has a key role in postischemic revascularization, we investigated this remodeling in mesenteric resistance arteries of normotensive (WKY) and spontaneously hypertensive rats (SHRs) aged 3 to 9 months. Sequential ligation of mesenteric resistance arteries allowed modifying blood flow in vivo, thus exposing arteries to low, normal, or high flow. After 1, 3, 8, or 24 weeks, arteries were isolated for in vitro study. High flow (HF) induced outward hypertrophic remodeling in WKY rats after 1 week and persisted until 24 weeks without change in wall to lumen ratio. In SHRs, diameter increase was delayed, occurring only after 3 weeks. Nevertheless, it was reduced at 8 weeks and no longer significant after 24 weeks. In parallel, media cross-section area increased more with time in SHRs than in WKY rats and this was associated with increased contractility and oxidative stress with decreased NO-dependent relaxation. Low flow induced progressive inward remodeling until 24 weeks in both strains with excessive hypertrophy in SHRs. Thus, a chronic increase in flow induced transitory diameter expansion and long-lasting hypertrophy in SHRs. This could contribute to the higher susceptibility of hypertensive subjects to ischemic diseases.
Highlights
Arterial hypertension is a major public health problem concern worldwide
We have shown that nitric oxide (NO) is essential to mesenteric resistance arteries remodeling induced by a chronic increase in blood flow [13, 14]
In High flow (HF) arteries blood flow ranged from 673 ± 52 to 724 ± 79 μL/min in WKY rats (n = 5 or 6 per group) and from 654 ± 45 to 688 ± 70 μL/min in spontaneously hypertensive rats (SHR) (n = 5 per group, P > 0.05)
Summary
Arterial hypertension is a major public health problem concern worldwide. This insidious disease that causes few if any symptoms or warning signs is an important risk factor for myocardial infarction, stroke, renal failure, and peripheral arterial disease. Chronic increase in blood pressure induces a structural vascular remodeling associated with endothelial dysfunction and increased vascular tone in resistance arteries [1, 2]. Hypertension-induced arterial remodeling is different along the vascular tree. Hypertrophic remodeling and increased stiffness may affect resistance arteries in more severe forms of essential hypertension or in renovascular (secondary) hypertension [4] and this may have dramatic consequences on local perfusion pressure and blood supply to target organs
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