Vascular Remodeling in Hypertension: Its Prevalence and Possible Mechanism

Abstract

The importance of the structural changes of the arteries in the development of hypertension has been championed by Folkow and his colleagues. Based on their perfusion studies in various animal models, and observations in hypertensive humans, Folkow suggested that the increase in vascular resistance and reactivity observed in the hypertensives can be explained by an alteration in vascular wall architecture, without the need to involve any change in sensitivity of the vasculature (14–17). There are two important aspects to this vascular wall alteration: [1] An increase in the medial wall thickness, which results in an increase in medial wall to lumen ratio; [2] An encroachment of the medial wall into the lumen, so that even at maximal relaxation, vascular resistance is increased in the hypertensives. Many histologic and morphometric studies of the arteries from hypertensive humans and animals have indeed documented the presence of medial wall hypertrophy, as well as an increase in media to lumen ratio in arteries from various vascular bed, and in different animal models (1,32,38–40). Encroachment of the medial wall into the lumen, i.e. a permanent narrowing of the lumen diameter, was found in some arteries from humans and in some animal models, but there is no consistency. In the spontaneously hypertensive rats (SHR), a narrower lumen in maximally relaxed arteries was found in the superior mesenteric and large mesenteric arteries of female SHR as compared with female Wistar-Kyoto normotensive rats (WKY)(41), whereas in the males, a smaller lumen was found only in the small mesenteric arteries from the SHR as compared with WKY (36), so that the difference in lumen size was dependent on sex and the calibre of the arteries.