Hypertension I: Structure of Small Arteries in Hypertension

Re: 0662 Struijker-Boudier Arteriolar growth and vascular resistance

h.struijker-boudier
h.struijkerboudier@farmaco.unimaas.nl

On Fri Dec 11, Russell L. Prewitt wrote
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>Dear Dr. Struijker-Boudier:
> In your introduction you mention that it is not clear if arteriolar rarefaction is an adaptation to hypertension rather than a possible contributing factor. We have shown that rarefaction develops after the pressure begins to rise. The arterioles first go through a period of functional rarefaction where they are closed to flow but can be opened with vasodilators. After more time, the closed vessels are lost completely. This occurs in the SHR as well as renal hypertensive models where there is no genetic predisposition for rarefaction. Both rarefaction and inward, eutrophic remodeling were not seen in the cremaster muscle of rats subjected to aortic coarctation, suggesting that pressure is the stimulus for both of these phenomena. Would you agree that these results suggest that rarefaction is an adaptation to elevated pressure?

Dear Russell,

Rarefaction can indeed be the consequence of a peristent elevated blood pressure. This is certainly true in many models of secondary hypertension. However, in primary (genetic) forms of hypertension rarefaction can occur in very early stages before significant elevation of pressure. This was shown in the SHR, but also in human essential hypertension. We therefore believe that there are two forms of rarefaction: a primary one related to a decreased angiogenic capacity and a secondary one as you have described it in several earlier papers due to pressure increase. Perhaps it would be better to restrict the term "rarefaction" to the latter form and refer to the first form as "decreased angiogenesis".

Harry Struijker-Boudier.

Sun Dec 13