Hypertension in rat models impairs endothelium-dependent relaxation due to impaired coupling between endothelium and smooth muscle cells, rather than diminished release of endothelium-derived relaxing factor.
Impaired endothelium-smooth muscle coupling in hypertensive models; hypothesis-generating and should not yet change clinical practice.
The relaxation effects of endothelium-dependent (acetylcholine, histamine) and endothelium-independent (nitroprusside, nitrite) relaxing substances were comparatively examined on contracted thoracic aortic rings from normotensive and experimental renal and desoxycorticosterone acetate (DOCA)-salt hypertensive Wistar rats. On the aorta preparations from hypertensive animals a highly significant depression of the maximal relaxation effect of histamine and acetylcholine was observed. This was not seen with nitroprusside and nitrite. By use of a bioassay technique it was demonstrated that the depression of the endothelium-mediated response is not due to a diminished release of endothelium-derived relaxing factor. Impaired coupling between the endothelium and the smooth muscle cells is suggested to be responsible for that depression.
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Voorde et al. (1986) studied this question.
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