Hypertension, the microcirculation and serotonin.

Essential hypertension in humans and most experimental animal models of hypertension is hemodynamically characterized by an increased vascular resistance. The site of resistance increase has been localized by recent intravital microscopic studies in most vascular beds primarily in the microcirculation, i.e. in arterioles smaller than 150 microns. Three mechanisms are held responsible for the resistance increase: (1) a rarefaction of the smallest arterioles and capillaries, (2) an increased wall to lumen ratio and (3) a decreased internal diameter. The latter two effects have been localized primarily in the larger arterioles and arteries. The contribution of each of the three factors to the rise in total peripheral resistance depends on the vascular bed, the model of hypertension and its stage of development. Serotonin is one of the endogenous mediators of vascular tone. Its effects have thus far been mostly studied in relation to alterations of internal vascular diameter. Larger arterioles and arteries constrict, but resistance-sized smaller arterioles dilate in response to the exogenous application of serotonin.