Impaired skin capillary recruitment in essential hypertension is caused byboth functional and structural capillary rarefaction

Capillary rarefaction occurs in many tissues in patients with essential hyp ertension and may contribute to an increased vascular resistance and impair ed muscle metabolism. Rarefaction may be caused by a structural (anatomic) absence of capillaries, functional nonperfusion, or both. The aim of this s tudy was to assess the extent of structural versus functional capillary rar efaction in the skin of subjects with essential hypertension. We examined s kin capillary density with video microscopy before and during maximization of the number or perfused capillaries by venous congestion (structural capi llary number) and before and during postocclusive reactive hyperemia (capil lary recruitment, which may have a structural and/or functional basis). The study group was composed or 26 patients with never-treated essential hyper tension and 26 normotensive control subjects. In both groups, intermittentl y perfused capillaries in the resting state were an important functional re serve for recruitment during postocclusive hyperemia. Recruitment of perfus ed capillaries during postocclusive reactive hyperemia was decreased in the hypertensive subjects compared with normotensive control subjects (47.9 +/ -6.8 versus 55.3 +/-8.2 capillaries/mm(2), respectively; P<0.01). During ve nous occlusion, maximal capillary density was significantly lower in the hy pertensive subjects than in the control subjects (52.5<plus/minus>6.6 versu s 57.2 +/-8.6 capillaries/mm(2), respectively; P<0.05), suggesting structur al rarefaction. However, in the hypertensive subjects compared with the nor motensive subjects, a smaller proportion of the maximal number of capillari es was perfused during postocclusive hyperemia (91.6<plus/minus>7.5% versus 97.2 +/-2.7%, respectively; P<0.05), suggesting an additional functional i mpairment of capillary recruitment. If the difference in capillary numbers during venous congestion (<approximate to>4.6 capillaries/mm(2)) truly refl ects the structural difference between the normotensive and hypertensive su bjects, then, at most, 62% (4.6/7.4X100%) of the difference in capillary nu mbers during postocclusive hyperemia (approximate to7.4 capillaries/mm(2)) can be explained by structural defects, and at least 38% can be explained b y functional defects. In conclusion, in patients with essential hypertensio n, recruitment of perfused capillaries is impaired, which can be explained by both functional and structural rarefaction.