Capillary rarefaction occurs in many tissues in patients with essential hypertension and may contribute to an increased vascular resistance and impaired muscle metabolism. Rarefaction may be caused by a structural (anatomic) absence of capillaries, functional nonperfusion, or both. The aim of this study was to assess the extent of structural versus functional capillary rarefaction in the skin of subjects with essential hypertension. We examined skin capillary density with video microscopy before and during maximization of the number of perfused capillaries by venous congestion (structural capillary number) and before and during postocclusive reactive hyperemia (capillary recruitment, which may have a structural and/or functional basis). The study group was composed of 26 patients with never-treated essential hypertension and 26 normotensive control subjects. In both groups, intermittently perfused capillaries in the resting state were an important functional reserve for recruitment during postocclusive hyperemia. Recruitment of perfused 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/mm², respectively;P<0.01). During venous occlusion, maximal capillary density was significantly lower in the hypertensive subjects than in the control subjects (52.5±6.6 versus 57.2±8.6 capillaries/mm², respectively;P<0.05), suggesting structural rarefaction. However, in the hypertensive subjects compared with the normotensive subjects, a smaller proportion of the maximal number of capillaries was perfused during postocclusive hyperemia (91.6±7.5% versus 97.2±2.7%, respectively;P<0.05), suggesting an additional functional impairment of capillary recruitment. If the difference in capillary numbers during venous congestion (≈4.6 capillaries/mm²) truly reflects the structural difference between the normotensive and hypertensive subjects, then, at most, 62% (4.6/7.4×100%) of the difference in capillary numbers during postocclusive hyperemia (≈7.4 capillaries/mm²) can be explained by structural defects, and at least 38% can be explained by functional defects. In conclusion, in patients with essential hypertension, recruitment of perfused capillaries is impaired, which can be explained by both functional and structural rarefaction.

Background —A strong but presently unexplained inverse association between blood pressure and insulin sensitivity has been reported. Microvascular vasodilator capacity may be a common antecedent linking insulin sensitivity to blood pressure. To test this hypothesis, we studied 18 normotensive and glucose-tolerant subjects showing a wide range in insulin sensitivity as assessed with the hyperinsulinemic, euglycemic clamp technique. Methods and Results —Blood pressure was measured by 24-hour ambulatory blood pressure monitoring. Videomicroscopy was used to measure skin capillary density and capillary recruitment after arterial occlusion. Skin blood flow responses after iontophoresis of acetylcholine and sodium nitroprusside were evaluated by laser Doppler flowmetry. Insulin sensitivity correlated with 24-hour systolic blood pressure (24-hour SBP; r =−0.50, P <0.05). Capillary recruitment and acetylcholine-mediated vasodilatation were strongly and positively related to insulin sensitivity ( r =0.84, P <0.001; r =0.78, P <0.001, respectively), and capillary recruitment was inversely related to 24-hour SBP ( r =−0.53, P <0.05). Waist-to-hip ratio showed strong associations with insulin sensitivity, blood pressure, and the measures of microvascular function but did not confound the associations between these variables. Subsequent regression analysis showed that the association between insulin sensitivity and blood pressure was not independent of the estimates of microvascular function, and part of the variation in both blood pressure ( R ² =38%) and insulin sensitivity ( R ² =71%) could be explained by microvascular function. Conclusions —Insulin sensitivity and blood pressure are associated well within the physiological range. Microvascular function strongly relates to both, consistent with a central role in linking these variables.

Chronic renal transplant dysfunction (CRTD) remains a leading cause of renal allograft loss. Evidence suggests that immunological and ischemic insults are mainly associated with CRTD occurring within the first year after transplantation, whereas nonimmunological insults are predominantly associated with CRTD beyond the first year. Several cardiovascular risk factors, such as obesity, dyslipidemia, hypertension, and diabetes mellitus have been identified as important nonimmunological risk factors for CRTD. These risk factors constitute the metabolic syndrome (MS). As renal allograft function is a surrogate marker of renal allograft loss, we investigated the association of MS with impairment of renal allograft function beyond the first year after transplantation in a cross-sectional study of 606 renal transplant outpatients. Metabolic syndrome was defined using the definition of the National Cholesterol Education Program. Renal allograft function was assessed as the 24-h urinary creatinine clearance. A total of 383 out of 606 patients (63%) suffered from MS at a median time of 6 years (2.6–11.4) post-transplant. Presence of MS was associated with impaired renal allograft function beyond 1 year post-transplant [−4.1 mL/min, 95%CI (−7.1, −1.1)]. The impact of MS did not change appreciably after adjustment for established risk factors for CRTD [−3.1 mL/min, 95%CI (−6.0, −0.2)]. However, not all component criteria of MS contributed equally. Only systolic blood pressure and hypertriglyceridemia were independently associated with impaired renal allograft function beyond 1 year post-transplant in multivariate analyses.