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.

Abstract-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 (47.9Ϯ6.8 versus 55.3Ϯ8.2 capillaries/mm 2 , respectively; PϽ0.01). During venous occlusion, maximal capillary density was significantly lower in the hypertensive subjects than in the control subjects (52.5Ϯ6.6 versus 57.2Ϯ8.6 capillaries/mm 2 , respectively; PϽ0.05), 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 (91.6Ϯ7.5% versus 97.2Ϯ2.7%, respectively; PϽ0.05), suggesting an additional functional impairment of capillary recruitment. If the difference in capillary numbers during venous congestion (Ϸ4.6 capillaries/mm 2 ) truly reflects the structural difference between the normotensive and hypertensive subjects, then, at most, 62% (4.6/7.4ϫ100%) of the difference in capillary numbers during postocclusive hyperemia (Ϸ7.4 capillaries/mm 2 ) 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.

It has been proposed that insulin-mediated changes in muscle perfusion modulate insulin-mediated glucose uptake. However, the putative effects of insulin on the microcirculation that permit such modulation have not been studied in humans. We examined the effects of systemic hyperinsulinemia on skin microvascular function in eight healthy nondiabetic subjects. In addition, the effects of locally administered insulin on skin blood flow were assessed in 10 healthy subjects. During a hyperinsulinemic clamp, we measured leg blood flow with venous occlusion plethysmography, skin capillary density with capillaroscopy, endothelium-(in)dependent vasodilatation of skin microcirculation with iontophoresis of acetylcholine and sodium nitroprusside combined with laser Doppler fluxmetry, and skin vasomotion by Fourier analysis of microcirculatory blood flow. To exclude nonspecific changes in the hemodynamic variables, a time-volume control study was performed. Insulin iontophoresis was used to study the local effects of insulin on skin blood flow. Compared to the control study, systemic hyperinsulinemia caused an increase in leg blood flow (؊0.54 ؎ 0.93 vs. 1.97 ؎ 1.1 ml ⅐ min ؊1 ⅐ dl ؊1 ; P < 0.01), an increase in the number of perfused capillaries in the resting state (؊3.7 ؎ 3.0 vs. 3.4 ؎ 1.4 per mm 2 ; P < 0.001) and during postocclusive reactive hyperemia (؊0.8 ؎ 2.2 vs. 5.1 ؎ 3.7 per mm 2 ; P < 0.001), an augmentation of the vasodilatation caused by acetylcholine (722 ؎ 206 vs. 989 ؎ 495%; P < 0.05) and sodium nitroprusside (618 ؎ 159 vs. 788 ؎ 276%; P < 0.05), and a change in vasomotion by increasing the relative contribution of the 0.01-to 0.02-Hz and 0.4-to 1.6-Hz spectral components (P < 0.05). Compared to the control substance, locally administered insulin caused a rapid increase (ϳ13.5 min) in skin microcirculatory blood flow (34.4 ؎ 42.5 vs. 82.8 ؎ 85.7%; P < 0.05). In conclusion, systemic hyperinsulinemia in skin 1) induces recruitment of capillaries, 2) augments nitric oxide؊mediated vasodilatation, and 3) influences vasomotion. In addition, locally administered insulin 4) induces a rapid increase in total skin blood flow, independent of systemic effects. Diabetes 51: 1515-1522, 2002

As in cardiovascular disease, CRP appears to be a risk marker for renal function loss. The mechanism of this relationship remains to be clarified. However, the association between CRP, body weight, and a relatively elevated creatinine clearance is a hypothesis-generating finding, suggesting that early inflammatory processes related to high body fat may predispose the kidney to glomerular hyperfiltration-related renal function loss.

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