Why the study?
Do aging and hypertension alter capillary pressure, density, and microvascular function?
Do aging and hypertension alter capillary pressure, density, and microvascular function?
Aging significantly increases capillary pressure without altering capillary density, while hypertension adds no additional effect on these parameters, suggesting normotensive aging relies on preserved NO-dependent vasodilatation at the expense of increased capillary pressure.
Aging-related capillary pressure rise warrants no practice change in hypertension; leaves open microvascular contributions to age-related CV risk.
Alterations of structure and function of the microcirculation in hypertension in the elderly and changes with normotensive aging have not been fully clarified. We studied capillary pressure, density, and skin microvascular function in 46 subjects in 3 groups: elderly subjects (aged >60 years) with untreated hypertension (n=16), elderly normotensive subjects (n=16), and young normotensive subjects (age <45 years, n=14). In a subgroup of 19 subjects, we also studied resistance artery function in the isometric myograph. Capillary pressure was higher in both elderly groups (elderly hypertensives: 18.6+/-4.7 mm Hg, elderly normotensives: 17.6+/-4.0 mm Hg) compared with young normotensives (13.9+/-2.6 mm Hg, P<0.05), but capillary density did not differ between the groups. Skin vasodilating responses to acetylcholine were greater in young normotensives compared with both elderly groups (P<0.05). In isolated resistance arteries, there was a greater inhibitory effect from blockade of the l-arginine-NO pathway in elderly normotensives (P<0.05) and a reduction in the maximal inhibitory effect of combined blockade of NO, prostanoids, and endothelium-derived hyperpolarizing factor in elderly hypertensives (P<0.05). This study has demonstrated a significant effect of aging but no additional effect of hypertension on capillary pressure and no effect of either on capillary density. Our findings with both in vivo and in vitro methods suggest that normotensive aging may depend on relative preservation of NO-dependent vasodilatation in resistance arteries at the expense of a rise in capillary pressure.
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James et al. (2006) studied this question.
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