Why the study?
Does captopril alter forearm vascular resistance and forearm venous volume in normal subjects during sodium loading and depletion?
Does captopril alter forearm vascular resistance and forearm venous volume in normal subjects during sodium loading and depletion?
The renin-angiotensin-aldosterone system contributes to the maintenance of blood pressure and limb vascular resistance only in sodium-depleted subjects, and does not regulate limb venous capacitance.
Supports RAAS contribution to BP and resistance only in sodium depletion; leaves open venous capacitance role and clinical translation.
It is not known whether the renin-angiotensin-aldosterone (RAA) system contributes to the regulation of the limb circulation in normal human beings. Accordingly, the effect of the angiotensin converting-enzyme inhibitor, captopril, on forearm vascular resistance (FVR) and forearm venous volume (FVV) was studied in nine normal subjects during states of both sodium loading and sodium depletion. All subjects were studied in the supine position and during 60 degrees head-up tilt. By analysis of variance, the combined intervention of sodium depletion and converting-enzyme inhibition was responsible for a decrease in both FVR and mean blood pressure (BP). In sodium-depleted subjects, converting-enzyme inhibition decreased supine mean BP 7.0% and supine FVR 22.8% but did not change FVV. Neither the fall in BP nor the fall in FVR, however, was significantly augmented by tilting from a supine to upright posture. In sodium-loaded subjects, captopril did not alter BP, FVR, or FVV in recumbent or upright positions. Therefore, the RAA system contributes to the maintenance of blood pressure and limb vascular resistance only in sodium-depleted subjects. Limb venous capacitance in normal subjects is not regulated by the RAA system.
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Creager et al. (1984) studied this question.
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