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Calcium and sodium handling during volume expansion in essential hypertension
No full textCalcium and sodium handling during volume expansion in essential hypertension.
Coruzzi P, Biggi A, Musiari L, Ceriati R, Mossini GL, Guerra A, Novarini A.
SourceInstitute of Semeiotica Medica, University of Parma, Italy.
Abstract
To evaluate the actual role of extracellular fluid volume (ECFV) expansion per se in modulating the rate of urinary calcium excretion, a thermoneutral water immersion (WI) study was conducted in 10 normal subjects and 30 patients with essential hypertension. Central hypervolemia by 2 hours of WI caused a significant diuretic and natriuretic response (P < .005) in normal subjects; no significant changes were detected in urinary calcium and magnesium excretion. WI provoked either an appropriate or exaggerated natriuresis (P < .001) in 21 hypertensive patients; these subjects also exhibited a highly positive correlation between urinary sodium and calcium excretion during WI (P < .001). In the remaining nine hypertensive patients, WI produced a significant diuretic response, but a barely discernible (P = NS) natriuresis (inappropriate response). These subjects also exhibited a significant reduction of urinary calcium (P < .001) and magnesium (P < .01) excretion. The data indicate that (1) volume expansion per se may have a role in regulating calcium excretion in hypertensive subjects; (2) a calcium leak may be attributable to a close relationship between urinary sodium and calcium metabolism, and causally related to a disturbance of sodium and volume homeostasis in hypertension
Measuring endothelial dysfunction - Reply
No full textWe thank Schlaich et al. for their [1] useful comments on
our recent paper [2].
We agree that there is no doubt that nitric oxidemediated,
endothelium-dependent mechanisms play a
key role in alterations of renal haemodynamics induced in
humans by systemic L-arginine infusion, which remains
an important tool of research in that field [3]. Such
changes, however, may not be considered solely as a
measure of the endothelial control of kidney circulation,
but reflect a more complex sequence of events, including
changes in tubulo-glomerular feedback (TGF)
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