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—The aim of the  present study was to demonstrate rapid effects of  aldosterone on the Na+ -H+ exchanger  in strips of human vascular vessels and to determine whether  11β-hydroxysteroid dehydrogenase enzyme (11β-HSD) could play a  protective role in this response, such as that described for the  classic type I mineralocorticoid receptor (MR). The activity of  11β-HSD isoforms 1 and 2 were measured in fetal and adult arteries.  Both isoforms are present in adult and fetal vessels. However, a  significant difference in the proportion of each isoform was found.  Isoform 1 activity (in pmol · min−1 · 100  mg−1 protein) was 42±5 in fetal vessels and 29±2 in  adult arteries, and isoform 2 activity was 78±7 in fetal and 12±2 in  adult tissue. The nongenomic effect of aldosterone on  Na+ -H+ exchanger activity was measured in  strips of chorionic and radial uterine arteries loaded with the  pH-sensitive dye  2′,7′-bis(2-carboxyethyl)-5,6-carboxyfluorescein.  Recordings of intracellular pH (pHi ) were made by  videofluorescence microscopy. Aldosterone (0.5  nmol/L) rapidly increased pHi , with a half-maximal effect  between 2 and 3 nmol/L in both fetal and adult vessels.  Ethylisopropylamiloride, a specific inhibitor of the  Na+ -H+ exchanger, inhibited this effect. The  hormone-mediated increase in pHi was unaffected by  spironolactone, a classic antagonist of MR, but was  completely blocked by RU28318. Cortisol (up to 1 μmol/L) had no  effect on pHi , but when applied in the presence of  carbenoxolone, a dramatic increase in Na+ -H+ exchanger activity was evident. The increments on pHi for  each cortisol concentration were similar to those observed for  aldosterone. These findings suggest that vascular 11β-HSD  plays an active role in maintaining the specificity of the rapid  effects of aldosterone.

Role of 11β-Hydroxysteroid Dehydrogenase in Nongenomic Aldosterone Effects in Human Arteries