Affiliation:
1. the Central Research Laboratory, Ministry of Public Health, Moscow, Russia.
Abstract
We measured Na
+
-H
+
exchange as the amiloride-inhibited fraction of H
+
efflux from red blood cells into a sodium-containing medium (pH
o
7.95 to 8.05) at pH
i
values of 6.05 to 6.15, 6.35 to 6.45, 6.95 to 7.05, and 7.35 to 7.45 in 12 drug-free patients with primary aldosteronism before and after excision of histologically proven aldosterone-producing adrenal adenoma, 12 drug-free essential hypertensive patients, and 12 healthy control subjects. Red blood cell Na
+
-H
+
exchange was increased in patients with primary aldosteronism similarly to the mean exchanger velocity in essential hypertensive patients compared with values in healthy subjects (334±25 and 310±29 versus 139±21 μmol H
+
/L cells per minute, respectively;
P
<.001 and .01). The kinetic parameters of Na
+
-H
+
exchange returned to normal on day 2 after removal of the aldosterone-producing mass.
K
m
for [Na
+
]
o
was not affected by aldosterone, whereas
K
m
for [H
+
]
i
was decreased in patients with primary aldosteronism. The kinetic characteristics did not differ in essential hypertensive patients and control subjects. Protein kinase C inhibition in vitro by calphostin C (60 nmol/L) increased
K
m
for [H
+
]
i
and caused up to a 65% suppression of Na
+
-H
+
exchange (pH
i
6.05 to 6.15), while diminishing
K
m
for [Na+]
o
in red blood cells of patients with primary aldosteronism. The calmodulin antagonist W-13 (60 mmol/L) decreased exchanger velocity and increased
K
m
for both H
+
and Na
+
. We conclude that aldosterone stimulates red blood cell Na
+
-H
+
exchange by a nongenomic mechanism that augments the exchanger affinity to Na
+
and H
+
. In primary aldosteronism, protein kinase C and calmodulin seem to have synergistic stimulatory effects on red blood cell Na
+
-H
+
exchange, and both increase the affinity of the exchanger to H
+
, while their effect on Na
+
binding is opposite.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Reference26 articles.
1. Kinetic abnormalities of the red blood cell sodium-proton exchange in hypertensive patients.
2. Koren W Postnov IY Kuznetzov SV Postnov YuV. Na + /H + exchange in erythrocytes of patients with arterial hypertension. In: Abstracts of the 4th International Symposium on Hypertension in the Community Jerusalem Israel; 1992:83.
3. Amiloride-sensitive Na+ transport in human red cells: Evidence for a Na/H exchange system
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