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(Hypertension. 1997;29:587-591.)
© 1997 American Heart Association, Inc.

Articles

Increased Na⁺-H⁺ Exchange in Red Blood Cells of Patients With Primary Aldosteronism

Wladimir Koren; Ilya Y. Postnov; Yuvenaly V. Postnov

the Central Research Laboratory, Ministry of Public Health, Moscow, Russia.

Correspondence to Wladimir Koren, MD, Department of Medicine C, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel.

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.

Key Words: hypertension, essential • sodium-hydrogen antiporter • primary aldosteronism

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