The mechanism of change in the rate of agglutination of human erythrocytes under the influence of adrenaline

Abstract

The study of erythrocytes of 80 men showed that adrenaline (10⁻¹⁰–10⁻⁶ g/mL) and phenylephrine (10⁻¹⁰–10⁻⁶ g/mL) dose-dependently increase the rate of agglutination of erythrocytes, judging by the decrease in the start time of agglutination, whereas ginipral (10⁻¹⁰–10⁻⁷ g/mL), on the contrary, decreases it. The effect of adrenaline and phenylephrine is blocked by nicergoline (10⁻⁶ g/mL), enhanced by obzidan (10⁻⁶ g/mL), and is not changed by yohimbine (10⁻⁶ g/mL) and atenolol (10⁻⁶ g/mL). These data indicate that the rate of agglutination increases with the activation of α1-adrenergic receptor (AR) and decreases with the activation of β₂-AR, whereas the activation of α₂- and β₁-AR does not affect it. Trifluoperazine (10⁻⁶ g/mL) as a calmodulin antagonist, barium chloride (10⁻⁶ g/mL) as a Ca²⁺-dependent K⁺-channel blocker, and indomethacin (10⁻⁶ g/mL) as an inhibitor of cyclooxygenase and phospholipase A₂ inhibit the ability of adrenaline to increase the rate of agglutination of erythrocytes. This suggests that this effect of adrenaline is caused by an increased Ca²⁺ entry into the erythrocyte, activation of calmodulin, cyclooxygenase, and phospholipase A₂, and subsequent K⁺ release from the erythrocytes through the Ca²⁺-dependent K⁺ channels, which is regarded as a manifestation of eryptosis. Indirectly, this means that the potentiation of activation of α₁-AR and β₂-AR, respectively, increases and, conversely, decreases the rate of eryptosis.