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

• Published in: Human physiology 2014-03, Vol.40 (2), p.171-178
• Main Authors: Volodchenko, A. I., Tsirkin, V. I., Kostyaev, A. A.
• Format: Article
• Language: English
• Subjects: Biomedical and Life Sciences; Biomedicine; Human Physiology; Life Sciences
• ISSN: 0362-1197; 1608-3164
• DOI: 10.1134/S0362119714010198

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 β 2 -AR, whereas the activation of α 2 - and β 1 -AR does not affect it. Trifluoperazine (10 −6 g/mL) as a calmodulin antagonist, barium chloride (10 −6 g/mL) as a Ca 2+ -dependent K + -channel blocker, and indomethacin (10 −6 g/mL) as an inhibitor of cyclooxygenase and phospholipase A 2 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 Ca 2+ entry into the erythrocyte, activation of calmodulin, cyclooxygenase, and phospholipase A 2 , and subsequent K + release from the erythrocytes through the Ca 2+ -dependent K + channels, which is regarded as a manifestation of eryptosis. Indirectly, this means that the potentiation of activation of α 1 -AR and β 2 -AR, respectively, increases and, conversely, decreases the rate of eryptosis.