Contribution of erythrocytes to phenylephrine-mediated vascular contraction responses

Objective: This study aimed to examine the effect of erythrocytes on phenylephrine-mediated vasoconstriction and to investigate the mechanism of this effect. Methods: Thoracic aorta segments obtained from 8-10 week old Wistar albino rats were placed in a tissue bath and phenylephrine (10-9-3x10-4 M) concentration-response curves were examined in the presence of Krebs solution and erythrocyte suspension. Blood samples were taken from healthy volunteers aged 18-45. The protocols were repeated in the presence of adrenoceptor antagonist Carvedilol, non-selective cyclooxygenase inhibitor Indomethacin, Thromboxane synthase inhibitor Dazoxiben, Thromboxane-A2 receptor antagonist GR32191B and Prostaglandin-F2α receptor antagonist AL8810. Following these measurements, Thromboxane-B2 and free hemoglobin measurements were made in the samples taken in the tissue bath. Results: It was observed that the vasoconstriction obtained in the presence of erythrocyte suspensions were significantly higher compared to Krebs solution alone (p<0.001). Carvedilol inhibited vasoconstriction responses in all groups (p<0.001). This increase in vasoconstriction occurring in the presence of erythrocytes was suppressed in the presence of indomethacin (p<0.01). It was found that the difference in response between tissue baths with and without erythrocytes disappeared in the presence of Dazoxiben and GR32191B. It was observed that vasoconstriction responses in the presence of erythrocytes were not affected by AL8810 incubation (p<0.01). It was found that the amount of Thromboxane B2 increased in the erythrocyte suspension group in response to phenylephrine (p<0.001) and free hemoglobin levels did not differ between groups.