Fibrinogen Effects of Erythrocyte Nitric Oxide Metabolism in Presence of Timolol

Abstract

Timolol inhibits erythrocyte membrane acetylcholinesterase (AChE) enzyme activity originates less active enzyme complex forms unable to change the normal values of the nitric oxide (NO) efflux from erythrocytes. The active complex resulting from acetylcholine (ACh) binding to AChE induces higher values of NO efflux. Increased values of NO efflux were also observed in presence of high fibrinogen (Fib) concentration with return to normal levels of NO efflux when ACh is added. Association between NO efflux and erythrocyte deformability values has been evidenced.The objective of this study was to evaluate the effects of high fibrinogen concentration on the erythrocyte NO metabolism and deformability in presence of timolol without and plus adenylyl cyclase or plus guanylyl cyclase inhibitors.Blood samples from healthy donors were divided in aliquots without (control) or with Fib or Fib plus timolol in absence or presence of adenylyl cyclase inhibitor (MDL) or guanylyl cyclase inhibitor (Ly). Erythrocyte deformability (ED), NO efflux, S-nitrosoglutathione (GSNO), nitrite and nitrate values were evaluated by referenced methods. In conclusion fibrinogen plus timolol increased ED at high shear stress without or with MDL. Fibrinogen increased NO efflux from erythrocytes and GSNO, nitrite and nitrate levels in presence of timolol plus guanylyl cyclase inhibitor.