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Öğe Leptin Prevents U46619- and Angiotensin II-Elicited Contraction in Isolated Human Umbilical Vessels(Erciyes Univ Sch Medicine, 2022) Duman, Ipek; Soner, Burak Cem; Irian, Salim Yalcin; Sahin, Ayse SaideObjective: This study investigated the vasoactive responses of quiescent and pre-contracted isolated human umbilical veins and arteries to cumulative leptin. Materials and Methods: The vasoactive response of umbilical vessels pre-contracted with U46619 (10(-10)M) and angiotensin II (10(-6)M) to cumulative leptin (10(-11)-10(-7)M) were recorded in vitro. Results: Leptin did not affect the artery or vein basal tonus (p=1). The leptin-elicited relaxation in U46619-contracted vessels was greater in veins than in arteries (p<0.001). Incubation with N (omega)-nitro-L-arginine methyl ester (L-NAME) (10(-4)M) prevented the leptin-induced relaxation of the U46619 contraction response in the artery. The E-max and pD(2) values of the L-NAME-incubated veins were lower than those of the non-incubated veins (p<0.001 and p=0.001, respectively). The relaxation in angiotensin II-contracted veins was greater than that of the arteries (p<0.001). Incubation with L-NAME prevented leptin-induced relaxation in angiotensin II-contracted arteries. The E-max of leptin-induced relaxation of L-NAME-incubated veins was significantly lower than that of non-incubated veins (p=0.027); the pD(2) was similar. Conclusion: Leptin did not alter the resting tension of isolated umbilical vessels; however, the results indicated that leptin caused concentration-dependent relaxation in umbilical vessels pre-contracted with U46619 or angiotensin II. The maximum relaxation was greater in veins compared with arteries. Incubation with L-NAME completely inhibited leptin-induced relaxation in arteries and resulted in a significant inhibition in veins.Öğe Leptin Prevents U46619- and Angiotensin II-Elicited Contraction in Isolated Human Umbilical Vessels(Erciyes Univ Sch Medicine, 2022) Duman, Ipek; Soner, Burak Cem; Irian, Salim Yalcin; Sahin, Ayse SaideObjective: This study investigated the vasoactive responses of quiescent and pre-contracted isolated human umbilical veins and arteries to cumulative leptin. Materials and Methods: The vasoactive response of umbilical vessels pre-contracted with U46619 (10(-10)M) and angiotensin II (10(-6)M) to cumulative leptin (10(-11)-10(-7)M) were recorded in vitro. Results: Leptin did not affect the artery or vein basal tonus (p=1). The leptin-elicited relaxation in U46619-contracted vessels was greater in veins than in arteries (p<0.001). Incubation with N (omega)-nitro-L-arginine methyl ester (L-NAME) (10(-4)M) prevented the leptin-induced relaxation of the U46619 contraction response in the artery. The E-max and pD(2) values of the L-NAME-incubated veins were lower than those of the non-incubated veins (p<0.001 and p=0.001, respectively). The relaxation in angiotensin II-contracted veins was greater than that of the arteries (p<0.001). Incubation with L-NAME prevented leptin-induced relaxation in angiotensin II-contracted arteries. The E-max of leptin-induced relaxation of L-NAME-incubated veins was significantly lower than that of non-incubated veins (p=0.027); the pD(2) was similar. Conclusion: Leptin did not alter the resting tension of isolated umbilical vessels; however, the results indicated that leptin caused concentration-dependent relaxation in umbilical vessels pre-contracted with U46619 or angiotensin II. The maximum relaxation was greater in veins compared with arteries. Incubation with L-NAME completely inhibited leptin-induced relaxation in arteries and resulted in a significant inhibition in veins.