In this study, we investigated the effects of Nw -nitro-L-arginine (L-NNA) on arterial blood pressure (BP), plasma noradrenaline (NA) and adrenaline (A) levels and angiotensin-converting enzyme (ACE) activity. L-NNA was applied with tap water (1 mg/ml) from the 3rd to the 8th week of age (group L-NNA1). In Experiment 1, long-term L-NNA application increased BP compared to the control group (group C1) (L-NNA1 = 131.4 ± 6.3, n=6; C1= 82.7 ± 4.7 mm Hg, n=7) but decreased plasma noradrenaline and adrenaline levels and ACE activity (NA levels: C1 = 15.5 ± 0.8, n=7; L-NNA1= 8,6 ± 0.5 ng/ml, n=7; A levels: C1 = 15.5 ± 0.8, n=7; L-NNA1 = 6.0 ± 0.5 ng/ml, n=7; ACE activities: C1= 87.3 ± 3.1, n=6; L-NNA1 = 46.2 ± 1.9 U/l, n=5). On the other hand, in Experiment 2 (carried out under the same conditions and in age-matched chickens), blood pressure, plasma noradrenaline levels and ACE activity were found to differ in the control group (C2) (BP=141.4 ± 15.5 mm Hg, n=7; NA =1.1 ± 0.4 ng/ml, n=7; ACE = 57.2 ± 5.3 U/l, n=7) as compared to C1, while plasma adrenaline levels were similar. In this series, long-term L-NNA application (group L-NNA2) did not change the BP, but surprisingly increased noradrenaline and ACE values (values of L-NNA2: BP = 165.7 ± 15.6 mm Hg, n=7; NA = 9.3 ± 1.3 ng/ml, n=8; ACE = 149.4 ± 16 U/l, n=8) while decreasing plasma adrenaline levels. L-arginine addition to L-NNA treatment completely reversed plasma noradrenaline and ACE activity values. These results indicate the modulatory activity of an L-arginine-NO pathway on adrenaline release as well as on the renin-angiotensin system in chickens., H. E. Aksulu, I. Bingöl, F. Karatas, H. Sagmanligil, B. Üstündag., and Obsahuje bibliografii
Little is known about the effect of chronic angiotensin-converting enzyme inhibition on the catecholamine levels in fowls. In this study, we investigated the effects of chronic lisinopri1 dihydrate (Ld) application on the plasma levels of adrenaline and noradrenaline and on the blood pressure. Lisinopril was given in different concentrations (25, 75 and 250 mg/l drinking water) to the white Leghorn chickens for 9 weeks, while the control group drank tap water only. Twenty-eight hours after the last lisinopril application, arterial blood pressure (BP), plasma adrenaline and noradrenaline levels, plasma renin (PRA) and plasma angiotensin-converting enzyme (ACE) activities were determined. In all concentrations, lisinopril significantly increased PRA and decreased ACE activities. Arterial BP was decreased only in the group receiving high lisinopril concentration (Controls 119±10.27, Ld3 98±5.4 mm Hg). However, the lower lisinopril concentrations did not alter arterial BP compared to the control group. Plasma noradrenaline levels were decreased in a concentration-dependent manner (47-58 %), but plasma adrenaline levels remained unchanged. The heart weight/body weight ratio was not changed in any of the lisinopril-treated groups. The persistent decrease in the blood pressure after lisinopril treatment was not directly related to a decrease of plasma ACE activity or plasma noradrenaline levels. Its mechanism still remains to be elucidated., H. S. Ozdemir, H. E. Aksulu, F. Karataş, B. Ustündag, I. Bingöl., and Obsahuje bibliografii