Effect of coronary angiography on plasma endothelin-1 and nitric oxide concentrations.

Abstract

Endothelium takes part in the regulation of vascular tone through the production of endothelium-derived relaxing factor, nitric oxide (NO), and the contracting factor endothelin-(ET-1). Induction of ET-1 and NO is influenced by many stimuli including hypoxia and shear stress. Some of these stimuli may arise during coronary angiography (CAG). In this study, the authors aimed to show endothelial response in patients undergoing CAG by evaluating plasma ET-1 and NO end-products including nitrite and nitrate concentrations. Twenty-four male patients with a mean age of 54.3 years (age range: 37-70) were included in the study. The patients had no coronary atherosclerotic lesions established by CAG. The mean time of the CAG procedures was 24.8 minutes, with a range of 19-33 minutes. Immediately before blood sampling, systolic and diastolic blood pressures were recorded. The mean blood pressures before and after CAG were 140/90 and 150/95, respectively. End products of NO radical, nitrite and nitrate (NOx), in plasma were used as a marker for the production of NO radical. ET-1 concentrations were measured by ELISA method. Significant increases in ET-1 concentrations were observed during CAG while no change observed in NOx concentrations. Duration of the CAG procedure was found to be correlated with the percent increase of the plasma ET-1 concentrations during CAG (r = 0.45, p<0.05, Figure 1), but not with NOx concentrations. Plasma ET-1 concentrations in patients who were cigarette smoking were found higher than those of patients who were nonsmokers (1.26 +/- 0.38 and 2.97 +/- 0.87 fmol/L, respectively). It was concluded that endothelial cells show increased ET-1 production as a response of some mechanical or emotional stimuli during CAG procedure that may play an important role in the regulation of vascular tonicity and some pathological processes. The authors suggest that duration and manipulation of CAG may be an important factor in plasma ET-1 concentrations.