Nitric oxide (NO) mediates many biological processes including vasodilatation induced by endothelial derived relaxing factor (EDRF) and nitrovasodi1ators. Endothelial cells produce NO and Superoxide anion (02-). NO reacts with O2y-to form cytotoxic peroxynitrite. Superoxide dlsmutase (SOD) scavenges 02- and protects NO. Pathophysiological production of 02- and NO in endothelium is involved in cardiovascular diseases such as ischemia and reperfusion injury. Thus. SOD might play an important role in cardiovascular system in normal and disease status. We have previously reported colocalization of neuronal NO synthase (nNOS) with and protection of nitrergic neurotransmission by copper zinc SOD (CuZn SOD). Here we report colocalization of endothelial NO synthase (eNOS) and CuZn SOD in the canine basal, coronary, kidney, pulmonary arteries and thoracic aorta. Immunohistochemical studies using anti-eNOS antibody and anti-CuZn SOD antibody revealed intense staining for eNOS in endothelial cells in these tissues. These eNOS-containing endothelial cells were also intensely stained for CuZn SOD. Endothelial immunoreactivities for eNOS and CuZn SOD were not observed with preimmune sera and with the primary antibodies preabsorbed by relevant antigens. Immunoreactivities were also not observed in blood vessels gently rubbed on their interior surfaces with cotton swabs prior to tissue fixation. These data Indicate that eNOS is colocalized with CuZn SOD in the canine basal, coronary, kidney, pulmonary arteries and thoracic aorta. (Supported by NIH grant DK17?38.).
|Original language||English (US)|
|State||Published - Dec 1 1996|
ASJC Scopus subject areas
- Molecular Biology