Immunocytochemical localization of endothelial nitric oxide synthase (e-NOS) and inducible nitric oxide synthase (i-NOS) in rat neurohypophysis after transient cerebral ischemia.

The expression pattern of endothelial and inducible forms of nitric oxide synthase (e-NOS, i-NOS) in rat neurohypophysis after transient ischemia was investigated using post-embedding immunogold method. We demonstrate that ischemia induced an early (10 min) expression of e-NOS not only in endothelium but also in the mast cells. Expression of i-NOS was almost exclusively confined to glial cells (pituicytes) and perivascular macrophages of experimental animals, and peaked at 24 h after ischemia. This evidence indicates that NO plays a significant role in mechanisms of cerebral ischemia. Taking into account the known beneficial role of e-NOS in ischemia it is likely that mast cells protect against post-ischemic brain damage by producing vasodilatation via nitric oxide. In contrast, cerebral macrophages and pituicytes may mediate neuronal and endothelial damage in late period after ischemia in rat neurohypophysis.