Enhanced destruction of nitric oxide by superoxide is associated with a number of cardiovascular and neural pathologies including hypertension, atherosclerosis, thrombosis, ischaemia-reperfusion injury, stroke and diabetes. Consequently, we are presently pursuing the concept that low molecular weight, membrane permeant SOD mimetic compounds may have a role as therapeutic agents. This involves the dual approach of screening agents for SOD mimetic activity using biochemical assays and examining their actions in biological systems under conditions of oxidant stress. Our long term aim is to develop ways of alleviating the deficient activity of nitric oxide in the above pathological conditions. Phase-contrast micrograph of porcine aortic endothelial cells in culture Role of nitric oxide in control of cerebrovascular tone and in migraine.
Most blood vessels possess sympathetic vasoconstrictor nerves but lack vasodilator nerves.
Vasodilatation is generally controlled by release of vasodilator agents, most notably nitric oxide, from the vascular endothelium. The major cerebral arteries, however, are members of a small group of highly specialised blood vessels which possess parasympathetic vasodilator nerves and, indeed, these too release nitric oxide as their neurotransmitter. Thus, control of cerebrovascular tone is regulated by release of nitric oxide from two distinct cellular sources. Furthermore, nitric oxide is now regarded as a central mediator of the profound vasodilatation and inflammation of migraine. Transverse section of porcine cerebral artery Role of nitric oxide in reproduction.