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Stimulation of several second messenger pathways induces the expression of immediate early genes such as c-fos, cjun, junB, and junD, but little is known about their induction via the stimulation of the cyclic GMP pathway . Here we looked at the expression of early genes in pheochromocytoma PC12 cells after activation of cytosolic guanylate cyclase by sodium nitroprusside . This compound spontaneously releases NO, a molecule known to be involved in cell communication . We found that expression of c-fos and junB but not of c jun or junD is increased upon activation of cyclic GMP pathway . c-fos mRNA expression was the most activated (fourfold at 30 min), whereas junB response was more modest (2 .2-fold activation at 60 min) . Nuclear extracts of stimulated cells show increased binding capacity to the AP1 binding site consistent with the dose-response curve . The activating effect of nitroprusside could be reproduced by dipyridamole, a selective cyclic GMP phosphodiesterase inhibitor and by 8-p-chlorophenylthio-cyclic GMP, a permeant selective cyclic GMP-dependent protein kinase activator, and abolished by KT5823, an inhibitor of that kinase . The results show that NO promotes early gene activation and APi binding enhancement through the stimulation of the cyclic GMP pathway . Key Words: Cyclic GMP-Early genes-fos-Guanylate cyclase-jun-Cyclic GMP-dependent protein kinase .

Risk factors for cerebrovascular disease were noted for each individual aetiology. Hypertension was defined as blood pressure greater than 160/95 mm Hg recorded on three occasions during admission to hospital or in patients previously treated for hypertension. Diabetes mellitus was generally diagnosed before the onset of cerebral infarction. Hyperlipidaemia was defined as an excess in serum cholesterol (more than 10 mmol/l) with or without hypertriglyceridaemia. The index for being overweight was considered to be 15% above the ideal weight. Smoking was noted as a risk factor beyond consumption of 15 cigarettes daily.A probable cause of ischaemic stroke was diagnosed on the basis of clinical, biological and radiological data. Atherosclerosis was considered contributory if typical lesions were found on arteriography. This cause was also presumed if the patient had three or more risk factors leading to atherosclerosis in cases where no arteriographic lesions or identifiable causes were detected. Besides the usual haematological tests, antithrombin III, coagulating factors and platelet activity were measured in the patients having haematological abnormalities. Blood viscosity and fibrinolysis were studied in six patients. C and also S protein were measured in five cases.Circulating anticoagulants were looked for in three cases. Tissue plasminogen activator was measured in two patients. The use of oral contraceptives was considered as a cause and not just a risk factor for cerebral infarction in the absence of any known aetiology leading to brain ischaemia. We attributed cerebral infarction to migraine only in cases of classic migraine. Despite diagnostic investigations,