Biomedical subjects

G Gulec

Publications and source records attributed to G Gulec.

3 recordsLinked to original sources

PubMed2001

Do recurrent febrile convulsions decrease the threshold for pilocarpine-induced seizures? Effects of nitric oxide.

The aim of the study was to determine whether (1) number of febrile convulsions is a predictor of development of temporal lobe epilepsy, (2) the susceptibility of rats to pilocarpine-induced seizures is increased due to febrile convulsions and (3) nitric oxide is a mediator in the pathogenesis of febrile convulsions. Rat pups were exposed to single or multiple hyperthermic seizures. Subconvulsant doses of pilocarpine (100 mg/kg and 150 mg/kg) were injected intraperitoneally to these rats at 60--70 days of age. Also L-arginine was applied to some rats before a single hyperthermic seizure. We found that risk of future epilepsy increases parallel to the number of febrile convulsions and nitric oxide does not have a pathogenetic role at given doses.

Animals↗

PubMed2001

A central link between angiotensinergic and cholinergic systems; role of vasopressin.

Participation of central cholinergic system in the effects of intracerebroventricular (i.c.v.) injection of angiotensin II (Ang II) on blood pressure and heart rate was studied in conscious, freely moving rats. Ang II dose-dependently increased blood pressure and decreased heart rate. Both atropine and mecamylamine (i.c.v.) pretreatments prevented the cardiovascular effects of Ang II. Pretreatment with a vasopressin V1 antagonist also prevented the cardiovascular responses to Ang II. Our data suggest that the central pressor effect of Ang II is mediated in part by central acetylcholine via both muscarinic and nicotinic receptors, and vasopressin participates in this effect through V1 receptors.

Angiotensin II↗

PubMed2001

Central injection of captopril inhibits the blood pressure response to intracerebroventricular choline.

In the present study, we investigated the involvement of the brain renin-angiotensin system in the effects of central cholinergic stimulation on blood pressure in conscious, freely moving normotensive rats. In the first step, we determined the effects of intracerebroventricular (icv) choline (50, 100 and 150 microg) on blood pressure. Choline increased blood pressure in a dose-dependent manner. In order to investigate the effects of brain renin-angiotensin system blockade on blood pressure increase induced by choline (150 microg, icv), an angiotensin-converting enzyme inhibitor, captopril (25 and 50 microg, icv), was administered 3 min before choline. Twenty-five microg captopril did not block the pressor effect of choline, while 50 microg captopril blocked it significantly. Our results suggest that the central renin-angiotensin system may participate in the increase in blood pressure induced by icv choline in normotensive rats.

Angiotensin-Converting Enzyme Inhibitors↗