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Ion channels-related diseases.

100%

Dworakowska B. , Dołowy K.

nr 3

685-703

There are many diseases related to ion channels. Mutations in muscle voltage-gated sodium, potassium, calcium and chloride channels, and acetylcholine-gated channel may lead to such physiological disorders as hyper- and hypokalemic periodic paralysis, myotonias, long QT syndrome, Brugada syndrome, malignant hyperthermia and myasthenia. Neuronal disorders, e.g., epilepsy, episodic ataxia, familial hemiplegic migraine, Lambert-Eaton myasthenic syndrome, Alzheimer's disease, Parkinson's disease, schizophrenia, hyperekplexia may result from dysfunction of voltage-gated sodium, potassium and calcium channels, or acetylcholine- and glycine-gated channels. Some kidney disorders, e.g., Bartter's syndrome, policystic kidney disease and Dent's disease, secretion disorders, e.g., hyperinsulinemic hypoglycemia of infancy and cystic fibrosis, vision disorders, e.g., congenital stationary night blindness and total colour-blindness may also be linked to mutations in ion channels.

Involvement of prostaglandins in the nicotine-induced pituitary-adrenocortical response during social stress

84%

Bugajski J. , Gadek-Michalska A. , Bugajski A. J.

tom 53

nr 4,2

The present study examined the functional selectivity of nicotine for nicotinic acetylcholine receptors in the stimulation of the hypothalamic-pituitary-adrenal (HPA) axis, the effect of social crowding stress on HPA response to nicotine and the involvement of prostaglandins synthesized by constitutive cyclooxygenase (COX-1) and inducible cyclooxygenase (COX-2) in the nicotine-induced HPA response in rats crowded (24 per a box instead 7) for 7 days. Nicotine (2.5-5.0 mg/kg i.p.) significantly increased plasma ACTH and corticosterone levels measured 1 h after administration. Mecamylamine (50 mg i.c.v.), a selective nicotinic receptor antagonist, atropine (0.1 mg/kg i.p.) a non-selective cholinergic receptor antagonist, or COX inhibitors were injected 15 min prior to nicotine and the rats were decapitated 1 h after the last injection. Mecamylamine abolished the nicotine-induced ACTH response and significantly diminished corticosterone response. Atropine did not alter ACTH response and modestly diminished corticosterone response to nicotine. Crowding stress significantly impaired the nicotine-evoked ACTH and corticosterone secretion. Pretreatment with piroxicam (0.2-2.0 mg/kg), a COX-1 inhibitor, considerably diminished the nicotine-induced ACTH and corticosterone secretion in control and crowded rats. Compound NS-398 (0.2-5.0 mg/kg), a selective COX-2 blocker, did not markedly alter the nicotine-induced hormones secretion in either control or stressed rats. Indomethacin (2 mg/kg), a non-selective COX inhibitor diminished significantly, but to a lesser extent than piroxicam, the nicotine-stimulated ACTH and corticosterone response. These results indicate that systemic nicotine stimulates the HPA axis selectively via nicotinic acetylcholine receptors. Chronic social stress significantly impairs the nicotine stimulated ACTH and corticosterone secretion. Prostaglandins, generated by COX-1- but not by COX-2- isoenzyme, are of crucial significance in the nicotine-induced ACTH and corticosterone secretion in both control and stressed rats.