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1
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Nitric oxide in the adrenergic- and CRH-induced activation of hypothalamic-pituitary-adrenal axis

100%
Gadek-Michalska A., Bugajski J.
Journal of Physiology and Pharmacology
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2008
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tom 59
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nr 2
In this report we investigated the effect of 7-nitroindazole (7-NI), a specific neuronal inhibitor of nitric oxide synthase (nNOS) and L-NAME, a nonselective NOS inhibitor upon the adrenergic- and CRH-induced stimulation of the hypothalamic-pituitary-adrenal axis in nonanesthetized rast. 7-NI given i.p. and L-NAME administered i.c.v. considerably reduced ACTH and corticosterone secretion induced by phenylephrine (30 µg i.c.v.), an alpha1-adrenergic receptor agonist. These inhibitors also diminished the HPA response to isoprenaline (20 µg i.c.v.), a nonselective ß-adrenergic receptor agonist, and i.c.v. L-NAME significantly lowered the ACTH and corticosterone response to clenbuterol (10 µg i.c.v.), a selective ß2-adrenergic agonist. L-NAME abolished the noradrenaline (NA), an alpha- and ß-receptor agonist-evoked ACTH and corticosterone response, which was reversed by pretreatment with i.p. L-arginine, an endogenous NO substrate. 7-NI abolished the stimulatory action of corticotropin-releasing hormone (CRH 1 µg/kg i.p.) on ACTH but not corticosterone secretion. L-NAME only moderately diminished the CRH-induced ACTH secretion, suggesting that a major part of the CRH-induced HPA axis activation is of neuronal origin. Dihydropyridine, nifedipine, a specific L-type Ca2+ channel blocker, inhibited significantly the CRH-induced ACTH and corticosterone response in rats exposed to 3 days crowding stress but not in rats under basal conditions. This finding indicates the strategic importance of Ca2+ influx into the pituitary corticotrops to meet increased secretory requirement under stressful conditions. Collectively, our results point to complex functional relationship between NO, adrenergic agents CRH and Ca2+ in the regulation of HPA axis activity.
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No effect of 7-nitroindazole on the anticonvulsant action of vigabatrin and oxcarbazepine in pentylenetetrazole-induced seizures in mice

84%
Luszczki J. J., Szadkowski M., Zadrozniak A., Wojda E., Dudra-Jastrzebska M., Andres-Mach M.
Journal of Pre-Clinical and Clinical Research
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2008
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tom 02
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nr 2
3
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Hypotrophic effect of long-term neuronal NO-synthase inhibition on heart and conduit arteries of the Wistar rats

84%
Kristek F., Cacanyiova S., Gerova M.
Journal of Physiology and Pharmacology
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2009
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tom 60
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nr 2
21-27
We demonstrate the effect of long-term nNOS inhibition with 7-nitroindazole (7NI) on the heart and conduit arteries. Ten weeks old Wistar rats were used: two groups of controls and rats receiving 7-NI (10 mg/kg b.w./day) for 6 weeks in drinking water. Blood pressure (BP) was measured by the plethysmographic method. In first group mesenteric, carotid and coronary arteries were excised after perfusion fixation (120 mmHg) for morphological study, in second group mesenteric artery was taken for functional investigation. 7NI did not affect BP, heart/body weight was decreased. In all arteries inner diameter (ID) did not changed, wall thickness (WT) (intima+media), cross sectional area (CSA) (intima+media), and WT/ID decreased. In carotid artery volume density (VD) (percentual proportion) of intima and media did not change; VD and CSAs of endothelial and smooth muscle cells decreased, CSAs of extracellular matrix in intima and media did not change. No difference was found in relaxation of mesenteric artery to acetylcholine (10-9-10-5 mol/L). Contraction induced by transmural nerve stimulation (8Hz) augmented and contraction to exogennous noradrenaline (10-9-10-5 mol/L) attenuated. Long-term 7NI administration evoked pressure independent cardiac hypotrophy and due to decrease of endothelial and smooth muscle cell mass arterial wall hypotrophy associated with decreased contractile efficiency.
4
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Blood pressure-independent hypotrophy of the heart, kidneys and conduit arteries after 7-nitroindazole administration to Wistar rats from the prenatal period to adulthood

67%
Kristek F., Malekova M., Ondrias K., Cacanyiova S.
Journal of Physiology and Pharmacology
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2013
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tom 64
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nr 1
5
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Effect of chronic neuronal nitric oxide-synthase inhibition on arterial function and structure in spontaneously hypertensive rats

67%
Cacanyiova S., Kristek F., Malekova M., Ondrias K.
Journal of Physiology and Pharmacology
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2012
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tom 63
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nr 1
6
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7-nitroindazole enhances amphetamine-evoked dopamine release in rat striatum. An in vivo microdialysis and voltammetric study

67%
Nowak P., Brus R., Oswiecimska J., Sokola A., Kostrzewa R. M.
Journal of Physiology and Pharmacology
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2002
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tom 53
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nr 2
The intracellular second messenger nitric oxide (NO) is implicated in a variety of physiological functions, including release and uptake of dopamine (DA). In the described study, in vivo microdialysis and differential pulse voltammetric techniques were used to determine the involvement of NO in release of DA and its metabolites (dihydroxyphenylalanine, DOPAC; homovanillic acid, HVA) in neostriatum of freely moving rats. While the NO donor molsidomine (30.0 mg/kg; MOLS) and neuronal NO synthase- (nNOS-) inhbitor 7-nitroindazole (10.0 mg/kg; 7-NI) had no effect on the basal in vivo microdialysate level of DA, 7-NI specifically enhanced D,L-amphetamine- (1.0 mg/kg i.p.; AMPH) evoked release of DA. Basal or AMPH effects on DOPAC and HVA levels were not influenced by MOLS or 7-NI. Findings indicate that nitrergic systems have an important role in mediating effects of AMPH on dopaminergic systems.
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