Drugs online research references
Physiol Behav. 1986;38(5):657-62.
Suprachiasmatic nuclei lesions do not eliminate the circadian rhythms of electrolyte excretion in the rat.
Stoynev AG, Ikonomov OC, Vrabchev NC, Usunoff KG.
The 24-hour variations in 2-hour diuretic and saluretic action of furosemide (4 mg/kg) given at 8, 12, 16, 20, 24 or 4 hr and the circadian rhythms of food and water intake, urine and electrolyte excretion followed for two consecutive days at 4-hour intervals were investigated in suprachiasmatic nuclei (SCN)-lesioned or sham-operated male Wistar rats. The results showed that: a distinct 24-hour rhythm in furosemide-induced urine, sodium and chloride excretion persisted after SCN lesions, and the lesions abolished the circadian rhythms of food and water intake but only desynchronized the individual 24-hour variations in electrolyte excretion. We concluded that SCN play a role as a central synchronizer but not as a major oscillator of the circadian rhythms of electrolyte excretion in the rat.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3823179&dopt=Abstract
downeurobiology.org
Recent studies have established the presence of 5-hydroxytryptamine (5-HT)(2A) receptors on glial cells in culture and in the brain in situ. Here we used cultured C6 glioma cells to investigate the possibility that 5-HT(2A) receptors on glia regulate glutamate release from the cell. The efflux of endogenous glutamate from cultured C6 glioma cells was increased by addition of 5-HT in a concentration-dependent manner (maximal effect +200%). The efflux of serine and aspartate was not altered. The effect of 5-HT was mimicked by both the nonselective 5-HT receptor agonist quipazine and the selective 5-HT(2) receptor agonist 4-iodo-2,5-dimethoxyamphetamine (DOI; both 0.01-100 microM). The 5-HT(2A) receptor antagonists ketanserin (1 microM) and spiperone (1 microM) inhibited the glutamate response to 5-HT, quipazine, and DOI, whereas the effect of 5-HT was not inhibited by the 5-HT(2B/C) receptor antagonist SB200646 (1 microM). The effect of 5-HT on glutamate was specific in that it was reduced in low-calcium medium but was not prevented by furosemide (5 mM), which prevents cell swelling-induced glutamate release. Finally, the glutamate uptake inhibitor 2,4,trans-pyrollidine dicarboxylic acid (50 microM) did not block the 5-HT-induced efflux of glutamate, making involvement of glutamate transport unlikely. In conclusion, 5-HT stimulates the efflux of glutamate from C6 glioma cells following 5-HT(2A) receptor activation and involves a calcium-dependent mechanism. Copyright 2002 Wiley-Liss, Inc.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11813245&dopt=Abstract
Acta Otolaryngol. 1987 May-Jun;103(5-6):558-66.
Strial prostaglandins and leukotrienes. Biochemical characteristics and interrelationship with furosemide.
Tran Ba Huy P, Ferrary E, Escoubet B, Sterkers O.
Synthesis of prostaglandins (PGs) was characterized in the lateral wall (LW) of guinea-pig cochlea. Basal synthesis at 37 degrees C was about 480 pg/LW (12.8 ng X mg-1 protein) for PGI2 and 85 pg/LW (2.3 ng X mg-1 protein) for PGE2, levelling out after 10 min of incubation. Incubation with arachidonic acid (10(-5) M) increased PGI2 and PGE2 synthesis by 44% and 1020%, respectively, showing that arachidonic acid availability is a synthesis-limiting factor. The stimulating effect of the Ca++ ionophore A23187 (5 X 10(-6) M) on PG synthesis was weak (about +50%) but was enhanced (about +140%) by preincubation with arachidonic acid. Angiotensin II (10(-6) M), vasopressin (5 X 10(-7) M), and furosemide (10(-8) to 10(-3) M) did not alter PG secretion. Neither aspirin nor indomethacin prevented the development of furosemide ototoxicity (endocochlear potential) in the rat. Perfusion with PGI2 influenced the furosemide effect in some instances.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3113170&dopt=Abstract
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