Drugs online research references
Neurochem Res. 1988 Sep;13(9):837-48.
Sodium and potassium uptake in primary cultures of proliferating rat astroglial cells induced by short-term exposure to an astroglial growth factor.
Latzkovits L, Torday C, Labourdette G, Pettmann B, Sensenbrenner M.
Institute of Experimental Surgery, Medical School of Szeged, Hungary.
Primary cultures of rat astroglial cells were maintained in a serum-free medium. After 8-10 days of cultivation the cells were exposed to an astroglial growth factor (AGF2) for short periods (1-120 min). Subsequently, uptake of 22Na+ and 42K+ into control and AGF2-pretreated cells was studied. Assay of the Na+ and K+ values in the cells was also performed by atomic absorption spectrometry. Treatment of rat astroglial cells with AGF2 resulted in a significant increase of the uptake of both Na+ and K+ depending on the duration of the exposure period. To reach the maximum increase of cation uptake, 6-10 min and 30 min of AGF2 pretreatment were needed for Na+ and K+, respectively. Amiloride blocked this increase of Na+ and K+ uptake elicited by AGF2 pretreatment, but the control cells were amiloride resistant. Treatment with AGF2 increased the ouabain sensitivity of the K+ uptake as that: 10(-4) M ouabain inhibited K+ uptake of the AGF2-treated cells to the same degree as 5 X 10(-3) M ouabain with the control cells. The Na+ uptake of AGF2-treated cells, however, exhibited no relevant changes in the presence of ouabain. A significant part of the AGF2-induced K+ uptake could be inhibited by both ouabain and amiloride, but a ouabain-resistant and amiloride-sensitive component also was revealed. The furosemide sensitivity of both Na+ and K+ uptake into cultured astroglial cells was also significantly increased by AGF2. Our findings suggest that short-term exposure of cultured glial cells to AGF2 induces these very early ionic events: 1) The appearance of a relevant amiloride-sensitive Na+/H+ exchange, and as a consequence of increased Na+ entry into the cells, secondary activation of the ouabain-sensitive K+ uptake via the Na+,K+-pump. 2) A direct effect of AGF2 on the Na+,K+-pump assembly in the membrane, resulting in increased Na+ sensitivity of the inner pump sites and enhanced ouabain sensitivity of the external K+-binding sites. 3) An increase of ouabain-resistant but amiloride- or furosemide-sensitive Na+ and K+ uptake.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3226466&dopt=Abstract
J Physiol. 1988 Dec;406:147-62.
Intracellular pH regulation in cultured mouse oligodendrocytes.
Kettenmann H, Schlue WR.
Department of Neurobiology, University of Heidelberg, F.R.G.
1. Intracellular pH (pHi) and the mechanism of pHi regulation have been investigated in cultured oligodendrocytes from mouse spinal cord using double-barrelled neutral-carrier H+-selective microelectrodes. The distribution of H+ was not in electrochemical equilibrium. The pHi was more alkaline than the pH of the bathing medium (pHo), namely 7.5 at pHo 7.2 at 7.6 at pHo 7.4. 2. Removal of HCO3- from the bathing medium reduced the steady-state pHi by 0.4 units. An increase in extracellular K+ caused, with a delay, an increase in pHi. A decrease in pHo to 6.2 caused an acidification of pHi by 0.5 units. 3. The pHi regulation was studied by applying and subsequently removing NH4+ which resulted in an acidification of the cell. The subsequent recovery of pHi could then be analysed. The recovery from an acidification by 1 pH unit lasted 3-10 min. In HCO3- -free solution pHi recovery was slowed. 4. In HCO3- -free solution pHi recovery was completely blocked when either Na+ was removed or when amiloride was applied indicating an exclusive activation of the Na+-H+ exchanger. 5. In the presence of HCO3-, removal of Na+ also completely blocked pHi recovery. When Na+ was readded, pHi recovered. In HCO3- -containing solution amiloride slightly slowed, but did not block pHi recovery. 6. Removal of Cl- or application of SITS, DIDS or furosemide, blockers of Cl- -coupled transport mechanisms, did not affect the pHi recovery in the presence of HCO3-. 7. In conclusion, oligodendrocytes possess two mechanisms regulating pHi, a Na+-H+ exchanger and a Na+-HCO3- co-transporter while the latter is clearly more potent. It follows that pHi regulation of oligodendrocytes is dependent on the transmembrane Na+ gradient and is strictly separated from regulation of internal Cl-.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3254411&dopt=Abstract
J Physiol. 1987 Dec;393:555-68.
Salt appetite in the pigeon in response to pharmacological treatments.
Epstein AN, Massi M.
Department of Biology, University of Pennsylvania, Philadelphia 19104.
1. In response to furosemide-induced sodium depletion pigeons showed a robust salt appetite. Following the 1st depletion they started to ingest 3% NaCl after a latency of 373 +/- 69 s and in 24 h they took 21.16 +/- 3.07 ml of this solution (vs. a daily mean intake of 1-2 ml prior to the depletion). 2. The appetite was selective as shown by the fact that when, after depletion, 0.34 M-CaCl2 was offered (which is equiosmotic to 3% NaCl) pigeons took just a trivial amount of it. 3. Analysis of sodium losses following the natriuretic treatment revealed that pigeons respond to sodium depletion with an excessive overconsumption of NaCl solution. In the 2 h after access to salt they took about 3 times the amount of sodium lost. 4. Repeated sodium depletions sharply reduced the latency to the ingestion of salt and produced larger intakes. However, the overall amount of salt taken in 24 h after the later depletions was very similar and statistically indistinguishable from that taken following the 1st depletion. 5. Subchronic deoxycorticosterone acetate treatment (2 mg pigeon-1 day-1 I.M.) increased daily 3% NaCl intake, but large variability was observed in the response. 4 mg pigeon-1 day-1 evoked a reliable 3% NaCl intake which was particularly marked from the 5th day of the treatment. 6. Pulse intracerebroventricular (I.C.V.) injection of purified hog renin evoked water intake within about 1 min of injection, followed (about 6 h later) by increased salt intake. In the 24 h after renin injection pigeons took 16.58 +/- 2.89 ml of 3% NaCl. On the 2nd day following injection salt intake was still higher than in controls. 7. In conclusion, our results show that pigeons respond to sodium depletion with a robust salt appetite. Moreover, salt appetite can be evoked by deoxycorticosterone acetate as well as by renin. These findings suggest that in the pigeon salt appetite may be an endocrine-induced behaviour controlled by mineralocorticoids and by the renin-angiotensin system.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3328783&dopt=Abstract
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