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Proc Natl Acad Sci U S A. 1985 Jul;82(13):4433-7.
Inositol trisphosphate modification of ion transport in rough endoplasmic reticulum.

Muallem S, Schoeffield M, Pandol S, Sachs G.

The ion transport properties of the rough endoplasmic reticulum (RER) from liver have been defined by using measurements of active and potential gradient-driven transport. The Ca2+ pump is shown to be electrogenic, and both ATP and potential difference is able to drive vanadate-inhibitable Ca2+ uptake into the RER. ATP-dependent Ca2+ transport into the RER depends on the presence of tetraethylammonium-sensitive cation conductance and a furosemide-inhibited cation/chloride cotransport pathway. Inositol trisphosphate does not affect either of the monovalent ion translocation systems but activates a Ca2+ conductance in the RER, allowing efflux of RER Ca2+ stores into the cytosol in exchange for K+ uptake.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3874400&dopt=Abstract




Am J Physiol. 1998 Nov;275(5 Pt 2):R1639-46.
Evidence that brain angiotensin II is involved in both thirst and sodium appetite in baboons.

Blair-West JR, Carey KD, Denton DA, Weisinger RS, Shade RE.

Southwest Foundation for Biomedical Research, San Antonio, Texas 78245-0549, USA.

The roles of ANG II in the brain mechanisms subserving thirst and Na appetite in baboons were investigated by chronic intracerebroventricular infusions of ANG II and AT1-receptor antagonists using subcutaneous miniosmotic pumps and by oral administration of captopril. ANG II at 3 or 5 micrograms/h for 7 days increased water intake from 2,455 +/- 107 to 7,052 +/- 562 ml/day by day 6 and 300 mM NaCl intake from 8.3 +/- 1.1 to 275 +/- 87 mmol/day by day 5. Concurrent intracerebroventricular losartan (300 micrograms/h) did not substantially reduce these responses, but they were abolished by intracerebroventricular ZD-7155 (50 micrograms/h). The increase of 300 mM NaCl intake when it was offered after intramuscular injection of furosemide, 2 mg . kg-1 . day-1 for 3 days, was unaltered by intracerebroventricular losartan (300 micrograms/h) but was reduced by intracerebroventricular ZD-7155 (50 micrograms/h) infused throughout Na depletion/repletion; oral captopril (1 g, 3 and 18 h before access to 300 mM NaCl) also reduced NaCl intake. Restriction of water intake to 25% of daily intake for 3 days caused a high intake of water on day 4, and this was reduced by intracerebroventricular losartan (300 micrograms/h) infused throughout the period of water restriction/rehydration. These novel results in a primate species suggest that brain ANG II is involved in both thirst and Na appetite, acting via AT1 receptors.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9791085&dopt=Abstract




Brain Res. 1998 Mar 16;787(1):171-4.
Acute sodium depletion modifies septo-preoptic neuron sensitivities to neurohormones.

Lienard F, Galaverna O, Thornton SN, Meile MJ, Nicolaidis S.

CNRS UPR 9054 Groupe de Neurobiologie des Regulations, I.E.S.G.C.A., Campus de l'Universite de Bourgogne, 15 rue Hugues Picardet, 21000 Dijon, France.

Sodium (Na+) depletion induces sodium appetite to replenish Na+ loss. It appears to be a consequence of enhanced levels of aldosterone (Aldo) and angiotensin II (AII) in the plasma as well as in the brain. Mineralocorticoid pretreatment modifies the sensitivity of septo-preoptic neurons to locally applied AII and Aldo. Therefore, we investigated septo-preoptic neuronal sensitivities to AII and Aldo, as well as to the specific AII type-1 receptor (AT-1) non-peptide antagonist losartan (Los) and to the specific AII type-2 receptor (AT-2) non-peptide antagonist PD123319 after one Na+ depletion without repletion. We found that one Na+ depletion induced increases in the proportion of neurons inhibited by iontophoretic application of AII (20.5% vs. 7.8%, p=0.004) whereas, the proportion of neurons excited by Aldo was increased, (23.7% vs. 5%, p=0.001). Moreover, the proportion of neurons changing sensitivity to AII after one application of Aldo was increased in the furosemide group (44.2% vs. 20.4%, p=0.0123). The proportion of neurons inhibited by application of losartan was enhanced, (26.4% vs. 9.3%, p=0.03). No significant changes were found in response to PD123319 by itself. Moreover, there were more neurons which co-localized responses to both Los and PD123319 in the furosemide group than in the control group (29.7% vs. 8.6%, p=0.027). It is known that multidepletions induce an increased need-free sodium appetite and our present findings could well form part of the neuronal basis of this behavior. Copyright 1998 Elsevier Science B.V.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9518596&dopt=Abstract













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