Drugs online research references
Kidney Blood Press Res. 1997;20(4):247-50.
Urinary calcium excretion and renal calbindin-D28k.
Hemmingsen C, Staun M, Meibom K, Bang K, Olgaard K.
Department of Nephrology, Institute of Experimental Pathology, Rigshospitalet, University of Copenhagen, Denmark.
The present investigation examined the possible influence of urinary calcium excretion on the concentration of renal calbindin-D28k. Thiazide diuretics stimulate calcium transport across the epithelial cells of the distal tubule, which express calbindin-D28k in high concentrations. Calbindin-D28k is assumed to facilitate transcellular Ca diffusion. Reduced urine calcium excretion and increased urine output were induced in Wistar rats by infusion of bendroflume-thiazide 1 mg/kg/day. The two control groups had infusions of either furosemide 20 mg/kg/day or vehicle, n = 8 in each group. Urinary Ca excretion was reduced to 10% in the thiazide group and increased by 50% in the furosemide group. Renal concentrations of calbindin-D28 showed no difference between vehicle, thiazide- and furosemide-treated rats. No differences in plasma concentrations of calcium, magnesium, phosphorus, urea, PTH, calcitonin and 1,25-(OH)2D were found between the groups. The present study describes that urine calcium excretion selectively can be manipulated without accompanying changes in renal calbindin-D28k concentrations. The data, therefore, suggest that urinary calcium excretion is not a significant determinator of cytosolic concentrations of renal calbindin-D28k.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9398030&dopt=Abstract
Am J Med. 1988 Sep 23;85(3B):25-30.
Pharmacokinetics of lisinopril.
Beermann B.
Department of Drugs, National Board of Health and Welfare, Uppsala, Sweden.
The angiotensin-converting enzyme inhibitor, lisinopril, has an oral bioavailability of 25 percent +/- 4 percent, which is unaffected by food. The accumulation half-life averages 12.6 hours despite a terminal serum half-life of approximately 40 hours. Steady state is attained after two daily doses (every 24 hours) in healthy volunteers. The drug is not metabolized but is eliminated via the kidneys. Lisinopril probably undergoes glomerular filtration, tubular secretion, and tubular reabsorption. There is no pharmacokinetic interaction between lisinopril and furosemide.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2844083&dopt=Abstract
Clin Exp Hypertens A. 1985;7(10):1409-26.
The relationship of lithium-potassium cotransport and the passive lithium leak to hypertension in Utah subjects.
Hunt SC, Williams RR, Smith JB, Ash KO, Kuida H.
Rate constants for lithium-potassium cotransport (kLPC) and the lithium efflux into MgCl2 with furosemide (passive lithium leak) along with sodium-lithium countertransport (SLC) were measured in erythrocytes from 351 normotensive adults age 18 and over, 220 youth under age 18 and in 27 hypertensives. The kLPC was significantly higher in the hypertensives than the adult normotensives with means and standard deviations of 13.9 +/- 9.2 vs. 8.7 +/- 5.9 10(-3)/hr (p less than 0.01). Adjusting for the significant weight (p = 0.014) and sex (p = 0.066, normotensive males higher than females) associations with kLPC in an analysis of covariance, increased the significant difference between the hypertensives and normotensives (p = 0.0004). The passive lithium leak rate constant was also higher in hypertensives than normotensives (20.2 +/- 7.6 vs. 15.5 +/- 5.3 10(-3)/hr, p less than 0.01). Weight (p=0.0003), but not sex, was related to the leak but did not account for the difference between hypertensives and normotensives (p = 0.0009). Mean blood pressure was positively associated with the lithium leak but not the kLPC or SLC values in a multivariate regression.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=4075541&dopt=Abstract
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