nystatin-a1 and Hypertension

nystatin-a1 has been researched along with Hypertension* in 4 studies

Trials

1 trial(s) available for nystatin-a1 and Hypertension

ArticleYear
Outward Na-K-Cl cotransport in human red blood cells: a methodological evaluation of method for epidemiologic investigations.
    American journal of epidemiology, 1987, Volume: 125, Issue:5

    The present report evaluates a method for the determination of the maximal velocity of the outward sodium, potassium, chlorine (Na-K-Cl) cotransport in erythrocytes. The loading procedure was carried out using the ionophore nystatin. The technical error for this assay, based on concurrent analysis of randomized blind duplicate samples, was 8.04% of the sample mean and 27.5% of the sample standard deviation. The assay was stable over time and reproducible. Fasting was not necessary. The ratio of intra- to interindividual variances was small. The cells can be safely preserved in an appropriate preservation solution without modification of the ion transport assay. The assay appears to be adequate for use in large-scale field trials.

    Topics: Chlorides; Epidemiologic Methods; Erythrocytes; Humans; Hypertension; Nystatin; Potassium; Sodium

1987

Other Studies

3 other study(ies) available for nystatin-a1 and Hypertension

ArticleYear
Colonization of the oral cavity by yeasts in patients with chronic renal failure undergoing hemodialysis.
    Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology, 2013, Volume: 42, Issue:3

    To determine the frequency of yeast in the oral cavity of patients with chronic renal failure, undergoing hemodialysis (PCRFH); identification and antifungal susceptibility profile of yeast and demographic profile of patients.. We performed mouthwash in 146 PCRFH; the rinse fluid was collected and cultured, yeasts grown were identified by phenotypic and molecular methods. The antifungal susceptibility profile was determined against nystatin, amphotericin B, fluconazole, voriconazole, and caspofungin based in Clinical and Laboratory Standards Institute (document M27-A3).. Positive culture was observed in 39% of patients, of whom 53% were women; the median of dialysis time was 2.9 years. The age of the colonized patients varied between 26 and 84 years, with a median of 52.5 years. PCRFH over 45 years were significantly more colonized (P = 0.0108) as well as denture wearers (84.0%). We isolated 81 yeasts, predominantly Candida albicans (63%) followed by Candida glabrata. In general, yeasts were sensitive to the evaluated antifungal agents, but there was significant variation in the minimum inhibitory concentration, especially among non-C. albicans Candida (NCAC) compared to fluconazole, caspofungin, and amphotericin B. NCAC required significantly higher concentrations of fluconazole (P < 0.01).. The rate of colonization by yeasts in PCRFH was high, and there was variability in species distribution and antifungal susceptibility profile. These results are little known in this group of patients and are important for controlling the risk of developing invasive fungal infections.

    Topics: Adult; Aged; Aged, 80 and over; Amphotericin B; Antifungal Agents; Candida; Candida albicans; Candida glabrata; Candida tropicalis; Caspofungin; Colony Count, Microbial; Dentures; Diabetes Complications; Echinocandins; Female; Fluconazole; Humans; Hypertension; Kidney Failure, Chronic; Lipopeptides; Male; Microbial Sensitivity Tests; Middle Aged; Mouth; Mycology; Nystatin; Phenotype; Pyrimidines; Renal Dialysis; Time Factors; Triazoles; Voriconazole

2013
Vasopressin-stimulated CFTR Cl- currents are increased in the renal collecting duct cells of a mouse model of Liddle's syndrome.
    The Journal of physiology, 2005, Jan-01, Volume: 562, Issue:Pt 1

    Liddle's syndrome is a genetic form of hypertension linked to Na(+) retention caused by activating mutations in the COOH terminus of the beta or gamma subunit of the epithelial sodium channel (ENaC). In this study, we used the short-circuit current (I(sc)) method to investigate the effects of deamino-8-d-arginine vasopressin (dDAVP) on Na(+) and Cl(-) fluxes in primary cultures of cortical collecting ducts (CCDs) microdissected from the kidneys of mice with Liddle's syndrome carrying a stop codon mutation, corresponding to the beta-ENaC R(566) stop mutation (L) found in the original pedigree. Compared to wild-type (+/+) CCD cells, untreated L/+ and L/L CCD cells exhibited 2.7- and 4.2-fold increases, respectively, in amiloride-sensitive (Ams) I(sc), reflecting ENaC-dependent Na(+) absorption. Short-term incubation with dDAVP caused a rapid and significant increase (approximately 2-fold) in Ams I(sc) in +/+, but not in L/+ or L/L CCD cells. In sharp contrast, dDAVP induced a greater increase in 5-nitro-2-(3-phenylpropamino)benzoate (NPPB)-inhibited apical Cl(-) currents in amiloride-treated L/L and L/+ cells than in their +/+ counterparts. I(sc) recordings performed under apical ion substituted conditions revealed that the dDAVP-stimulated apical secretion of Cl(-), which was absent in cultured CCDs lacking CFTR, was 1.8-fold greater in L/+ and 3.7-fold greater in L/L CCD cells than in their +/+ CCD counterparts. After the basal membrane had been permeabilized with nystatin and a basal-to-apical Cl(-) gradient had been imposed, dDAVP also stimulated larger Cl(-) currents across L/L and L/+ CCD layers than +/+ CCD layers. These findings demonstrate that vasopressin stimulates greater apical CFTR Cl(-) conductance in the renal CCD cells of mice with Liddle's syndrome than in wild-type mice. This effect could contribute to the enhanced NaCl reabsorption observed in the distal nephron of patients with Liddle's syndrome.

    Topics: Animals; Cells, Cultured; Chloride Channel Agonists; Chloride Channels; Chlorides; Codon; Cystic Fibrosis Transmembrane Conductance Regulator; Deamino Arginine Vasopressin; Electrophysiology; Epithelial Sodium Channels; Hypertension; Kidney Tubules, Collecting; Mice; Mice, Knockout; Nephrons; Nystatin; Organ Culture Techniques; Phenotype; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Sodium; Sodium Channels; Syndrome; Vasopressins

2005
The regulation of Na-K cotransport system and essential hypertension.
    Klinische Wochenschrift, 1985, Volume: 63 Suppl 3

    We have determined in human red cells the equilibrium position between outward and inward furosemide-sensitive (FS) Na-K cotransport, by measurements of unidirectional 22Na and 42K influx and efflux. At physiological Na and K concentrations, the system performs net Na and K extrusion. In vascular endothelial cells, the Na-K cotransport system performs net Na influx and is stimulated by vasoactive peptides (bradykinin and vasopressin). Measurements of red cell Na-K cotransport performed by other investigators are discussed. Measurements of outward cotransport as a function of internal Na (nystatin loading) indicate that a subset of hypertensive subjects has higher K0.5 for internal Na to promote FS Na efflux.

    Topics: Biological Transport; Erythrocytes; Furosemide; Humans; Hypertension; Kinetics; Nystatin; Potassium; Sodium

1985