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Results for “NICOTINIC ACID”

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At least 523 records · Page 29Linked to original sources
PubMed1986

Combined treatment with cholestyramine and nicotinic acid in heterozygous familial hypercholesterolaemia: effects on biliary lipid composition.

In ten patients with heterozygous familial hypercholesterolaemia, combination therapy with cholestyramine and nicotinic acid was instituted for a minimum of 2 months. During therapy, plasma low-density lipoprotein levels were reduced by 32%, and low-density lipoprotein to high-density lipoprotein ratios by 40%. The cholesterol saturation of fasting gall-bladder bile was reduced by 33% during treatment. We conclude that long-term combination therapy with cholestyramine and nicotinic acid is practically feasible in heterozygous familial hypercholesterolaemia, normalizes plasma cholesterol and low-density lipoprotein levels in many patients, and does not result in unwanted side-effects on biliary lipids. It should therefore be considered as the therapy of choice in this condition.

Adult↗
PubMedDate not supplied

[The dynamic biosynthesis of nicotinamide coenzymes from nicotinamide and nicotinic acid in rat tissues].

Dynamics of nicotinamide coenzyme biosynthesis in rat tissues has been studied systematically with previous injection of two main precursors nicotinic acid and nicotinamide (50 mg/100 g of weight. This process is characterized by exact tissue specificity. As a precursor of NAD-biosynthesis nicotinamide was used more intensively in the liver and brain tissues. In the mucous tissue of intestine nicotinic acid was utilized more intensively. An increase in the NADP+ content in tissues with high level of NAD+ biosynthesis is limited as a result of competition between these two processes for the intracellular ATP level.

Animals↗
PubMed1981

Human adipose tissue blood flow during prolonged exercise, III. Effect of beta-adrenergic blockade, nicotinic acid and glucose infusion.

Subcutaneous adipose tissue blood flow (ATBF) was measured in six male subjects by the 133Xe-washout technique during 3-4 h of exercise at a work load corresponding to an oxygen uptake of about 1.71/min. The measurements were done during control conditions, during blockade of lipolysis by nicotinic acid, during acute i.v. beta-adrenergic blockade by propranolol, and during continuous i.v. infusion of glucose. The most pronounced lipid mobilization and utilization during work was seen in the control experiments where ATBF rose 3-fold on average from the initial rest period to the third hour of work. No increase in lipolysis and no increase in ATBF were found when lipolysis was blocked by nicotinic acid (0.3 g/h). Propranolol treatment (0.15 mg/kg) reduced lipolysis and nearly abolished the increase in ATBF during exercise. Intravenous administration of glucose (about 0.25 g/min) did not influence lipid metabolism (evaluated by the respiratory quotient) nor did it reduce the ATBF response to exercise. These results are inconsistent with the hypothesis that increase in ATBF during exercise is elicited via direct stimulation of vascular beta1-receptors, while they are not in disagreement with the hypothesis that adipose tissue vasodilation during exercise is secondary to metabolic events connected to lipolysis.

Adipose Tissue↗
PubMed2005

Calcium mobilization by nicotinic acid adenine dinucleotide phosphate (NAADP) in rat astrocytes.

Nicotinic acid adenine dinucleotide phosphate (NAADP) has been shown to release intracellular Ca(2+) in several types of cells. We have used Ca(2+)-sensitive fluorescent dyes (Fura-2, Fluo-4) to measure intracellular Ca(2+) in astrocytes in culture and in situ. Bath-applied NAADP elicited a reversible and concentration-dependent Ca(2+) rise in up to 90% of astrocytes in culture (EC(50)=7 microM). The NAADP-evoked Ca(2+) rise was maintained in the absence of extracellular Ca(2+), but was suppressed after depleting the Ca(2+) stores of the ER with ATP (20 microM), with cyclopiazonic acid (10 microM) or with ionomycin (5 microM). P(2) receptor antagonist pyridoxalphosphate-6-azophenyl-2'4'-disulfonic acid (PPADS, 100 microM), IP(3) receptor blocker 2-aminoethoxydiphenyl borate (2-APB, 100 microM) and PLC inhibitor U73122 (10 microM) also reduced or suppressed the NAADP-evoked Ca(2+) rise. NAADP still evoked a Ca(2+) response after application of glycyl-l-phenylalanine-beta-naphthylamide (GPN, 200 microM), which permeabilizes lysosomes, or preincubation with H(+)-ATPase inhibitor bafilomycin A1 (4 microM) and of p-trifluoromethoxy carbonyl cyanide phenylhydrazone (FCCP, 2 microM), that impairs mitochondrial Ca(2+) handling. In acute brain slices, NAADP (10 microM) evoked Ca(2+) transients in cerebellar Bergmann glial cells and in hippocampal astrocytes. Our results suggest that NAADP recruits Ca(2+) from inositol 1,4,5-trisphosphate-sensitive Ca(2+) stores in mammalian astrocytes, at least partly by activating metabotropic P(2)Y receptors.

Animals↗
PubMed2003

[Epigenetic variability induced by nicotinic acid in Triticum aestivum L].

The effect of nicotinic acid (NA) on hereditary traits of spring common wheat cultivar Kazakhstanskaya 126 (K.126) were studied under the laboratory and field conditions. Treatment of seeds and vegetating plants with 0.01-0.1% NA (aqueous solution) induced heritable epigenetic changes in wheat. As a result, strong tall plants with the long productive spike, large seeds, and several quantitative and qualitative characters other than in the original cultivar were obtained in the second and further generations after treatment. Crosses of changed plants with each other did not result in segregation with respect to leaf downiness or anthocyan stem color in F2-F4, suggesting the same epigenetic state of genes responsible for changed characters. In crosses with the original cultivar, characters of the changed plants always dominated in F1. Basing on the current views, the changes were attributed to a transition of the hl1 and pc recessive marker genes into new, dominant epiallelic states Hl1 and Pc, which respectively determine downy leaves and the colored stem. The NA effect was specific, since only one type of the variation was observed. The changed characters were stable, and no reversion to the original phenotype was detected in 57 generations.

Genes, Plant↗
PubMed1998

Efficacy and safety of one-year treatment with slow-release nicotinic acid. Monitoring of drug concentration in serum.

The paper is aimed at evaluation of the efficacy and safety of one-year therapy with slow-release nicotinic acid (NA-SR). The study involved a group of 30 patients with hyperlipidemia of type II. The concentration of nicotinic acid in serum was determined using capillary electrophoresis. After the placebo period (2 months), NA-SR was applied at the dose of 1.5 g/d (2 months), and subsequently 2-3 g/d (10 months), on average 2.13 g/d. During the treatment with 2.0 g/d dose, the steady-state concentration of NA in serum was within a range of 2.7-4.9 microg/ml and with 3.0 g/d of 6.17-7.75 microg/ml. These doses of the drug were tolerated well and advantageously modified the serum lipids.

Adult↗
PubMed1980

Absorption of nicotinic acid and nicotinamide from rat small intestine in vitro.

Intestinal absorption of nicotinic acid and nicotinamide was studied using everted sacs of rat small intestine. Transport down the concentration gradient showed saturation kinetics at low concentrations and linear kinetics at higher concentrations. Addition of ouabain or omission of sodium ions decreased absorption. Neither compound was absorbed against a concentration gradient. The mode of transport was thought to be carrier-mediated facilitated diffusion at lower concentrations masked by passive diffusion at higher concentrations.

Animals↗
PubMed1979

Prostaglandins contribute to the vasodilation induced by nicotinic acid.

The significance of endogenously formed prostaglandins in the vasodilation induced by nicotinic acid (NIC) was investigated. The forearm venous plasma level of radioimmunoassayed PGE (R-PGE) and the forearm blood flow (FBF) were measured in 13 healthy male volunteers at rest and during infusion of NIC. Each subject was subsequently re-studied after pretreatment with the PG synthesis inhibitor, naproxen. In the absence of naproxen, NIC infusion resulted in an almost four-fold rise in the release of R-PGE and a 60% increase in FBF. Pretreatment with naproxen did not affect the basal release of R-PGE or the basal FBF but inhibited both the release of R-PGE and the increase in FBF following NIC. The data support the hypothesis that the vasodilating effect of NIC is largely dependent upon an increased vascular formation of PG.

Adult↗
PubMed1979

Studies on nicotinic acid interaction with bilirubin metabolism.

The mechanism by which intravenous administration of nicotinic acid (NA) increases serum unconjugated bilirubin in patients with the Gilbert's syndrome has been investigated. Studies using the technique of percutaneous transhepatic catheterization of the splenic vein and coil planet centrifuge suggested that following intravenous injection of NA some of the circulating erythrocytes were rendered osmotically fragile and trapped by the spleen and that unconjugated bilirubin increased in the splenic vein blood. In patients with liver cirrhosis, the increments of unconjugated bilirubin were closely correlated with the weights of the spleens removed for the management of varices. In rats, intravenous NA injection enhanced heme oxygenase activities in the spleen, but not uridine-5'-diphosphate (UDP)-glucuronyltransferase activity in the liver. These results are consistent with the hypothesis that NA-induced unconjugated hyperbilirubinemia is a result of complex reactions which include increased erythrocyte fragility, increased splenic heme oxygenase activity, and increased formation of bilirubin in the spleen.

Adult↗
PubMed2000

Nicotinic acid adenine dinucleotide phosphate-induced Ca(2+) release. Interactions among distinct Ca(2+) mobilizing mechanisms in starfish oocytes.

An intracellular mechanism activated by nicotinic acid adenine dinucleotide phosphate (NAADP(+)) contributes to intracellular Ca(2+) release alongside inositol 1,4,5-trisphosphate (Ins-P(3)) and ryanodine receptors. The NAADP(+)-sensitive mechanism has been shown to be operative in sea urchin eggs, ascidian eggs, and pancreatic acinar cells. Furthermore, most mammalian cell types can synthesize NAADP(+), with nicotinic acid and NADP(+) as precursors. In this contribution, NAADP(+)-induced Ca(2+) release has been investigated in starfish oocytes. Uncaging of injected NAADP(+) induced Ca(2+) mobilization in both immature oocytes and in oocytes matured by the hormone 1-methyladenine (1-MA). The role of extracellular Ca(2+) in NAADP(+)-induced Ca(2+) mobilization, which was minor in immature oocytes, was instead essential in mature oocytes. Thus, the NAADP(+)-sensitive Ca(2+) pool, which is known to be distinct from those sensitive to inositol 1,4,5-trisphosphate or cyclic ADPribose, apparently migrated closer to (or became part of) the plasma membrane during the maturation process. Inhibition of both Ins-P(3) and ryanodine receptors, but not of either alone, substantially inhibited NAADP(+)-induced Ca(2+) mobilization in both immature and mature oocytes. The data also suggest that NAADP(+)-induced Ca(2+) mobilization acted as a trigger for Ca(2+) release via Ins-P(3) and ryanodine receptors.

Adenine↗
PubMed1984

[Possibility of correcting brain bioenergetics in neuroses using nicotinic acid derivatives].

Experiments were made to study the effect of the animals' neurosis status on the synthesis of macroergs according to the oxidative phosphorylation data and macroerg utilization via the ATPase system. It was demonstrated that in the stage of metabolic deadaptation , neurosis leads to dramatic inhibition of oxidative phosphorylation and its dissociation, decreases the content of macroergs , discoordinates the ATPase system. The prophylactic administration of nicotinic acid derivatives stimulated oxidative phosphorylation, making return to normal the content of macroergs and the ATPase activity. According to some data, the action of chlorodiazepoxide aggravated adverse effects of neurosis. The possibility of correcting brain bioenergetics with nicotinic acid derivatives has been shown.

Adenosine Diphosphate↗