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Results for “NICOTINIC ACID”

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At least 613 records · Page 34Linked to original sources
PubMed2005

Strategies for modifying high-density lipoprotein cholesterol: a role for nicotinic acid.

Statin-mediated lowering of low-density lipoprotein cholesterol (LDL-C) is regarded as the foundation of lipid-modifying therapy. However, the residual cardiovascular risk for statin-treated patients remains high, indicating the need for therapeutic intervention against other lipid targets as well as non-lipid risk factors. Low levels of high-density lipoprotein cholesterol (HDL-C) are established as a strong independent risk factor for cardiovascular disease. Intervention studies have also demonstrated clinical benefits associated with HDL-C raising. Although lifestyle modification does play an important role in raising HDL-C, most patients with a low HDL-C and at high risk of coronary events also require pharmacological treatment to achieve the target. Of the available treatment options, nicotinic acid is the most potent agent for raising HDL-C (by 26% at clinically recommended doses), while substantially lowering triglycerides and LDL-C. The addition of nicotinic acid to primary statin therapy is a logical approach to dyslipidaemia management, given their complementary mechanism of action, and is supported by recent clinical trials such as the Arterial Biology for the Investigation of the Treatment Effects of Reducing cholesterol (ARBITER) 2 study. Raising HDL-C will increasingly become an important secondary focus of dyslipidaemia management.

Cardiovascular Diseases↗
PubMed1977

[Elucidation of the mechanism of nicotinic acid flush in the animal experiment (author's transl)].

The reddening of the ears of guinea pigs following the administration of nicotinic acid and its derivatives is regarded as an animal experiment for the human flush-reaction. In agreement with the observations in humans we found that the reddening effects decreased after repeated administration of xantinol nicotinate (Complamin). The results demonstrate that the reddening of the ears of guinea pigs--and presumably flushing in humans as well--is a complex event. The liberation of prostaglandins, histamine and serotonin, and first of all, cholinergic reactions, seem to be involved.

Adrenergic beta-Antagonists↗
PubMed2001

Effect of nicotinic acid adenine dinucleotide phosphate on ryanodine calcium release channel in heart.

Nicotinic acid adenine dinucleotide phosphate (NAADP), a molecule derived from nicotinamide adenine dinucleotide phosphate (NADP+), is a recently identified nucleotide that activates Ca2+ release from intracellular stores in invertebrate eggs and in mammalian cells. NAADP could function as an intracellular messenger for mobilizing internal Ca2+ stores, however the targets and nature of NAADP-induced Ca2+ release are unknown. We report here that NAADP (3-10 microM) induces Ca2+ release from rat heart microsomes and that NAADP (1-10 microM) activates single ryanodine receptor/calcium release channels (RyR2) from dog heart incorporated into bilayer lipid membranes. The results indicate that NAADP may play a role in cardiac excitation-contraction coupling by acting on RyR2 channels.

Animals↗
PubMed2005

Extracellular application of nicotinic acid adenine dinucleotide phosphate induces Ca2+ signaling in astrocytes in situ.

Nicotinic acid adenine dinucleotide phosphate (NAADP+) has been identified as a novel second messenger triggering Ca2+ release from intracellular stores. Here we report that murine cortical astrocytes in culture and in acute slices respond with transient intracellular Ca2+ increases to extracellularly applied NAADP+ and express the NAADP+-producing enzyme CD38. The Ca2+ transients triggered by NAADP+ occurred with an average delay of 35 s as compared with ATP-triggered Ca2+ signaling, suggesting that NAADP+ may have to enter the cell to act. Blockage of connexin hemichannels (a possible entry route for NAADP+ into the cell) reduced the number of astrocytes responding to NAADP+. Disruption of lysosomes as the suggested site of NAADP+ receptors reduced the number of astrocytes responding to NAADP+ strongly. The NAADP+-triggered Ca2+ signal also depended on intact endoplasmic reticulum Ca2+ stores linked to activation of inositol 1,4,5-trisphosphate receptors and on the activity of voltage-gated Ca2+ channels. Adenosine receptor-mediated signaling contributes to the NAADP+-evoked signal, since it is strongly reduced by the adenosine receptor blocker CGS-15943. Moreover, NAADP+ triggered responses in all other cell types (cultured cerebellar neurons, microglia, and oligodendrocytes) of the central nervous system.

ADP-ribosyl Cyclase 1↗
PubMed2006

Second messenger function of nicotinic acid adenine dinucleotide phosphate revealed by an improved enzymatic cycling assay.

Nicotinic acid adenine dinucleotide phosphate (NAADP) is the most potent activator of Ca2+ release from intracellular stores known today. Although recent reports have suggested an important function of NAADP in human T lymphocytes, direct evidence for receptor-induced formation of NAADP is yet missing in these cells. Thus, we developed a highly sensitive and specific enzyme assay capable of quantifying low fmol amounts of NAADP. In unstimulated T cells, the NAADP concentration amounted to 4.4 +/- 1.6 nm (0.055 +/- 0.028 pmol/mg of protein). Stimulation of the cells via the T cell receptor/CD3 complex resulted in biphasic elevation kinetics of cellular NAADP levels and was characterized by a bell-shaped concentration-response curve for NAADP. In contrast, the NAADP concentration was elevated neither upon activation of the ADP-ribose/TRPM2 channel Ca2+ signaling system nor by an increase of the intracellular Ca2+ concentration upon thapsigargin stimulation. T cell receptor/CD3 complex-mediated NAADP formation was dependent on the activity of tyrosine kinases because genistein completely blocked NAADP elevation. Thus, we propose a regulated formation of NAADP upon specific stimulation of the T cell receptor/CD3 complex, suggesting a function of NAADP as a Ca2+-mobilizing second messenger during T cell activation.

Biochemistry↗
PubMed2001

Nicotinic acid adenine dinucleotide phosphate: a new Ca2+ releasing agent in kidney.

Nicotinic acid adenine dinucleotide phosphate (NAADP), a molecule derived from beta-NADP, has been shown to trigger Ca2+ release from intracellular stores of invertebrate eggs and mammalian cell microsomes. NAADP-induced Ca2+ release occurs through a mechanism distinct from that of inositol-1,4,5-trisphosphate- or cyclic ADP-ribose-elicited Ca2+ release. This study investigated whether NAADP can be synthesized in rat kidney. Extracts from glomeruli, mesangial cells, and papilla have high NAADP synthetic capacities. Conversely, synthesis of NAADP in kidney cortex was almost undetectable. Furthermore, 9-cis-retinoic acid significantly up-regulated NAADP synthesis in mesangial cells. Authenticity of NAADP biosynthesis in glomeruli was affirmed by HPLC analysis. NAADP stimulated Ca2+ release from mesangial cell microsomes through a pathway distinct from that of inositol-1,4,5-trisphosphate or cyclic ADP-ribose. NAADP-triggered Ca2+ release may play an important role in regulation of renal function.

Animals↗
PubMedDate not supplied

[Effect of the diethylamide of nicotinic acid (cordiamine) on the hydroxylating function of the liver].

Diethylamide of nicotinic acid (subcutaneously, 40 and 120 mg/kg, once a day for 4 days) was shown to exert no influence on p-hydroxylation of aniline and to increase the rate of N-demethylation of amidopyrine and ethylmorphine in the rat liver microsomal fraction by 21 and 47% as compared with the control. At the same dose of 40 mg/kg and the same schedule of administration the drug was found to increase urine excretion of antipyrine metabolites: nor-antipyrine, 4-hydroxy-antipyrine and the sum of metabolites by 229, 89 and 80%, respectively, during the first 90 min of the experiment. Excretion of antipyrine, 3-hydroxymethyl-antipyrine and 3-carboxymethyl-antipyrine underwent no significant changes. The duration of hexobarbital-induced sleep of the rats was shown to be decreased by 26%.

Aminopyrine↗
PubMed1991

Effects of yohimbine and nicotinic acid on insulin secretion in islet transplanted streptozotocin-diabetic rats.

Whether insulin secretion from transplanted islets is normally regulated has not been established. We have studied the effects of either alpha-adrenoceptor antagonism or induction of insulin resistance on glucose-stimulated insulin secretion in streptozotocin (70 mg/kg)-diabetic rats transplanted with 1000 freshly isolated islets to the left kidney subcapsular space. The alpha 2-adrenoceptor antagonist yohimbine (15 micrograms/min) increased basal and potentiated glucose-stimulated insulin secretion in control rats. In contrast, yohimbine did not affect basal or glucose-stimulated insulin secretion in transplanted rats. This suggests that the alpha-adrenoceptor islet tonus is lost following islet transplantation. Induction of insulin resistance by nicotinic acid (6 mg orally twice daily for 10 days) was followed by increased basal insulin levels without any effect on basal plasma glucose levels, both in control and islet transplanted rats, as an adaptation to insulin resistance. Furthermore, after nicotinic acid, the plasma insulin response during glucose infusion was adequate to maintain the normal hyperglycemic response, both in controls and in islet transplanted rats. This suggests that transplanted islets retain the capability to adapt to insulin resistance.

Animals↗
PubMed1979

[Mechanisms of detecting organic cholephilic anions in man: comparative studies on plasma depuration of rifamycin-SV. Interference of nicotinic acid and phenobarbital].

We have studied plasmatic half-life of R-SV administered alone and in association with nicotinic acid, before and after treatment with phenobarbital, in 10 normobilirubinaemic subjects and in 10 patients Gilbert's syndrome, used like controls. Ouer results confirm the existence of some alterations of drug-metabolism produced by associated administration of other drugs, in both healthy and hyperbilirubinaemic subjects, and in these one even more.

Adolescent↗
PubMedDate not supplied

[Dynamics and kinetics of 14C-nicotinic acid uptake by leukocytes and erythrocytes as an index of vitamin PP transport regulation].

Isolated leukocytes with the presence of 14C-nicotinate in physiological concentrations (1 mg%) uptake it intensely from the dilute plasm for 6h. Dynamics of the uptake is characterized by two maxima (30-50 min and 3-5 h) which might reflect metabolic transformation of vitamin PP in leukocytes. Isolated erythrocytes and blood plasma proteins under these conditions accumulate the labelled vitamin in the largest amounts for first minutes of incubation without subsequent changes, accumulation of the labelled nicotinate by erythrocytes is 20 times as low as that by leukocytes. Kinetics of 14C-nicotinate uptake in increasing concentrations (from 4.0 up to 50.0 mM) by isolated leukocytes indicates to a system of this vitamin intake through the plasmatic membrane ensuring its intensive transport into cells with the present of 3.0-6.5 mM of nicotinic acid and a step inhibition of the label accumulation at higher concentrations which reflects decompensation of the vitamin-barrier function of the leukocytes plasma membranes with a rise in the nicotinate concentration in the medium from 6.5 to 16.3 mM the label accumulation is inhibited not only by leukocytes but also by erythrocytes. However the blood plasma proteins still bind 14C-nicotinate when it is present in the medium in linearly increasing high concentrations (16.0 = 50 mM).

Biological Transport, Active↗
PubMed1980

Effects of combined procetofene--nicotinic acid therapy in treatment of hypertriglyceridaemia.

Eight males with hypertriglyceridaemia were treated with a combination of procetofene (400 mg/day) and nicotinic acid (4 g/day) for 6 weeks. Previous therapy with only procetofene (400 mg/day) had given a certain, but not complete degree of normalisation. The combined treatment lowered the VLDL TG concentration values from 3.21 to 1.11 mmol/l and increased the HDL cholesterol concentration from 1.04 to 1.43 mmol/l (P less than 0.05 for both). The significant LDL cholesterol increase from 4.45 to 5.27 mmol/l, observed during treatment with procetofene only, reverted to 4.05 mmol/l when combined therapy was given. This drug combination may be a valuable tool to obtain maximum reduction of elevated TG in the therapy of hypertriglyceridaemia.

Aged↗
PubMedDate not supplied

[Adrenal cortex and vitamin PP. The effect of corticosteroids on the NAD level in the rat liver after the administration of excess nicotinic acid or nicotinamide].

The NAD content in the liver was experimentally studied in intact, adrenalectomized rats and those given hydrocortisone following nicotinic acid and nicotinamide administration. The NAD concentration in the liver rose linearly and equally during the first 4 experimental hours after the nicotinamide administration (200 mg/kg). A conclusion was drawn that in administration of exogenous precursors the coenzyme biosynthesis did not depend on the initial hormonal background.

Adrenal Cortex↗