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At least 19 recordsLinked to original sources
PubMed1964

NICOTONIC ACID BIOSYNTHESIS: CONTROL BY AN ENZYME THAT COMPETES WITH A SPONTANEOUS REACTION.

Extracts of livers from diabetic rats contain normal amounts of the enzymes needed to convert 3-hydroxyanthranilic acid to nicotinic acid nucleotide. The decreased capacity of diabetic animals to synthesize nicotinic acid is therefore attributed to increased amounts of picolinic carboxylase, which competes for a common intermediate with the spontaneous reaction in which quinolinic acid is formed as a precursor of nicotinic acid. These studies were facilitated by the synthesis of 3-hydroxyanthranilic acid labeled with carbon-14 in positions 3 and 6

Adenosine Triphosphate↗
PubMed2003

Hemodynamic effects of nicotinic acid infusion in normotensive and hypertensive subjects.

Nicotonic acid (NA) infusions are associated with peripheral vasodilation from the generation of vascular prostaglandins with minimal effects on blood pressure (BP) in normotensive subjects. We studied the effects of a NA infusion in 10 hypertensive and 11 normotensive individuals to further characterize systemic hemodynamic responses to NA using pulse waveform analysis. Blood pressure, stroke volume, cardiac output, total peripheral resistance, large and small artery elasticity were determined before and after a 1-h NA infusion. In the normotensives, systolic, diastolic, mean BP, and pulse pressure were not affected by NA. In contrast, the hypertensive subjects experienced a decrease in mean BP from 105 +/- 2 mm Hg to 100 +/- 3 mm Hg (P <.01) accompanied by significant decreases in systolic, diastolic, and pulse pressures. The differential BP response occurred despite comparable increases in heart rate (11% to 13%, P </=.05) and similar decreases in total peripheral resistance (6%, P </=.05) in both groups. However, the normotensive group demonstrated a decrease in overall vascular compliance, measured as stroke volume to pulse pressure ratio, from 2.12 +/- 0.09 to 1.93 +/- 0.09 mL/mm Hg (P <.05). This finding was supported by a decrease in C1 (large artery compliance), assessed by pulse waveform analysis, from 15.8 +/- 1 to 14.2 +/- 1 mL/mm Hg (P <.05). In contrast, overall compliance and C1 were unchanged after the NA infusion in the hypertensive group. These results suggest that there is a differential hemodynamic response to NA infusion in normotensive and hypertensive individuals. The adjustment in vascular compliance may be an important factor in determining overall BP response to NA.

Adult↗
PubMed1967

Studies on the mechanism of kinin formation in inflammation.

1. Injection of autologous plasma into the subcutaneous space leads to kinin formation in man. Kinin formation was also observed after similar injections of homologous plasma in the rat, dog and guinea-pig. The material withdrawn from the subcutaneous tissue following the injection of plasma was characterized as kinin by inhibition of its formation with trasylol, by inactivation with chymotrypsin and by its pharmacologic effects.2. Kinins were also demonstrated in subcutaneous tissue following injections of compound 48/80, a histamine liberator.3. A slightly acid pH greatly favours the accumulation of kinins in subcutis.4. Human plasma kallikrein was not activated in vitro by histamine, serotonin, nicotonic acid or endotoxin. Human polymorphonuclear leukocytes initiated the formation of kinins in plasma.5. It is suggested that in inflammation, ;primary mediators' such as histamine, do not activate plasma kallikrein directly, but rather increase vascular permeability, permitting plasma to enter the extravascular space where conditions for activation exist. Kinin accumulation is enhanced in inflammation where pH is slightly lowered.

Animals↗
PubMed1986

Integrated metabolic control of food intake.

Inhibition of glycolysis and fatty acid oxidation by combined treatment with 2-deoxyglucose (2DG) and methyl palmoxirate, or inhibition of glycolysis and lipolysis by combined treatment with 2DG and nicotonic acid synergistically increased food intake in rats. Methyl palmoxirate treatment alone increased food intake in rats fed a high-fat, but not low-fat diet. These results provide direct evidence for a mechanism in the control of food intake that integrates signals generated by the metabolism of glucose and fatty acids. In addition, they strongly indicate a role for fatty acid oxidation in the control of eating and raise the possibility that an interaction between glucose and fat metabolism underlies the link between regulation of body fat stores and short-term food intake.

Animals↗
PubMed1991

Sleep deprivation-induced dermatitis: further support of nicotinic acid depletion in sleep deprivation.

It is noted that some of the manifestations of prolonged sleep deprivation are similar to changes seen in pellagra. Dermatitis is one of the cardinal clinical manifestations of human pellagra. Prolonged sleep deprivation also typically induces a dermatitis in experimental animals. Both dermatidities are histopathologically similar. It is plausible that both may have a similar etiology, i.e. depletion of nicotonic acid and products derived from it.

Animals↗