Abstract
Acute fluoride intoxication increases intracellular calcium (Cai), manifested by increased twitch tension in cardiac muscle, and by potassium efflux (mediated by Ca2+-dependent K+ channels) in fluoridated erythrocytes. Fluoride, like isoproterenol, stimulates adenylate cyclase, and could increase Cai via the effects of cAMP on Ca2+ channels. However, while the inotropic effects of fluoride mimicked isoproterenol in rat atria, their effects on the time course of isometric contraction were quite different. In addition, acetylcholine negated isoproterenol’s effect on twitch tension but did not modulate the effects of fluoride. Further, the Ca2+ channel antagonist verapamil had no effect on fluoride-stimulated K+ efflux from erythrocytes. Fluoride also inhibits Na+-K+ ATPase, and increases intracellular Na+, so could increase Cai via Na+-Ca2+ exchange. Lanthanum, which blocks Na+-Ca2+ exchange, blocks fluoride-induced K+ efflux in erythrocytes. We conclude that the effects of fluoride on adenylate cyclase are not important in intact tissue, and that inhibition of Na+-K+ ATPase and subsequent Na2+-Ca2+ exchange may be the mechanism of increased Cai in acute fluoride toxicity.
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Delayed fatal hyperkalemia in a patient with acute fluoride intoxication.
A 19-year-old man presented with acute fluoride poisoning. Initially his serum electrolytes were normal, but two hours later he developed ECG evidence of hyperkalemia followed by refractory ventricular fibrillation, suggesting that hyperkalemia may be important in the cardiotoxicity of acute fluoride intoxication. Treatment of fluoride-induced hyperkalemia consists of removal of
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Further evidence for the involvement of cAMP in central blood pressure regulation
In order to test the hypothesis that the activity of cardiovascular centres is determined by their content of cAMP a number of drugs which influence the activity of either phosphodiestase or adenylcyclase were injected in doses of 100-1000 mug/kg into the lateral cerebral ventricle of cats. The effects on blood
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Stimulation of cAMP accumulation in rat aorta and diaphragm by fluorine containing compounds
Evidence is presented that accumulation of cAMP in isolated rat thoracic aorta and diaphragm is stimulated by several fluorine containing compounds (NaF, Na2PO3F (MFP) and SnF2). Time course experiments with NaF showed that maximal stimulation of cAMP accumulation was observed within 2.5 min. NaF and MFP produced significant increases in
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Protective effect of quercetin against sodium fluoride induced oxidative stress in rat's heart
The antioxidative and cardioprotective properties of quercetin were investigated against sodium fluoride (NaF) induced oxidative stress in rat hearts. Experimental rats were divided into five groups. The first group served as the untreated (normal) control. The second group received NaF at a dose of 600 ppm through drinking water for
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The effects of fluoridated water on rat urine and tissue cAMP levels
Male Wistar rats were fed a fluoride deficient diet (less than 0.5 parts/10(6) F), and either distilled water or fluoridated water (1.0 parts/10(6)). By week 3, the control group had urinary excretions of 106 +/- 5 nmol cAMP/day (mean +/- SEM) whereas the experimental group excreted 129 +/- 6 nmol
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