Abstract

The modulatory actions of fluoride on the function of the dihydropyridine-sensitive (L-type) Ca2+ channel were studied in rabbit cardiac myocytes. In cell-attached voltage-clamp experiments, using barium as the charge carrier, fluoride increased the activity of the Ca2+ channel dose-dependently. Low concentrations (<10 mM) of fluoride increased the number of traces with channel activities, and decreased the number of traces without channel activities, resulting in a net increase in the open-channel probability. The effect of 5 mM fluoride on the Ca2+ channel was inhibited by the presence of non-hydrolyzable guanosine diphosphate analog in the cell. On the other hand, high concentrations (>10 mM) of fluoride increased the open-channel duration, resulting in a marked increase in open-channel probability. A pretreatment of myocytes with a phosphatase inhibitor, okadaic acid, virtually abolished the additional effect of fluoride on the open-channel duration or open probability. A concentration of up to 75 mM fluoride had no effect on the Ca2+-channel activity when the myocytes were pretreated with a potent inhibitor of protein kinases, indicating that fluoride increased the Ca2+- channel activity via modulation of the phosphorylation state of the myocyte or the channel protein alone.

• Related Studies :

  • The pathophysiological profile of the acute cardiovascular toxicity of sodium fluoride.

    The mechanism of sodium-fluoride (7681494) cardiovascular toxicity was examined. Spontaneously breathing or mechanically ventilated male Wistar-rats instrumented with carotid and aorta arterial transducers and thermistors were infused intravenously with 2mg/kg per minute (min) sodium-fluoride until death. Arterial blood pressure, heart rate, cardiac output, peripheral resistance, respiration frequency, oxygen consumption (VO2),

  • Chronic fluorosis: the disease and its anaesthetic implications..

    Abstract Chronic fluorosis is a widespread disease-related to the ingestion of high levels of fluoride through water and food. Prolonged ingestion of fluoride adversely affects the teeth, bones and other organs and alters their anatomy and physiology. Fluoride excess is a risk factor in cardiovascular disease and other major diseases, including

  • Fluoride-induced hyperkalemia: the role of Ca2+-dependent K+ channels.

    Acute fluoride poisoning is associated with sudden cardiac death by an unknown mechanism. Because F- binds to Ca2+ to cause marked hypocalcemia, lowered serum Ca2+ concentrations have been thought to be a major underlying factor in the ventricular irritability of F(-)-toxic patients. However, correction of the hypocalcemia does not prevent

  • Dose effect relationship between high fluoride intake and biomarkers of lipid metabolism in endemic fluorosis

    Fluorosis is a metabolic hard tissue disease caused by ingestion of excessive amount of fluoride mainly through drinking water. We aimed to explore the dose effect correlation among some biochemical indexes of lipid metabolism in fluoride toxicity. Blood samples from 705 patients, age 20–60, with endemic fluorosis living in seven

  • Association of vascular fluoride uptake with vascular calcification and coronary artery disease

    Objective: The feasibility of a fluoride positron emission tomography/computed tomography (PET/CT) scan for imaging atherosclerosis has not been well documented. The purpose of this study was to assess fluoride uptake of vascular calcification in various major arteries, including coronary arteries. Methods: We retrospectively reviewed the imaging data and cardiovascular history of

• Related FAN Content :

  • Fluoride & Arteriosclerosis

    Healthy arteries are flexible and elastic, allowing efficient transfer of blood and nutrients from the heart to the rest of the body. Arteriosclerosis refers to a stiffening of the arteries, including loss of elasticity. This is a slow, progressive disease that may begin early in life from damage to the

  • Fluoride & Electrocardiogram Abnormalities

    An electrocardiogram (ECG) is a diagnostic test that measures the electrical activity of the heart. An ECG can reveal heart rate, heart rhythym (i.e. steady or irregular), and the strength and timing of the heart’s natural electrical signals. ECGs are described in terms of “waves” (e.g. amplitude and duration). Problems

  • Fluoride & Myocardial Damage

    Structural damage to the heart resulting from fluoride toxicity has been observed in numerous human and animal studies. The general features of this damage include cloudy swelling, vacuolization or vacuolar degeneration, hemorrhages, interstitial edema, fibrous necrosis, dissolution of nuclei, and thickening of the vessel walls in the heart muscle (Basha

  • Fluoride, Blood Pressure and Hypertension

    Individuals with blood pressure readings that exceed 140/90 are considered hypertensive. Hypertension can increase the risk of stroke, heart attack, heart failure, aortic aneurysms, and peripheral arterial disease. An association between increased fluoride in ground water and increased prevalence of hypertension has been observed, especially among adult males (Amini et

  • Fluoride & Arterial Calcification

    The major change involved with cardiovascular disease is development of atherosclerosis in critical arteries, which is partially characterized by vascular calcification. The level of coronary artery calcification is thought to be the most important indicator of future cardiovascular events. Increased arterial calcifications have frequently been reported in those with skeletal fluorosis