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.
-
-
Review of the Bartlett-Cameron survey: a ten year fluoride study.
Analysis of the data produced the following conclusions: 1. As was expected, dental fluorosis was significantly greater in Bartlett than in Cameron (all of the participants born and in continuous residence in Bartlett during the tooth formative period exhibited positive evidence of dental fluorosis). 2. The incidence of cardiovascular disease was higher
-
Possible protective role of calcium against fluoride induced cardio toxicities in adult male albino rats
Fluoride contamination in drinking water due to natural and anthropogenic activities has been recognized as one of the major problems worldwide imposing a serious threat to human health. Excessive exposure to fluoride appears to be serious and causes metabolic, functional and structural damages in many organs especially in the heart.
-
Fluorosis in Aden
The cases to be described here occurred in the Aden Protectorate where for the last 12 years mass screening of the chest to exclude pulmonary tuberculosis has been carried out. The patients had all drunk the brackish water from the wells, and the analysis of the water from a well
-
Fatal systemic fluorosis due to hydrofluoric acid burns.
A patient with a 70% hydrofluoric acid burn developed systemic dissemination of fluoride ion from a 9% to 10% body surface area exposure on the lower extremities. Severe hypocalcemia and intractable ventricular arrhythmias resulted. This case is the second documented occurrence of hypocalcemia from hydrofluoric acid burns. It is the
-
Fluoride stimulates in vitro vascular prostacyclin synthesis: interrelationship of G proteins and protein kinase C
The role of G proteins in mediating adrenoceptor-prostacyclin synthesis coupling was investigated using the G protein activator, sodium fluoride. Sodium fluoride (NaF) stimulated in vitro rat aortic prostacyclin (PGI2) synthesis (EC50 = 5 x 10(-3) mol.l-1), an action inhibited completely by the presence of EDTA (10(-2) mol.l-1). The NaF-PGI2 dose-response
Related Studies :
-
-
-
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 & 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 & 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 & 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
Related FAN Content :
-