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PubMed2004

Fire-diffuse-fire calcium waves in confined intracellular spaces.

The propagation of fire-diffuse-fire Ca(2+) waves through a three-dimensional rectangular domain is considered. The domain is infinite in extent in the direction of propagation but with lateral barriers to diffusion which contain Ca(2+) pumps. The Ca(2+) concentration profile due to the firing of a release site (spark) is derived analytically based on the Green's function for the diffusion equation on the domain. The existence, stability and speed of these waves is shown to be critically dependent on the dimensions of the domain and the Ca(2+) pump rate. It is shown that the smaller the dimensions of the region, the lower the Ca(2+) release flux required for wave propagation, and the higher the wave speed. Also it is shown that the region may support multiple Ca(2+) wavefronts of varying wave speed. This model is relevant to subsarcolemmal waves in atrial myocytes (Kockskämper et al., 2001, Biophys. J. 81, 2590-2605), and the results may be of importance in understanding the roles of the endoplasmic/sarcoplasmic reticulum, surface membranes and Ca(2+) pumps in the intracellular Ca(2+) dynamics of cells.

Calcium↗
PubMed1978

[Distribution of water between the extracellular and intracellular space in rats].

In anesthetized rats the renal pedicules were clamped and the solution with THO, antipyrine, thyocyanate, inulin, 22Na, 36Cl, 82Br was injected into the tail artery. The space of distribution of THO was 65.1% body weight, antipyrine--81.9%. The volumes of distribution of 22Na (27.4%) and thyocyanate (26.9%) were higher than the 36Cl (24.8%) and 82Br (25.6%) spaces. Inulin space was 13.8%. There was no difference between the volume of distribution of the substances in female and male rats. The same spaces of the substances (except inulin) were determined in rats with intact kidneys. After i.a. administration of 5 ml/100 g body weight of Ringer's solution the recovery of all the substances was about 100%. The data obtained indicate that antipyrine cannot be used for estimation of the total body water in rats. For the measurement of extracellular fluid it is better to use radioisotopes 82Br, 36Cl or 22Na; more variable data were observed with thyocyanate and inulin.

Animals↗
PubMed2002

Exploring intracellular space: function of the Min system in round-shaped Escherichia coli.

The MinCDE proteins help to select cell division sites in normal cylindrical Escherichia coli by oscillating along the long axis, preventing unwanted polar divisions. To determine how the Min system might function in cells with multiple potential division planes, we investigated its role in a round-cell rodA mutant. Round cells lacking MinCDE were viable, but growth, morphology and positioning of cell division sites were abnormal relative to Min+ cells. In round cells with a long axis, such as those undergoing cell division, green fluorescent protein (GFP) fusions to MinD almost always oscillated parallel to the long axis. However, perfect spheres or irregularly shaped cells exhibited MinD movement to and from multiple sites on the cell surface. A MinE-GFP fusion exhibited similar behavior. These results indicate that the Min proteins can potentially localize anywhere in the cell but tend to move a certain maximum distance from their previous assembly site, thus favoring movement along the cell's long axis. A new model for the spatial control of division planes by the Min system in round cells is proposed.

Adenosine Triphosphatases↗
PubMed1992

Airway hyperresponsiveness, increased intracellular spaces of bronchial epithelium, and increased infiltration of eosinophils and lymphocytes in bronchial mucosa in asthma.

Inflammation of the airway wall and airway hyperresponsiveness are consistent features of chronic asthma. We investigated how damage of the bronchial epithelium is related to airway hyperresponsiveness and how bronchial infiltration of eosinophils and lymphocytes is related to bronchial epithelial damage. We examined the biopsy specimens of bronchial mucosa taken from 19 patients with chronic asthma by electron microscopy. We also measured the incidence of opening of epithelial tight junctions, the widening of intercellular spaces in the epithelium, and the density of infiltrated eosinophils and lymphocytes in bronchial mucosa. Airway responsiveness was accessed by measuring PC20-acetylcholine (PC20-ACh). The inflammatory cells in the airway mucosa were counted by electron microscopy. Lymphocytes were most abundant, being 54.5% of the cells counted; eosinophils were 22.1%, neutrophils were 4.9%, and mast cells were 4.6%. A significant correlation was noted between the density of eosinophils and that of lymphocytes infiltrated in the airway mucosa (r = 0.80, p less than 0.01), suggesting that T cells may potentiate eosinophil infiltration. With increased density of eosinophils infiltrated in bronchial mucosa, both the incidence of opening of tight junctions of epithelial ciliary cells and the degree of widening of intercellular spaces in epithelium increased significantly (r = 0.51, p less than 0.05; r = 0.52, p less than 0.05), suggesting that eosinophils are related to damage of the bronchial epithelium. No correlation was observed between the density of lymphocyte infiltration and the degree of epithelial damage.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMedDate not supplied

Role of magnesium in insulin action, diabetes and cardio-metabolic syndrome X.

Magnesium (Mg) is one of the most abundant ions present in living cells and its plasma concentration is remarkably constant in healthy subjects. Plasma and intracellular Mg concentrations are tightly regulated by several factors. Among them, insulin seems to be one of the most important. In vitro and in vivo studies have demonstrated that insulin may modulate the shift of Mg from extracellular to intracellular space. Intracellular Mg concentration has also been shown to be effective in modulating insulin action (mainly oxidative glucose metabolism), offset calcium-related excitation-contraction coupling, and decrease smooth cell responsiveness to depolarizing stimuli. A poor intracellular Mg concentration, as found in noninsulin-dependent diabetes mellitus (NIDDM) and in hypertensive patients, may result in a defective tyrosine-kinase activity at the insulin receptor level and exaggerated intracellular calcium concentration. Both events are responsible for the impairment in insulin action and a worsening of insulin resistance in noninsulin-dependent diabetic and hypertensive patients. By contrast, in NIDDM patients daily Mg administration, restoring a more appropriate intracellular Mg concentration, contributes to improve insulin-mediated glucose uptake. The benefits deriving- from daily Mg supplementation in NIDDM patients are further supported by epidemiological studies showing that high daily Mg intake are predictive of a lower incidence of NIDDM. In conclusion, a growing body of studies suggest that intracellular Mg may play a key role in modulating insulin-mediated glucose uptake and vascular tone. We further suggest that a reduced intracellular Mg concentration might be the missing link helping to explain the epidemiological association between NIDDM and hypertension.

Diabetes Mellitus, Type 2↗
PubMed1997

Hypertension, diabetes mellitus, and insulin resistance: the role of intracellular magnesium.

Magnesium is one of the most abundant ions present in living cells and its plasma concentration is remarkably constant in healthy subjects. Plasma and intracellular magnesium concentrations are tightly regulated by several factors. Among them, insulin seems to be one of the most important. In fact, in vitro and in vivo studies have demonstrated that insulin may modulate the shift of magnesium from extracellular to intracellular space. Intracellular magnesium concentration has also been shown to be effective on modulating insulin action (mainly oxidative glucose metabolism), offset calcium-related excitation-contraction coupling, and decrease smooth cell responsiveness to depolarizing stimuli, by stimulating Ca2+-dependent K+ channels. A poor intracellular magnesium concentration, as found in non-insulin-dependent diabetes mellitus (NIDDM) and in hypertensive (HP) patients, may result in a defective tyrosine-kinase activity at the insulin receptor level and exaggerated intracellular calcium concentration. Both events are responsible for the impairment in insulin action and a worsening of insulin resistance in non-insulin-dependent diabetic and hypertensive patients. By contrast, in NIDDM patients daily magnesium administration, restoring a more appropriate intracellular magnesium concentration, contributes to improve insulin-mediated glucose uptake. Similarly, in HP patients magnesium administration may be useful in decreasing arterial blood pressure and improving insulin-mediated glucose uptake. The benefits deriving from daily magnesium supplementation in NIDDM and HP patients are further supported by epidemiological studies showing that high daily magnesium intake to be predictive of a lower incidence of NIDDM and HP. In conclusion, a growing body of studies suggest that intracellular magnesium may play a key role on modulating insulin-mediated glucose uptake and vascular tone. We further suggest that a reduced intracellular magnesium concentration might be the missing link helping to explain the epidemiological association between NIDDM and hypertension.

Animals↗
PubMed1976

The kinetics of efflux of 5,5-dimethyl-2,4-oxazolidinedione (DMO) from the myocardium.

1. The efflux of 14C-labelled 5,5-dimethyl-2,4-oxazolidinedione (DMO) from the myocardium of the rabbit has been studied. The perfusate pH was 7-38. 2. The effluent curve is complex and appears to be the resultant of movement between at least four compartments. 3. The first two probably represent intravascular and extracellular compartments; the last two have smaller rate constants and may represent intracellular spaces. Intracellular pH (pHi) calculated from the effluent curve was 7-23 +/- 0-05. pHi estimated from the steady-state distribution volume of DMO was 7-28 +/- 0-02. The existence of two intracellular compartments suggests that DMO is not homogeneously distrubted in the myocardium. It is suggested that the apparent greater buffering capacity of cardiac than skeletal muscle can be explained by the greater number and volume of mitochondria in the myocardium, compartmentalization of DMO and assumptions inherent in the DMO method for the measurement of pHi.

Animals↗