The Effects of Manganese on the Rabbit Anterior Mesenteric–Portal Vein

1972 ◽  
Vol 50 (4) ◽  
pp. 300-309 ◽  
Author(s):  
G. A. Collins ◽  
M. C. Sutter ◽  
J. C. Teiser

The effects of manganese and lanthanum were tested on the contractile responses of the rabbit anterior mesenteric–portal vein (A.M.V.). Since these ions have been shown to block calcium fluxes in other tissues, examining their effects may give information concerning the importance of calcium influx for contractions of the A.M.V. The effects of the two cations on the A.M.V. were found to be similar except that lanthanum was more potent and its inhibitory effects were not readily reversible. Spontaneous action potentials and their associated contractions were abolished by the addition of 0.5 mM Mn2+. This inhibition could be rapidly reversed by adding EDTA to chelate the manganese. Manganese inhibited the responses to all agonists tested (noradrenaline, histamine, serotonin, procaine, and KCl). The inhibition of responses to all agonists but procaine could be partially reversed by raising the external calcium concentration. The interaction between calcium and manganese follows competitive kinetics. Adding manganese during the tonic phase of a contraction evoked by 10−6 g/ml noradrenaline resulted in a relaxation to a decreased, but sustained, tension. The inhibitory effects of manganese add further evidence that an influx of calcium from the extracellular fluid is required for spontaneous activity and for both the initiation and maintenance of contractions to agonists in the rabbit A.M.V.

1999 ◽  
Vol 82 (1) ◽  
pp. 429-435 ◽  
Author(s):  
James L. Costantin ◽  
Andrew C. Charles

GT1–1 cells exhibit spontaneous action potentials and transient increases in intracellular calcium concentration ([Ca2+]i) that occur in individual cells and as spatially propagated intercellular Ca2+ waves. In this study, simultaneous cell-attached patch-clamp recording of action currents (indicative of action potentials) and fluorescence imaging of [Ca2+]i revealed that Ca2+transients in GT1–1 cells were preceded by a single action current or a burst of action currents. Action currents preceded Ca2+transients in a similar pattern regardless of whether the Ca2+ transients were limited to the individual cell or occurred as part of an intercellular Ca2+ wave. Both the action currents and Ca2+ transients were abolished by 1 μM tetrodotoxin. Removal of extracellular Ca2+ abolished all spontaneous Ca2+ transients without inhibiting the firing of action currents. Nimodipine, which blocks L-type Ca2+ currents in GT1–1 cells, also abolished all spontaneous Ca2+ signaling. Delivery of small voltage steps to the patch pipette in the cell-attached configuration elicited action currents the latency to firing of which decreased with increasing amplitude of the voltage step. These results indicate that spontaneous intercellular Ca2+ waves are generated by a propagated depolarization, the firing of action potentials in individual cells, and the resulting influx of Ca2+ through L-type Ca2+ channels. These patterns of spontaneous activity may be important in driving the pulsatile release of GnRH from networks of cells.


1976 ◽  
Vol 68 (1) ◽  
pp. 29-41 ◽  
Author(s):  
G Plishker ◽  
H J Gitelman

Intact human erythrocytes can be readily loaded with calcium by incubation in hypersomotic media at alkaline pH. Erythrocyte calcium content increases from 15-20 to 120-150 nmol/g hemoglobin after incubation for 2 h at 20 degree C in a 400 mosmol/kg, pH 7.8 solution containing 100 mM sodium chloride, 90 mM tetramethylammonium chloride, 1 mM potassium chloride, and 10 mM calcium chloride. Calcium uptake is a time-dependent process that is associated with an augmented efflux of potassium. The ATP content in these cells remains at more than 60% of normal and is not affected by calcium. Calcium uptake is influenced by the cationic composition of the external media. The response to potassium is diphasic. With increasing potassium concentrations, the net accumulation of calcium initially increases, becoming maximal at 1 mM potassium, then diminishes, falling below basal levels at concentrations above 3 mM potassium. Ouabain inhibits the stimulatory effect of low concentrations of potassium. The inhibitory effects of higher concentrations of potassium are ouabain insensitive and independent of the external calcium concentration. Sodium also inhibits calcium uptake but this inhibition can be modified by altering the external concentration of calcium. The effux of calcium from loaded erythrocytes is not significantly altered by changes in osmolality, medium ion composition, or ouabain. It is concluded that hypertonicity increases the net uptake of calcium by increasing the influx of calcium and that some part of the sodium potassium transport system is involved in this influx process.


1972 ◽  
Vol 50 (4) ◽  
pp. 289-299 ◽  
Author(s):  
G. A. Collins ◽  
M. C. Sutter ◽  
J. C. Teiser

Studies were done measuring contractile activity in the isolated rabbit anterior mesenteric–portal vein (A.M.V.). The rabbit A.M.V. requires external calcium for both spontaneous activity and the initiation and maintenance of contractions to agonists.After bathing the tissues in calcium-free Krebs' solution containing 1 mM ethyleneglycoltetraacetic acid (EGTA) for 10 min, and then washing out the EGTA, the re-addition of calcium produced a contraction. The pre-addition of a small amount of calcium (0.1 mM) after EGTA treatment (while not inducing a contractile response) alters subsequent contractile responses to larger concentrations of calcium. This is interpreted as the ability of membrane-bound calcium to control membrane permeability to calcium.Other experiments involved bathing the tissues in calcium-free solution until no response was obtained to agonists, and then re-adding calcium. The time course of the responses to noradrenaline after calcium re-addition depended on the length of calcium incubation. This suggests that noradrenaline can release a loosely bound calcium fraction which may be involved in controlling calcium influx. This bound calcium, however, does not provide a major source of activator calcium in normal Krebs' solution.


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