Search

Calcium levels in the blood and in cells are maintained within narrow limits in normal animals, although variations occur in dietary constituents and absorption. This blood balance is maintained primarily by using the calcium reserves in skeletal tissues and modulating its loss in the kidney (15). It is thus essential to understand the underlying role of the cells of these tissues in effecting selective ion distribution, as calcium plays a major role in physiologic processes, and maintenance of appropriate distribution and concentration is mandatory (16). All cells regulate and utilize calcium in some activity, and the means employed by different cell types may be used to give clues to the mechanisms involved in regulating calcium ion distribution in mineralized systems. The following examples are selected to illustrate the diverse distribution and mechanisms of regulation that may by employed.

1. Calcium efflux from guinea-pig auricles followed saturation kinetics when [Ca](o) and [Na](o) were changed while the ratio [Ca](o)/[Na](o) (2) was kept constant. The Michaelis constant, K(m) (Ca+Na) = 40 mM, suggests that a hypothetical carrier system, responsible for sodium-calcium exchange, is far from saturation with the inside concentrations of these ions.2. [Na](i) was altered in the auricles between 12.5 and 60 mM/kg fibre water while total cellular calcium concentration ([Ca](t)) at the beginning of the influx period was not significantly different in the various groups of preparations.3. (45)Ca influx increased appreciably with increasing [Na](i). (45)Ca influx from sodium-poor solution corresponded to an almost equal increase in [Ca](t), while [Ca](t) did not change much in preparations loaded with (45)Ca in Tyrode solution. When the sodium-activated fraction of calcium influx was plotted against [Na](i) (2) the resulting curve indicated saturation with K(m) (Na) = 3500 (mM [Na](i))(2) and maximal influx rate, J(i, max) (Ca') = 1.35 mM/kg wet weight x 10 min.4. When the preparations were re-equilibrated for various times in normal Tyrode solution after [Na](i) had been increased, both the sodium-activated component of calcium influx and [Na](i) (2) decreased with approximately the same rate constants.5. Calcium efflux from auricles with high [Na](i) was increased when it was measured in Tyrode solution while the efflux in sodium-poor solution was inhibited.6. Auricles with increased [Na](i) showed a positive inotropic contractile response.7. The main conclusion reached by these experiments is that calcium influx is affected by [Na](i) in a way which is compatible with a carrier-mediated sodium-calcium exchange system.

Im K-depolarisierten Myometrium ist die mechanische Aktivitat durch die extrazellulare Ca-Konzentration graduierbar. Zugabe von Acetylcholin in die Ca-freie, depolarisierende Losung ergibt mechanische Spannungsentwicklung des Myometriums.

Electron-dense deposits were found along the inner side of the cell membrane of chicken erythrocytes when fixed in a CaCl2-containing glutaraldehyde solution. Osteoblasts and osteoclasts were studied in an attempt to determine whether the deposits are related to calcium metabolism. No electron-dense deposits adjacent to the cell membrane were found in either these cells or in rat erythrocytes. Therefore, it is assumed that the deposits are not calcium-binding protein necessary for the cellular calcium uptake.

Calcium ions (Ca2+) are accumulated by a cellular depot in isolated rabbit ileal longitudinal smooth muscle during incubation of this tissue in high Ca2+ medium. Transfer of the muscle to Ca2+-free solution results in a transient contractile response. The magnitude of the contraction appears to be a rectangular hyperbolic function of the Ca2+ concentration in the cellular compartment. When 10−6M acetylcholine (ACh) is present in the Ca2+-free solution, the muscle is stimulated, and the magnitude and duration of the mechanical activity occurring in the Ca2+-free environment is enhanced. When 10−6 or 10−7M epinephrine (Epi) is present in the Ca2+-free medium, the magnitude and duration of the contraction occurring in the Ca2+-free solution is reduced. Neither agent alters significantly the rate of loss of radioactive 45Ca from the muscle strips. Rather, these agents may be acting by influencing the operation of a saturable Ca2+ transport system located between the cellular Ca2+ pool and the contractile machinery. Evidence indicates that ACh increases and Epi decreases the turnover rate and/or number of active Ca2+ sites associated with this transport mechanism.

IT has been suggested, on the basis of indirect evidence, that heparin may extract calcium from cells1.

Acetylcholine 5 × 10−8 g/ml reduces the Ca45 uptake of the beating left atria of guinea-pig; the tissue calcium is not altered. In resting atria, acetylcholine 5 × 10−7 g/ml has no influence upon the calcium content and Ca45 uptake. It is concluded that acetylcholine acts by shortening the action potential duration and thereby reduces the release of cellular calcium per excitation.

The effect of adrenaline on the cellular calcium exchange during the K-depolarization of myocardium was studied in isolated left auricles of guinea-pigs by means of the45Ca. Increasing the extracellular K-concentration from 2.7–30 mM without corresponding reduction in sodium concentration results in a depression of contraction strength of the myocardium when current is applied. The depression is immediately reversible by using adrenaline. This was associated with a significant increase of the45Ca exchange.