THE EFFECTS OF NEW DIURETICS ON NET ION MOVEMENTS IN SODIUM-RICH SMOOTH MUSCLES

1967 ◽  
Vol 45 (1) ◽  
pp. 149-159 ◽  
Author(s):  
E. E. Daniel
Keyword(s):  
Active Transport ◽  
Ethacrynic Acid ◽  
Smooth Muscles ◽  
Convincing Evidence ◽  
Small Concentration ◽  
K Uptake ◽  
Aldosterone Antagonist ◽  
Ion Movements ◽  
Sufficient Concentration

The effects of furosemide, ethacrynic acid, triamterene, and an aldosterone antagonist (Su-11927) were studied on recovery of electrolyte gradients by Na-rich pieces from rabbit uteri and aortas. In sufficient concentration furosemide and ethacrynic acid appeared to inhibit Na extrusion. Only furosemide inhibited K uptake as well. A small concentration of ethacrynic acid (0.1 μg/ml) increased Na extrusion from Na-rich uterine pieces but did not increase K uptake. Thus K gain and Na extrusion were not always reciprocally related. Triamterene and Su-11927 altered recovery of electrolyte gradients, but convincing evidence for inhibition of Na active transport was not obtained. Whether inhibition of Na extrusion without inhibition of K uptake, as by ethacrynic acid, could be considered convincing evidence of inhibition of active transport was discussed.

scholarly journals Cat Heart Muscle In Vitro

1964 ◽  
Vol 47 (3) ◽  
pp. 531-543 ◽  
Author(s):  
Ernest Page ◽  
R. J. Goerke ◽  
S. R. Storm
Keyword(s):  
Active Transport ◽  
Sucrose Solution ◽  
Ion Movements ◽  
K Concentration ◽  
Ouabain Inhibition ◽  
External Face ◽  
Cat Heart ◽  
Water Contents ◽  
Physiological Value

Cellular concentrations, [K]i, [Na]i, and [Cl]i, and cell water contents were measured in vitro at 27°C in cat papillary muscles. Measurements were made with and without ouabain at varying concentrations of K and ouabain, at pH 5.2 and 9.0, in absence of O2, and in NaCl-free solution. Large losses of cell K and increases of cell Na occurred in presence of ouabain, at 2–3°C, and in K-free medium. The dependence of inhibition of cation transport by ouabain on external K concentration, studied at constant initial [K]i, was consistent with a competition between K and ouabain localized to the external face of the membrane. In NaCl-free sucrose solution [K]i remained at its physiological value and was not affected by exposure to ouabain or low temperature, except when Ca was also omitted. Ouabain inhibition persisted at pH 9.0 and in Ca-poor media. Cells swelled and lost K at pH 5.2, and residual ouabain effect was small. At pH 9.0, or in absence of O2, or in Ca-poor solutions cells became permeable to mannitol. The ion movements observed after inhibition of active transport are compatible either with a passive K distribution and a primary inhibition of Na extrusion or with inhibition of a coupled active transport of both K and Na.

II. Ion distribution and the role of calcium in cellular function - Ion distribution and ion movements in smooth muscle

1973 ◽  
Vol 265 (867) ◽  
pp. 35-46 ◽  
Keyword(s):  
Steady State ◽  
Smooth Muscles ◽  
Temperature Sensitive ◽  
Ion Distribution ◽  
Sodium Permeability ◽  
Ionic Distribution ◽  
High K ◽  
Ion Movements ◽  
Calcium Exchange

The steady-state fluxes of K + , Cl - and Na + from smooth muscles in normal Krebs solution are described, and some of the problems encountered in the interpretation of such results are discussed. Sodium fluxes are particularly difficult to analyse, and the type of model used to estimate sodium permeability from flux curves, determines the value calculated to a large extent. In order to simplify the ionic distribution in the tissue, in the hope of obtaining more information about the handling of Na and K by the guinea-pig taenia coli, potassium-free (high Na) tissues and sodium-free (high K) tissues were prepared by soaking for 4 h in the relevant solution. The tissues reach a steady state, and the effluxes of 42 K from high K tissues and 24 Na from high Na tissues were measured and compared. In these two conditions the electrochemical gradients for Na + and for K + are probably identical. Nevertheless, the fluxes are markedly different. At 37 °C the Na flux is much faster than the K flux, and a part of the Na exchange is very temperature sensitive. There is also some evidence for a sodium calcium exchange mechanism. It is hoped that further experiments will produce results that will help to understand the processes involved in these exchanges.

Dysfunction of calcium handling by smooth muscle in hypertension

1985 ◽  
Vol 63 (4) ◽  
pp. 366-374 ◽  
Author(s):  
C. Y. Kwan
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Cardiovascular System ◽  
Control Systems ◽  
Active Transport ◽  
Smooth Muscles ◽  
Peripheral Resistance ◽  
Calcium Handling ◽  
Experimental Hypertension

Dysfunction of ion handling, including binding and fluxes (passive and active transport) of physiologically important ions such as potassium, sodium, calcium, and magnesium, by vascular smooth muscle cell membranes has repeatedly been reported to be associated with the pathophysiology of hypertension. The specific purpose of this review is to summarize and evaluate the evidence for alterations of calcium ion (Ca2+) handling by vascular smooth muscle in various forms of hypertension in the animal model on the basis that regulation of cytoplasmic Ca2+ concentration is a complex and yet vitally important process for a normal function of vascular smooth muscle and that derangement of such a regulation may result in excessive retention of cytoplasmic Ca2+, contribute toward increase of total peripheral resistance, and ultimately lead to elevation of blood pressure. Emphasis is placed upon the consideration of the usefulness of the subcellular membrane fractionation technique in studies of binding and transport of Ca2+ by vascular and nonvascular smooth muscle membranes from genetic as well as experimental hypertensive rats. The limitations of the interpretation of data using such an approach are also considered. Decreased active transport of Ca2+ across isolated plasma membrane vesicles from large and small arteries occurs in several but not all forms of hypertension. This membrane abnormality also occurs in nonvascular smooth muscles and other tissues or cells not confined to the cardiovascular system in genetic hypertension, but not in experimental hypertension. A hypothesis of general membrane defects in spontaneous hypertension is proposed. Since the long-term regulation of blood pressure at the sites of resistant blood vessels is under finely integrated and interacting control systems, namely, the myogenic, neurogenic, and humoral controls, involving many tissues or cells not necessarily confined to cardiovascular system, membrane abnormalities in Ca2+ handling by tissues in each or a combination of these control systems can conceivably lead to hypertension.

scholarly journals K Fluxes in Frog Skin

1965 ◽  
Vol 48 (6) ◽  
pp. 1011-1033 ◽  
Author(s):  
Peter F. Curran ◽  
Marcelino Cereijido
Keyword(s):  
Epithelial Cells ◽  
Connective Tissue ◽  
Active Transport ◽  
Time Constant ◽  
Frog Skin ◽  
Bathing Solution ◽  
Na Transport ◽  
K Uptake ◽  
Low Concentrations ◽  
K Concentration

A method has been developed for measuring K influx into the epithelial cells of frog skin from the inside solution. Diffusion delay in the connective tissue has been taken into account. Ninety-four per cent of skin K was found to exchange with K42 in the inside solution with a single time constant. K influx showed saturation with increasing K concentration, was not altered by imposing a potential difference of ±200 mv across the skin, and was inhibited by dinitrophenol, fluoroacetate, and ouabain. Relatively low concentrations of dinitrophenol (5 x 10-5 M) and fluoroacetate (10-10 M) had no effect on k influx but caused a 40 per cent decrease in net Na flux. There was no correlation between the rate of K uptake at the "inner barrier" and the rate of net Na transport. Reduction of net Na transport by lowering Na concentration in the outside solution caused little change in K uptake. These observations indicate that there is not a significant Na-K exchange involved in active transport of Na across the skin. K influx was found, however, to require Na in the inside bathing solution.

Active transport, ion movements, and pH changes

1988 ◽  
Vol 19 (3) ◽  
pp. 225-236
Author(s):  
Norman E. Good
Keyword(s):  
Active Transport ◽  
Ph Changes ◽  
Ion Movements

scholarly journals PERMEATION AND DIFFUSION OF K IONS IN FROG MUSCLE

1957 ◽  
Vol 41 (1) ◽  
pp. 169-195 ◽  
Author(s):  
E. J. Harris
Keyword(s):  
Diffusion Constant ◽  
Membrane Resistance ◽  
Frog Muscle ◽  
K Uptake ◽  
Rich Region ◽  
Ion Movements ◽  
K Concentration ◽  
And Diffusion ◽  
Tracer Experiments ◽  
External K

The movements of tracer K and net changes of K have been measured in frog muscle. The quantities moving can be linearly related to the square root of the time after a delay of 4 to 30 minutes depending on the external K concentration. The slope of the uptake-t½ line is increased when the external K concentration is raised. The Q10 of the uptake is about 1.9 per unit t½. K uptake from 1 to 2 mM concentration is diminished by a factor of about 2 if strophanthin is applied. The output per unit t½ is increased by a factor of about 1.4 by strophanthin. Tetrabutylammonium substituted for 10 per cent of the Na in the medium causes a reversible slowing of K uptake and Na output. The rates of movement found in the tracer experiments can be used to calculate the net losses of K taking place in K-free or strophanthin-containing media. The results are interpreted on the basis of K movement being limited both by a resistive outer layer and by diffusion within a K-rich region. The internal diffusion constant is 10–11 to 10–10 cm.2 sec.–1 depending on the K concentration. The rate of movement of the K can be related to the electrochemical activity of the ion, the lability of the sites on which it is absorbed, and cation + anion pair diffusion within the cell. The surface resistance to K ions can be accounted for as the sum of a membrane resistance equal to that found by electrical methods and the resistance offered to the movement of K by an annulus sufficiently thick (ca. 3 µ) to accommodate the cell Na at a density equal to the mean density of cation within the cell through which K diffuses with the same diffusion constant as holds in the K-rich region. Na movement, if assumed to take place by diffusion from the annulus with diffusion constant equal to that for K ions, has a rate which agrees well with observed values. The influence of strophanthin and tetrabutylammonium on the ion movements is interpreted as being the result of these agents causing an expansion of the outer non-selective region, normally occupied mainly by Na, at the expense of the inner K-rich region.

Active transport, ion movements, and pH changes

1988 ◽  
Vol 19 (3) ◽  
pp. 237-250
Author(s):  
Roger P. Hangarter ◽  
Norman E. Good
Keyword(s):  
Active Transport ◽  
Ph Changes ◽  
Ion Movements

The relationship of the scleractinian corals to the rugose corals

Paleobiology ◽  
1980 ◽  
Vol 6 (02) ◽  
pp. 146-160 ◽  
Author(s):  
William A. Oliver
Keyword(s):  
Critical Points ◽  
Scleractinian Corals ◽  
Convincing Evidence ◽  
Early Triassic ◽  
Rugose Corals ◽  
History Of ◽  
The Subject ◽  
Relationship Of ◽  
The Relationship ◽  
Biologic Factors

The Mesozoic-Cenozoic coral Order Scleractinia has been suggested to have originated or evolved (1) by direct descent from the Paleozoic Order Rugosa or (2) by the development of a skeleton in members of one of the anemone groups that probably have existed throughout Phanerozoic time. In spite of much work on the subject, advocates of the direct descent hypothesis have failed to find convincing evidence of this relationship. Critical points are:(1) Rugosan septal insertion is serial; Scleractinian insertion is cyclic; no intermediate stages have been demonstrated. Apparent intermediates are Scleractinia having bilateral cyclic insertion or teratological Rugosa.(2) There is convincing evidence that the skeletons of many Rugosa were calcitic and none are known to be or to have been aragonitic. In contrast, the skeletons of all living Scleractinia are aragonitic and there is evidence that fossil Scleractinia were aragonitic also. The mineralogic difference is almost certainly due to intrinsic biologic factors.(3) No early Triassic corals of either group are known. This fact is not compelling (by itself) but is important in connection with points 1 and 2, because, given direct descent, both changes took place during this only stage in the history of the two groups in which there are no known corals.

Sign in / Sign up

Export Citation Format

Share Document