Axonal Adaptations to Osmotic and Ionic Stress in an Invertebrate Osmoconformer (Mercierella Enigmatica Fauvel): III. Adaptations to Hyposmotic Dilution

1978 ◽  
Vol 76 (1) ◽  
pp. 221-235
Author(s):  
J. A. BENSON ◽  
J. E. TREHERNE
Keyword(s):  
Axonal Swelling ◽  
Osmotic Concentration ◽  
Bathing Medium ◽  
Axon Membrane ◽  
Ionic Stress ◽  
Sodium Inactivation ◽  
Sodium Extrusion ◽  
Potassium Gradient ◽  
Sodium And Potassium

The giant axons of this extreme osmoconformer were adapted, in vitro, to progressive hyposmotic dilution of the bathing medium (from 1024 m-Osmol to concentrations as low as 76.8 m-Osmol). Hyposmotic adaptation is associated with reductions in the intracellular concentrations of both sodium and potassium ions. These reductions do not appear to result from appreciable axonal swelling. The different electrical responses to isosmotic and hyposmotic dilution suggest that reduction in [Na+]1 results from ouabain-dependent sodium extrusion, in response to ionic dilution, and that reduction in [K+]1 is induced by a combination of ionic and osmotic dilution. The reduced level of intracellular potassium achieved during hyposmotic adaptation represents a balance between the necessity to contribute to osmotic equilibration and to maintain a potassium gradient across the axon membrane sufficient to produce appreciable axonal hyperpolarization during dilution of the bathing medium. This hyperpolarization tends to maintain the amplitude of the action potential, by compensating for reduction in overshoot (with decline in ENa), and by reducing sodium inactivation. This, together with the reduction in [Na+]1, enables overshooting action potentials of relatively large amplitude and rapid rise time to be maintained during more than tenfold dilution of the ionic and osmotic concentration of the bathing medium.

Long-term Adaptations of Sabella Giant Axons to Hyposmotic Stress

1978 ◽  
Vol 75 (1) ◽  
pp. 253-263
Author(s):  
J. E. TREHERNE ◽  
Y. PICHON
Keyword(s):  
Sea Water ◽  
Potassium Concentration ◽  
Resting Potential ◽  
Sodium Permeability ◽  
Bathing Medium ◽  
Appreciable Change ◽  
Axon Membrane ◽  
Giant Axons

Reprint requests should be addressed to Dr Treherne. Sabella is a euryhaline osmoconformer which is killed by direct transfer to 50% sea water, but can adapt to this salinity with progressive dilution of the sea water. The giant axons were adapted to progressive dilution of the bathing medium (both in vivo and in vitro) and were able to function at hyposmotic dilutions (down to 50%) sufficient to induce conduction block in unadapted axons. Hyposmotic adaptation of the giant axon involves a decrease in intracellular potassium concentration which tends to maintain a relatively constant resting potential during adaptation despite the reduction in external potassium concentration. There is no appreciable change in the intracellular sodium concentration, but the relative sodium permeability of the active membrane increases during hyposmotic adaptation. This increase partially compensates for the reduction in sodium gradient across the axon membrane, during dilution of the bathing media, by increasing the overshoot of the action potentials recorded in hyposmotically adapted axons.

Na+ transport properties of the peritubular membrane of cortical collecting tubule

1982 ◽  
Vol 242 (6) ◽  
pp. F664-F671 ◽  
Author(s):  
E. Natke ◽  
L. C. Stoner
Keyword(s):  
Efflux Rate ◽  
Bathing Medium ◽  
Sodium Efflux ◽  
Collecting Tubule ◽  
Potassium Influx ◽  
Collecting Tubules ◽  
Low K ◽  
Sodium And Potassium ◽  
Cortical Collecting Tubule

The effects of varying endogenous aldosterone levels on the passive and active properties of the peritubular membrane were studied. Rabbits that were fed either a low Na+ (normal K+) diet or a high Na+, low K+ diet increased or decreased plasma aldosterone, respectively. Tubules were dissected, filled with oil, and incubated in 0 K+ medium to increase intracellular sodium. Cellular sodium and potassium content was measured by helium-glow photometry. The degree to which cells accumulate sodium and lose potassium is a function not only of time of exposure but also of diet. Tubules from animals on a low Na+ diet are about 6 times more permeable to sodium than those from animals fed a high Na+ diet. When tubules were loaded with sodium and returned to a normal (5 mM K+) bathing medium, net sodium efflux and potassium influx occurred. The rate of sodium efflux by cortical collecting tubules dissected from animals on the low Na+ diet was 2.3 times greater than the efflux rate of tubules from animals on the high Na+ diet. These data suggest that high levels of endogenous aldosterone enhance sodium transport measured in vitro across the peritubular membrane of cortical collecting tubule.

Axonal Adaptations to Osmotic and Ionic Stress in an Invertebrate Osmoconformer (Mercierella Enigmatica Fauvel): II. Effects of Ionic Dilution on the Resting and Action Potentials

1978 ◽  
Vol 76 (1) ◽  
pp. 205-219
Author(s):  
J. A. BENSON ◽  
J. E. TREHERNE
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Prolonged Exposure ◽  
Giant Axon ◽  
Sodium Concentration ◽  
Ionic Concentration ◽  
Osmotic Concentration ◽  
Bathing Medium ◽  
Axon Membrane ◽  
Wide Range

The giant axon of this extreme euryhaline osmoconformer possess an unusual ability to produce action potentials of large amplitude over a wide range of ionic dilution when constant osmotic concentration is maintained by the addition of mannitol to the bathing medium. Ionic dilution under these circumstances causes a decline in the overshoot of the action potential (resulting largely from reduction in [Na+]0) and an appreciable axonal hyperpolarization (primarily as a result of decrease in [K+]0). This hyperpolarization tends to compensate for the reduction in the extent of the overshoot and so maintains the amplitude of the sodium-mediated action potentials during isosmotic dilution of the bathing medium. The axonal hyperpolarization also appears to reduce sodium inactivation so as to maintain a rapid rate of rise of the action potential despite drastic reduction in the ionic concentration of the bathing medium. Prolonged exposure to reduced ionic concentrations appears to induce a ouabain sensitive reduction in intracellular sodium concentration which increases the sodium gradient across the axon membrane during isosmotic dilution of the external medium.

Effects of Osmotic Stress on the Electrical Activities of the Giant Axon of a Marine Osmoconformer, Sabella Penicillus

1978 ◽  
Vol 75 (1) ◽  
pp. 237-251
Author(s):  
A. D. CARLSON ◽  
Y. PICHON ◽  
J. E. TREHERNE
Keyword(s):  
Giant Axon ◽  
Ionic Concentration ◽  
Rapid Decline ◽  
Osmotic Concentration ◽  
Bathing Medium ◽  
Axonal Membrane ◽  
Abrupt Changes ◽  
Slow Potassium ◽  
Electrical Activities

Reprint requests should be addressed to Dr Treherne. The giant axons of the polychaete, Sabella penicillus, can withstand, in vitro, abrupt changes in osmotic and ionic concentration of the bathing medium in the range measured in the blood of this osmoconformer (543–1236 m-osmol) at different external salinities. Isosmotic dilution of the external ions (i.e. when osmotic concentration was maintained by sucrose) induced a modest hyperpolarization of the axonal membrane and a rapid decline in the overshoot of the action potential. In contrast, abrupt hyposmotic dilution resulted in a relatively slow and complex decline in overshoot in the absence of axonal hyperpolarization. A slow potassium depolarization and rate of decrease in overshoot in sodium-free conditions suggests that there is a reduced intercellular access to the axon surfaces following exposure to hyposmotic media. It is suggested that this restricted access could provide short-term protection from fluctuations in blood osmotic concentration.

Fluid secretion in the nephron: Relation to renal failure

1976 ◽  
Vol 56 (1) ◽  
pp. 248-258 ◽  
Author(s):  
J. J. Grantham
Keyword(s):  
Fluid Transport ◽  
Fluid Secretion ◽  
Cystic Kidney Disease ◽  
Rabbit Kidney ◽  
Cystic Kidney ◽  
Obstructive Nephropathy ◽  
Bathing Medium ◽  
Pars Recta ◽  
Uremic Syndrome

It had been generally accepted that glomerular filtration and tubular reabsorption were the basic modes of fluid transport in mammalian nephrons. Recently, evidence was obtained to indicate that net fluid secretion may occur in mammalian nephrons as well. In the pars recta portion of proximal tubules of rabbit kidney net fluid secretion was observed in vitro in response to PAH and other aryl acids in the peritubular bathing medium. Net fluid secretion appeared to be coupled to the transcellular transport of aryl acid from bath to lumen. Serum from uremic subjects stimulated net fluid secretion in the pars recta in a manner similar to PAH. The accumulation of high levels of endogenous aryl acids may contribute to the general organ dysfunction that is a part of the uremic syndrome of advanced renal insufficiency. Futhermore, there is evidence to suggest that the fluid-secretion phenomenon in association with aryl acids may significantly affect renal excretion and morphology in slow-flow states, in patients with cystic kidney disease, and in obstructive nephropathy.

Phorbol ester inhibition of Na-H exchange in rabbit proximal colon

1985 ◽  
Vol 249 (5) ◽  
pp. C527-C530 ◽  
Author(s):  
J. Ahn ◽  
E. B. Chang ◽  
M. Field
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Intracellular Ph ◽  
Phorbol Ester ◽  
Proximal Colon ◽  
Bathing Medium ◽  
Two Agents ◽  
Luminal Membrane ◽  
Kinase C

In rabbit proximal colon, in vitro addition of phorbol 12,13-dibutyrate (PDB, 10(-7) M) to the serosal bathing medium inhibits mucosal (m)-to-serosal (s) unidirectional Na flux (JsmNa) without altering JsmNa or unidirectional Cl fluxes. Similar results were obtained when amiloride (2 X 10(-4) M) was added to the mucosal bathing medium. No additivity of effect was seen when tissues were exposed to both agents. Measurements with carboxyfluorescein reveal that the two agents cause equal decreases of intracellular pH (pHi), an effect that is dependent on the presence of extracellular Na (Na replacement also decreases pHi). No additivity of pHi effects is seen when both agents are added together. To determine the membrane site of this PDB-inhibitable Na-H exchange, Na influx across the luminal border of proximal colon was measured and was found to be inhibited equally by PDB and amiloride. We conclude that PDB, by activation of protein kinase C, inhibits electro-neutral amiloride-sensitive Na-H exchange in the luminal membrane of proximal colon.

Association between HCO3(-) absorption and K+ uptake by Amphiuma jejunum: relations among HCO3(-) absorption, luminal K+, and intracellular K+ activity

1984 ◽  
Vol 246 (6) ◽  
pp. G732-G744
Author(s):  
M. A. Imon ◽  
J. F. White
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Uptake Mechanism ◽  
Bathing Medium ◽  
The Media ◽  
Absorptive Flux ◽  
Free Media ◽  
Intracellular K Activity ◽  
K Activity

Titration techniques and K+- sensitive microelectrodes have been used to investigate the relations among HCO3(-) absorption, luminal K+, and intracellular K+ activity in in vitro Amphiuma jejunum. The HCO3(-) absorptive flux (JHCO3(-] measured by pH-stat under short circuit was reduced by removal of K+ from the medium but not by replacement of Na+ with choline. JHCO3(-) exhibited a seasonal variation when K+ was absent from the media and was increased to a maximum when K+ equaled 5 mM. Addition of K+ to a K+-free luminal medium stimulated JHCO3(-) much more than addition to the serosal medium. Acetazolamide (10(-4) M) blocked K+-stimulated HCO3(-) absorption while benzolamide reduced the short-circuit current associated with HCO3(-) absorption much more rapidly when added to the mucosal bathing medium. Intracellular K+ activity (aik) and mucosal membrane potential (psi m) of jejunal villus cells were measured with double-barreled microelectrodes. When bathed bilaterally with HCO3(-)-containing media, K+ was actively accumulated for many hours (aik = 58.5 mM) but in the presence of ouabain fell to equilibrium (16 mM) after 2 h. In contrast, when HCO3(-) absorption was induced by removal of serosal HCO3(-), aik was elevated to 83.6 mM and, after 4-h exposure to ouabain cell K+, remained far above electrochemical equilibrium at 33 mM. Tissues bathed in Na+-free (Tris) media containing ouabain retained cell K+ after 4 h at even higher levels (46 mM). Cell K+ activity was reduced by removal of K+ from either the mucosal or serosal medium. Acetazolamide reduced aik over 2 h in Na+-free media from 66 to 42 mM. The decline in aik was associated with a concomitant decline in the HCO3(-) absorptive current. It is concluded that K+ is actively accumulated across both luminal and serosal membranes of the jejunal absorptive cell and that the luminal uptake mechanism is linked to HCO3(-) absorption or an equivalent process.

THE WATER AND ELECTROLYTE METABOLISM OF RAT DIAPHRAGM IN VITRO

1956 ◽  
Vol 34 (1) ◽  
pp. 1069-1083 ◽  
Author(s):  
R. H. Rixon ◽  
J. A. F. Stevenson
Keyword(s):  
Intracellular Water ◽  
Diaphragm Muscle ◽  
Optimal Conditions ◽  
Rat Diaphragm ◽  
Concentration Gradients ◽  
Hypoxic Conditions ◽  
Diaphragm In Vitro ◽  
Sodium And Potassium

The distribution of water and of sodium and potassium between the cell and synthetic environments has been studied in rat diaphragm muscle. It has been found that: (1) the amount of intracellular water is markedly increased at 0 °C. in oxygen and at 37 °C. in nitrogen compared to that of tissue at 37 °C. in oxygen, in media up to 0.75 osmolar; (2) optimal conditions of temperature and oxygen are necessary to prevent or reduce the uptake of water; (3) swelling at reduced temperatures and under hypoxic conditions is related to the oxygen uptake; (4) the loss of tissue solids during incubation does not have any significant effect on the calculation of the total tissue and intracellular water; (5) the concentration of total sodium and potassium in the tissue, in vivo and in vitro at optimal conditions is slightly in excess of that in the plasma water or incubating medium—this is believed not to represent an active hypertonicity; (6) concomitant with the uptake of water there are marked redistributions of sodium and potassium, the gain of sodium being greater than the loss of potassium. It is concluded that the swelling of tissue cells under conditions that inhibit oxidative metabolism is primarily due to the redistribution of electrolytes and that the natural distribution of water in muscle is determined by active maintenance of the concentration gradients of sodium and potassium across the cell membrane.

scholarly journals Membrane Dysfunction Induced by In Vitro Ischemia in Rat Hippocampal CA1 Pyramidal Neurons

1999 ◽  
Vol 81 (4) ◽  
pp. 1872-1880 ◽  
Author(s):  
E. Tanaka ◽  
S. Yamamoto ◽  
H. Inokuchi ◽  
T. Isagai ◽  
H. Higashi
Keyword(s):  
Membrane Potential ◽  
Voltage Clamp ◽  
Pyramidal Neurons ◽  
Membrane Surface ◽  
Bathing Medium ◽  
Ca1 Pyramidal Neurons ◽  
In Vitro Ischemia ◽  
Hippocampal Ca1 ◽  
Electrode Voltage

Membrane dysfunction induced by in vitro ischemia in rat hippocampal CA1 pyramidal neurons. Intracellular and single-electrode voltage-clamp recordings were made to investigate the process of membrane dysfunction induced by superfusion with oxygen and glucose-deprived (ischemia-simulating) medium in hippocampal CA1 pyramidal neurons of rat tissue slices. To assess correlation between potential change and membrane dysfunction, the recorded neurons were stained intracellularly with biocytin. A rapid depolarization was produced ∼6 min after starting superfusion with ischemia-simulating medium. When oxygen and glucose were reintroduced to the bathing medium immediately after generating the rapid depolarization, the membrane did not repolarize but depolarized further, the potential reaching 0 mV ∼5 min after the reintroduction. In single-electrode voltage-clamp recording, a corresponding rapid inward current was observed when the membrane potential was held at −70 mV. After the reintroduction of oxygen and glucose, the current induced by ischemia-simulating medium partially returned to preexposure levels. These results suggest that the membrane depolarization is involved with the membrane dysfunction. The morphological aspects of biocytin-stained neurons during ischemic exposure were not significantly different from control neurons before the rapid depolarization. On the other hand, small blebs were observed on the surface of the neuron within 0.5 min of generating the rapid depolarization, and blebs increased in size after 1 min. After 3 min, neurons became larger and swollen. The long and transverse axes and area of the cross-sectional cell body were increased significantly 1 and 3 min after the rapid depolarization. When Ca2+-free (0 mM) with Co2+ (2.5 mM)-containing medium including oxygen and glucose was applied within 1 min after the rapid depolarization, the membrane potential was restored completely to the preexposure level in the majority of neurons. In these neurons, the long axis was lengthened without any blebs being apparent on the membrane surface. These results suggest that the membrane dysfunction induced by in vitro ischemia may be due to a Ca2+-dependent process that commences ∼1.5 min after and is completed 3 min after the onset of the rapid depolarization. Because small blebs occurred immediately after the rapid depolarization and large blebs appeared 1.5–3 min after, it is likely that the transformation from small to large blebs may result in the observed irreversible membrane dysfunction.

Actions of adrenergic agonists on isolated excretory ducts of submandibular glands

1978 ◽  
Vol 235 (6) ◽  
pp. F548-F556 ◽  
Author(s):  
A. R. Denniss ◽  
L. H. Schneyer ◽  
C. Sucanthapree ◽  
J. A. Young
Keyword(s):  
Sympathetic Nerve Activity ◽  
Physiological Changes ◽  
Adrenergic Agonists ◽  
Nerve Activity ◽  
Bathing Medium ◽  
Submandibular Glands ◽  
Low Concentrations ◽  
K Secretion ◽  
Prior Administration

The effects of norepinephrine and isoproterenol on the transepithelial potential difference (PD) and the net transepithelial fluxes of Na, K, Cl, and HCO3 of the main ducts of the submandibular glands of rats and rabbits have been studied by microperfusion of ducts incubated in vitro in an artifical bathing medium. In the rabbit duct, both catecholamines caused depolarization and reduced transepithelial Na reabsorption at concentrations above 10(-29) M. In the rat duct, norepinephrine reduced PD and net Na reabsorption and, in addition, inhibited net K secretion at concentrations of 10(-7) M and above. Isoproterenol also depolarized the duct and reduced net K reabsorption, but at concentrations of 10(-9) M it stimulated net Na reabsorption, whereas at concentrations of 10(-4) M it inhibited Na reabsorption. The stimulation caused by isoproterenol at low concentrations could be blocked by prior administration of propranolol. The results suggest that electrolyte transport, by both rat and rabbit ducts, may be influenced not only by sympathetic nerve activity but also by physiological changes in the concentrations of circulating catecholamines. Inconsistencies in the literature regarding the sensitivity of the rabbit duct to catecholamines and the response of the rat duct to isoproterenol have now been resolved.

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