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Biomedical subjects

T Clausen

Publications and source records attributed to T Clausen.

At least 181 records · Page 10Linked to original sources

Treatment of attacks in hyperkalaemic familial periodic paralysis by inhalation of salbutamol.

In fifteen patients with hyperkalaemic familial periodic paralysis, inhalation of salbutamol alleviated hyperkaleamia and paralysis precipitated by exercise or oral administration of potassium chloride. In-vitro studies with rat soleus muscles indicated that the hypokalaemic effect of salbutamol is related to stimulation of the active coupled transport of sodium and potassium in muscle cells. Follow-up studies proved that the inhalation of salbutamol is a simple and adequate method for the treatment of the paralytic episodes in these patients.

Adolescent↗

The relationship between the transport of glucose and cations across cell membranes in isolated tissues. IX. The role of cellular calcium in the activation of the glucose transport system in rat soleus muscle.

1. The role of cellular Ca2+ in the transport of glucose has been investigated by determining the time-course of tension development and the release of 45Ca and 3-0-[14C]methylglucose from preloaded rat soleus muscles. 2. Electrical stimulation, 2,4-dinitrophenol (0.05 mM) and hyperosmolarity (200 mM mannitol) were all found to induce a rapid rise in tension and the rate coefficient of 45Ca release, which coincided with an acceleration of 3-0-[14C]methylglucose efflux. 3. Caffeine (10 mM) or exposure to K+ -substituted buffer induced a rapid increase in tension and the release of 45Ca, but a much later stimulation of 3-0-methylglucose efflux. This delayed response may be related to the fact that both factors induce a pronounced suppression of the effect of various agents known to stimulate sugar transport.4. Following a washout period of 120 min at 0 degreesC, the return to 30 degrees C elicited a prompt transient rise in the rate coefficient for the release of 45Ca and 3-0-[14C]meth ylglucose to levels, respectively, 2.8 and 14.6 times the control levels measured at 30 degrees C. The magnitude of these peaks appeared to be a function of the duration of the exposure to 0 degrees C. Cooling also led to a stimulation of the uptake of 3-0-[14C]methylglucose, and phlorizin suppressed the rise. 5. It was not possible to detect any significant effect of insulin on basal tension or on the influx or efflux of 45Ca. However, in a hyperosmolar environment, insulin (10-100 munits/ml) induced a marked further rise in tension, indicating that the hormone can elicit a redistribution of cellular Ca2+. 6. It is concluded that a rise in the cytoplasmic concentration of free Ca2+ constitutes a part of the mechanism by which the glucose transport system is activated by a variety of stimuli, perhaps also insulin.

Animals↗

Relationships between the exchange of calcium and phosphate in isolated fat-cells.

The uptake and the washout of 45Ca2+ and 32Pi is described in free fat-cells and whole epididymal fat-pads from fed rats. 2. In isolated fat-cells, the uptake of 45Ca2+ proceeds with an initial rapid phase of about 1 min duration, followed by a slower subsequent accumulation. In contrast with the rapid phase, the slow phase is inhibited by 2,4-dinitrophenol, warfarin, oligomycin and verapamil, shows saturation, and presumably represents transport across the plasma membrane. 3. The washout of 45Ca2+ from preloaded cells consists of a rapid (1 min) initial phase and a slow phase which is non-monoexponential, suggesting that the radioactive isotope is released from several cellular pools. 4. When Pi is omitted from the incubation medium, the slow phase of 45Ca uptake is almost abolished, and the washout of 45Ca from preloaded fat-cells is markedly accelerated. At elevated extracellular concentrations of Pi (2,4-6.2mM), the uptake of 45Ca is stimulated by 2-10-fold, and the release of the radioactive isotope from preloaded cells is inhibited. In whole epididymal fat-pads, variations in the extracellular concentration of Pi have no detectable effect on the uptake or the washout of 45Ca. 5. In isolated fat-cells, the accumulation of 32Pi is inhibited by 2,4-dinitrophenol or the omission of glucose from the incubation medium. In a Ca2+-depleted buffer, the uptake of 32Pi is diminished, and hyperosmolarity, which stimulates 45Ca uptake, also accelerates the accumulation of 32Pi. 6. It is concluded that in free fat-cells, the uptake and release of Ca2+ and Pi take place by closely interrelated processes, which are dependent on mitochondrial energy production.

Adipose Tissue↗

The relationship between calcium exchange and enzyme secretion in the isolated rat pancreas.

1. The role of extracellular and intracellular Ca(2+) in pancreatic enzyme secretion has been assessed by correlating the exchange of (45)Ca with amylase secretion in the isolated uncinate pancreas of baby rats.2. The rate coefficient of (45)Ca efflux from pre-loaded glands declined continually (indicating that (45)Ca is retained in several different pools) and probably reflects changes in the concentration of cytoplasmic free (45)Ca, which is determined by the rate at which (45)Ca is released from intracellular organelles into the cytoplasm.3. The rate coefficient of (45)Ca release was not influenced by extracellular Ca(2+) or Mg(2+) concentrations.4. Cholecystokinin-pancreozymin (CCK-PZ) and acetylcholine accelerated the release of both (45)Ca and amylase in a dose-dependent fashion, even when extracellular Ca(2+) was reduced to 0.1 mM, but did not affect the initial rate of (45)Ca uptake by the tissue.5. In Ca(2+)-free media (containing 0.5 mM-EGTA) basal amylase secretion slowly declined and stimulated secretion was virtually abolished, but the accelerated release of (45)Ca was maintained.6. These observations indicate that natural stimuli of pancreatic enzyme secretion alter (45)Ca distribution in the cell by a process which is independent of extracellular Ca(2+) and which is associated with amylase secretion provided that the plasma membrane has not been depleted of Ca(2+).7. Secretin, glucagon and insulin did not influence (45)Ca release. Secretin slightly increased amylase secretion, but this may have been a washout effect.8. Replacement of extracellular Na(+) by Li(+) increased the release of (45)Ca and amylase, but only in the presence of extracellular Ca(2+). Li(+)-substitution also increased (45)Ca uptake. Thus, under special conditions, secretion may be stimulated when increased amounts of Ca(2+) are made available from extracellular sources.9. Hyperosmolarity (known to increase (45)Ca release in muscle) also accelerated (45)Ca release and amylase secretion.10. 2,4-Dinitrophenol markedly accelerated (45)Ca efflux but did not stimulate amylase secretion, indicating that a rise in cytoplasmic Ca(2+) will not initiate secretion if energy metabolism is impaired.11. CCK-PZ slightly increased the rate coefficient of (42)K release, indicating a changed membrane permeability.12. The stimulatory effects of CCK-PZ and acetylcholine were suppressed during Na(+)-substitution by Li(+), suggesting that the Na(+) concentration gradient across the membrane is important in secretion.13. It is concluded that the primary action of CCK-PZ and acetylcholine may be to increase the influx of Na(+) into the cell by changing membrane permeability. This in turn is responsible for the release of Ca(2+) from intracellular stores (probably endoplasmic reticulum), leading to a rise in Ca(2+) concentration close to the structures involved in enzyme secretion. Secretion then follows provided that ATP is available and the plasma membrane is not depleted of Ca(2+).

Acetylcholine↗