scholarly journals Aconitine-induced delayed afterdepolarization in frog atrium and guinea pig papillary muscles in the presence of low concentrations of Ca2+.

1987 ◽  
Vol 37 (1) ◽  
pp. 59-79 ◽  
Author(s):  
Tohru SAWANOBORI ◽  
Yuji HIRANO ◽  
Masayasu HIRAOKA
1988 ◽  
Vol 11 (5) ◽  
pp. 619-625 ◽  
Author(s):  
Noriaki Kondo ◽  
Shoji Shibata ◽  
Thomas E. Tenner ◽  
Peter K. Pang

1965 ◽  
Vol 48 (5) ◽  
pp. 797-823 ◽  
Author(s):  
L. Barr ◽  
M. M. Dewey ◽  
W. Berger

The hypothesis that the nexus is a specialized structure allowing current flow between cell interiors is corroborated by concomitant structural changes of the nexus and changes of electrical coupling between cells due to soaking in solutions of abnormal tonicity. Fusiform frog atrial fibers are interconnected by nexuses. The nexuses, desmosomes, and regions of myofibrillar attachment of this muscle are not associated in a manner similar to intercalated discs of guinea pig cardiac muscle. Indeed, nexuses occur wherever cell membranes are closely apposed. Action potentials of frog atrial bundles detected extracellularly across a sucrose gap change from monophasic to diphasic when the gap is shunted by a resistor. This indicates that action potentials are transmitted across the gap when sufficient excitatory current is allowed to flow across the gap. When the sucrose solution in the gap is made hypertonic, propagation past the gap is blocked and the resistance between the cells in the gap increases. Electron micrographs demonstrate that the nexuses of frog atrium and guinea pig ventricle are ruptured by hypertonic solutions.


1973 ◽  
Vol 44 (2) ◽  
pp. 163-179 ◽  
Author(s):  
Anne M. S. Grant ◽  
A. Neuberger

1. A specific and quantitative radioimmunoassay was developed for the measurement of low concentrations of human and rabbit Tamm—Horsfall glycoprotein in the presence of other proteins. Antibody-coated tubes were used as a solid phase in the assay and the optimum antibody concentration and duration of antibody coating were established. 2. Pure Tamm—Horsfall glycoprotein was labelled with 125I and, because of its apparent susceptibility to radiation damage, was labelled at weekly intervals. 3. Sodium dodecyl sulphate, an ionic detergent, was included in the assay at a final concentration of 0.0005% to disaggregate the glycoprotein. An overnight preincubation step in the presence of the detergent was necessary before the disaggregated glycoprotein solutions were allowed to react with the antibody. Pretreatment of the tracer with detergent was not necessary. 4. Two glycoprotein standards were prepared fresh for each assay from freeze-dried material. The average linear range of the assay was between approx. 150 ng/ml and 2.5 μg/ml. Albumin was only shown to interfere with the assay at concentrations greater than 100 μg/ml. 5. Urines were dialysed against water for 3 days before assay to remove inhibitory material. Urines were never frozen as this was found to affect the assay. 6. A recovery experiment showed that the pure freeze-dried standard behaved in an immunologically identical way to the urinary glycoprotein. 7. Human Tamm-Horsfall glycoprotein cross-reacted with guinea-pig anti-(rabbit Tamm—Horsfall) antiserum and rabbit Tamm—Horsfall glycoprotein cross-reacted with guinea-pig anti-(human Tamm—Horsfall) antiserum, but not with rabbit anti-(human Tamm—Horsfall) antiserum. This showed a partial immunological identity between Tamm-Horsfall glycoprotein from humans and rabbits which was only evident when the antiserum was raised in a third species. 8. The excretion rate of Tamm—Horsfall glycoprotein in normal humans was found to be 48.1 ± 9.6 (SD) mg/24 h for males and 50.5 ± 14.8 (SD) mg/24 h for females. The mean excretion rate of the glycoprotein in New Zealand White rabbits was 34.8 ± 7.9 mg/24 h.


1991 ◽  
Vol 260 (3) ◽  
pp. H785-H795
Author(s):  
C. Lynch

Contractions of guinea pig papillary muscles were studied at 37 degrees C under a variety of conditions and stimulation rates that markedly alter the pattern of tension development. When rested-state contractions (RSCs) were enhanced by treatments that increase intracellular adenosine 3',5'-cyclic monophosphate (0.1-1 microM isoproterenol, 1-10 microM forskolin), a markedly enhanced late peak tension developed after a 100-ms delay. Such late peak tension was selectively depressed by local anesthetics (200-400 microM procaine, 4-10 microM tetracaine, or 0.5-1 mM ethyl aminobenzoate). In contrast, 0.1-1 microM ryanodine had little effect on late peak tension, whereas 5 mM caffeine reduced the delay before tension development. Inotropic interventions such as increased external Ca2+ concentration or the Ca2+ channel agonist BAY K 8644 did not elicit such distinct late peaking RSCs. Rapid initial tension development observed under a variety of situations (short cycle lengths, stimulation rates of 0.25 Hz plus isoproterenol, decreased external Na+ concentration) was markedly depressed by 0.01-1 microM ryanodine and by caffeine, whereas local anesthetics had little effect. These results suggest two pharmacologically distinct types of sarcoplasmic reticulum Ca2+ release: 1) Ca2+ that accumulates during prior depolarizations is released immediately upon depolarization and decreased by ryanodine and caffeine; 2) extracellular Ca2+ that enters the myocyte is accumulated and released after an initial delay and is selectively depressed by low concentrations of local anesthetics.


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