[A serum factor blocking neuromuscular transmission in myasthenia gravis: electrophysiological study with intracellular microelectrodes (author's transl)].
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Cl- permeability in the reabsorptive sweat duct (RSD) epithelium from normal subjects was studied using electrophysiological techniques. The average basolateral membrane potential (Vb) of normal ducts was -36.8 +/- 0.8 mV and the average apical membrane potential (Va) was -27.2 +/- 0.8 mV (n = 45). Amiloride in the lumen of microperfused sweat ducts hyperpolarized Va by 34.3 +/- 3.1 mV and Vb by 25.7 +/- 3.1 mV (n = 12) with a small but significant increase in voltage divider ratio (Ra/Rb) from 4.2 +/- 0.8 to 5.0 +/- 0.8 (n = 8). Cl- substitution in the lumen depolarized Va by +37 +/- 4.2 (n = 11) accompanied by a significantly larger increase in Ra/Rb from 4.8 +/- 2.6 (n = 8) to 7.0 +/- 3.1 (n = 8). Bath Cl- substitution depolarized Vb by +24.3 +/- 2.7 mV (n = 15) while decreasing Ra/Rb from 3.2 +/- 0.7 to 1.9 +/- 0.4 (n = 7). These results indicated a significant Cl- permeability in both apical and basolateral membranes. Removing Cl- from the lumen significantly decoupled Va and Vb and restricted the amiloride-induced hyperpolarization to the apical membrane. This result may suggest that intracellular Cl- might be responsible for coupling Va and Vb and that hyperpolarization of Va and Vb by amiloride may result in changes in intracellular Cl-. Alternatively, Va and Vb could be coupled through a Cl- sensitive paracellular shunt. These results are consistent with Cl- permeability in both apical and basolateral membranes of duct cells. However, the question of whether paracellular Cl- permeability is important in Cl- uptake cannot be determined from the present data.
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The effects of bepridil on sinoatrial conduction were studied by perfusing 15 isolate rabbit right atrial preparations. In a preliminary series an increase in cycle length was observed with a dose-dependent effect with concentrations of between 5 X 10(-7) M and 1 X 10(-5) M. At the latter dose, sinoatrial block was observed. Bepridil was therefore used in a series of 10 preparations to induce sinoatrial block (SAB). After 10 minutes perfusion the cycle length increased significantly (14.3%, p less than 0.02). In 4 preparations SAB occurred 18.7 +/- 2.5 minutes after the onset of the perfusion. Sinoatrial block did not occur in 6 cases and in 4 cases an intrasinus shift of the dominant pacemaker was observed. The types of SAB observed were varied and their mechanisms were complex. Different types of SAB occurred in the same preparation. The different types of block recorded were: Blumberger type I SAB, anterograde 2/1 SAB, intrasinus 2/1 block, retrograde 2/1 and advanced block, complete atrio-sinusal dissociation.
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