Single freshly isolated smooth muscle cells of adult bovine trachea were voltage clamped, and the calcium inward current was separated from K+ currents by blocking the large outward currents with intra- and extracellular Cs+ and extracellular tetraethylammonium chloride. Isoproterenol stimulated peak calcium current (ICa) in a dose-dependent manner through the beta-adrenergic receptor. The isoproterenol effect was not mediated or caused by the stimulation of a K+ or Na+ current, a decrease in the intracellular concentrations of Ca2+ or H+, the stimulation of the Na(+)-H+ or the Na(+)-Ca2+ exchanger. Neither basal nor isoproterenol-stimulated ICa was affected by internal dialysis of the cell with adenosine 3',5'-cyclic monophosphate (cAMP), cAMP analogues, or the catalytic subunit of cAMP-kinase. Internal dialysis of the cells with guanosine 5'-O-(2-thiodiphosphate) (GDP beta S) blocked the stimulation of isoproterenol whereas dialysis with guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S) induced an isoproterenol-like maximal increase of ICa. These results show that the beta-adrenergic receptor stimulates the L-type calcium current of isolated tracheal smooth muscle cells independent of cAMP and cAMP-kinase through a GTP/GDP regulated protein.
In a family with synovial chondromatosis affecting at least three, presumably five members, the articular disorder was combined with dwarfism. The persons with joint disorders were below the third percentile in body height, but family members with normal articular function had normal height. We believe this to be the first description of a combination of synovial chondromatosis with genetically caused dwarfism.
The hormonal regulation of L-type calcium current was investigated in freshly isolated tracheal smooth muscle cells using the whole-cell configuration of the patch-clamp technique. Isoproterenol stimulated the L-type calcium current 2.6-fold through β-adrenoceptors. Dialysis of these cells with cyclic AMP, cyclic AMP analogues or the catalytic sub-unit of cyclic AMP kinase had no effect on basal or isoproterenol-stimulated calcium current. The calcium current was stimulated and inhibited by dialysis of the cells with GTPγS and GDPβS, respectively. Evidently, in some smooth muscle cells the β-adrenoceptor couples directly to L-type calcium channels via a G protein.
6 patients with AMPD-deficiency and 6 control subjects performed exercise on a bicycle ergometer until heart rate was 200 minus age. During exercise the increase of ammonia plasma concentrations was reduced in AMPD-deficient patients compared with that of control subjects. Plasma concentrations of lactate, pyruvate, inosine, hypoxanthine and xanthine increased during exercise in both groups. The concentrations of lactate, inosine and hypoxanthine were lower in AMPD-deficient patients during exercise, the difference was not significant. In AMPD-deficient patients the ATP-concentrations of red blood cells increased during exercise in contrast to control subjects, whereas the ADP amount did not change significantly. Our data suggest that in AMPD-deficient-patients AMP is mainly reduced to adenosine during exercise resulting in decreased ammonia concentrations. The increased concentrations of ATP in red blood cells may be the consequence of increased phosphorylation.
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