Effects of adrenaline and serotonin on the pump potential of sympathetic ganglion cell membrane in bullfrogs.
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Animals↗
Biomedical subjects
T Akasu
Publications and source records attributed to T Akasu.
Adrenaline and the electrogenic sodium pump in Rana catesbeiana sympathetic ganglion cells.
The effect of adrenaline on the Na+-pump in bullfrog (Rana catesbeiana) sympathetic ganglion cells was studied by use of electrophysiological methods. The rate of removal of excess Na+ injected into a ganglion cell was increased by adrenaline. The K+-activated hyperpolarization of cell membrane, which might be produced by an electrogenic Na+-pump, was also increased by adrenaline. These results suggested that adrenaline was able to accelerate the Na+-pump, possibly the electrogenic Na+-pump.
Action Potentials↗
The effect of adrenaline on the K+ -activated hyperpolarization of the sympathetic ganglion cell membrane in bullfrogs.
Effects of adrenaline on K+ -activated hyperpolarization of bullfrog sympathetic ganglion cells, preganglionic nerve axons and splanchnic nerve axons were studied. The K+ -activated hyperpolarization recorded from ganglion-postgangaline (0.3 mM). On the other hand, the K+ -activated hyperpolarization of postganglionic, preganglionic nerve axons and splanchnic nerve axons was not affected under the same experimental conditions. The facil-tatory effect of adrenaline on the K+ -activated hyperpolization was gradually intensified when the application of adrenaline was sustained for up to 60 min. The effect was reversible. The K+ -activated hyperpolarization recorded from ganglion cell-bodies by intracellular microelectrodes was similarly augmented by adrenaline (0.1 mM). Adrenaline in this concentration, however, caused no significant changes of the membrane potential and conductance in the presence of ouabain (0.002 mM) which completely and reversibly inhibited K+-activated hyperpolarization. Noradrenaline showed similar but less effected and isoproterenol showed no significant effect on the K+ -activated hyperpolarization. The facilitatory effect of adrenaline was inhibited in the presence of phentolamine but not of DCI. These results suggested that the intraganglionic membrane of ganglion cells possessed some kind of adrenergic alpha-receptors and the electrogenic Na+ pump of ganglion cells was accelerated by some unknown mechanism when adrenaline reacted to these receptors.
Animals↗
Nerve-sparing surgery with lateral node dissection for advanced lower rectal cancer.
133 patients who underwent nerve-sparing surgery with lateral dissection for lower rectal cancer were analysed for survival and functional results, operative burdens, and modes of recurrence. In 84% of patients an acceptable urinary function was preserved. Operative time averaged 334 min, and blood loss averaged 935 ml. The 5-year survival rate was 67% in all patients, and 88% for Dukes' A, 74% for Dukes' B and 59% for Dukes' C. According to the number of positive nodes, the 5-year survival rate comprised 83% of patients with up to three nodes, and 34% of those with more than four nodes. Local recurrent rates were 2.7% in patients with Dukes' B and 13% with Dukes' C. At present, pelvic nerve-sparing procedures with lateral dissection is the most promising surgery, guaranteeing both adequate lymphadenectomy and preservation of urinary function.
Autonomic Pathways↗
Adenosine mediates a slow hyperpolarizing synaptic potential in autonomic neurones.
Considerable evidence has accumulated suggesting that purines, adenosine and ATP function as neurotransmitters in the central and peripheral nervous systems. Burnstock has proposed that purinergic receptors be classified into two types, P1 and P2, having adenosine and ATP, respectively, as agonist prototypes. Recent data suggest that ATP may mediate a synaptic potential in guinea pig vas deferens, but no such evidence exists for adenosine. The presence of a non-cholinergic, non-adrenergic nerve supply to the urinary bladder has been postulated and termed purinergic, as these nerves have been shown to release ATP. Furthermore, atropine-resistant contractions of bladder smooth muscle are thought to be mediated by ATP, while in situ experiments in vesical parasympathetic ganglia have suggested that a purinergic modulatory mechanism may control urinary bladder function. We now report the presence of a slow hyperpolarizing synaptic potential (slow-h.s.p.) in neurones of cat vesical parasympathetic ganglia, produced by stimulating the preganglionic nerves, and provide evidence that the slow-h.s.p. is mediated by adenosine.
Adenosine↗