Effects of Sodium Fluoride on Frog Heart Motility

Effects of sodium fluoride (NaF) on the bullfrog heart were investigated. NaF (10 mM) inhibited the autonomic heart contraction, reducing the heart rate. This inhibitory action was recovered by per fusion with 2-Ca^ Ringer\u27s solution. The twitch tension of auricular muscle was reduced by 2 mM NaF as well as 1 mM sodium oxalate and low-Ca^ Ringer, but the latter two were less effective than the former. However, NaF (5 mM) induced a rise in resting tension similar to that in the case of DNP application. ATP, adrenaline, and theophylline all reversed the inhibitory action of NaF, while both DNP and iodo acetic acid promoted it. NaF (5 mM) decreased the tension of Na^+-deficient contracture. The results obtained suggest that the reduction in the heart motility by NaF might be caused by the following mechanism : Inhibition of Ca^ influx into the myocardial cell as a result of both decrease in the extracellular Ca^ concentration and inhibition of ATP production and the Na^+-Ca^ exchange

Effect of stability and photodynamic activity of lipid membrane-incorporated porphyrins by location of porphyrins

広島大学(Hiroshima University)博士(工学)Doctor of Engineeringdoctora

マウス運動神経末端における伝達物質遊離に対する塩化第一スズおよび塩化第二スズの作用

Stannous chloride (SnCl_2) is thought to facilitate the transmitter release from the motor nerve terminals. Stannous ions tend to become oxidized to stannic ions (Sn^) in the presence of water and oxygen. Therefore, the results seen with SnCl_2 until now might reflect the properties of Sn^. In the present study, to ascertain whether SnCl_2 facilitates the transmitter release from mouse motor nerve terminals, we compared the effects of stannic chloride (SnCl_4) on the miniature endplate potential (m. e. p. p.) frequency and the quantal content of the endplate potential (e. p. p.) with those of SnCl_2. We statistically analyzed the mean values of the differences of SnCl_2 (30μM) from its control and of SnCl_4 (30μM) from its control. There were significant differences between the two, both in the m. e. p. p. frequency and in the quantal content. The results obtained demonstrate that the actions of Sn^ are not involved in the effects shown by SnCl_2. We conclude that SnCl_2 facilitates the transmitter release from mouse motor nerve terminals

ラット神経筋伝達に対する塩化第一スズの作用

Stannous chloride (SnCl_2) facilitates frog neuromuscular transmission. Effects of SnCl_2 on the neuromuscular junction of the rat have been investigated to determine whether mammalian responses to SnCl_2 are the same as those of amphibians. SnCl_2 (30 μM) had no effect on the resting potential or the membrane resistance of the muscle fiber. SnCl_2 did not change the amplitude of the endplate potential. SnCl_2 significantly raised the frequency of the miniature endplate potential in the high potassium-medium. SnCl_2 decreased the amplitude of the miniature endplate potential. These results suggest that SnCl_2 may facilitate the transmitter release from the nerve terminals, but it may reduce the acetylcholine sensitivity of the endplate in the rat