Stereo- and enantio-selective topochemical photoreactions are described in relation with crystallographic results of starting compounds. It was confirmed that ethyl 4-[2-(4-pyridyl)ethenyl]cinnamate crystallized into the chiral form without any external chiral reagents and that the chiral crystal, obtained from each recrystallization batch without seeding, always gave one or the other enantiomeric dimer in a large excess. The result was presumed to be a model of the generation of chiral homogeneity in nature. Topochemical reaction of achiral crystals of achiral molecules, ethyl α-cyano-4-[2-(2-pyridyl)ethenyl]cinnamate, proceeded stereo-specifically through the topochemical induction due to steric hindrance in the crystal cavity, and resulted in a syndiotactic compound.
By measuring the isometric tension produced by thin strips of taenia coli smooth muscle, inhibitory effects of caffeine on the acetylcholine (ACh)-induced phasic contraction were examined under the high-K depolarized state. Caffeine (2mM) inhibited ACh-contraction by three different mechanisms: 1) by decreasing the efficiency of Ca-release from Ca-store, 2) by inhibiting the loading of Ca-store with Ca2+ and 3) by accelerating the depletion of Ca-store. In the presence of physiological concentration of Ca2+ the first mechanism was found to be dominant with a slight contribution of the second. Under the nominally Ca-free conditions the contribution of the third was also important.
The offspring raised from parathyroid-transplanted male and female rats possesses heritable hypercalcitoninemia. These rats at the 7th generation were examined for the response of thyroid C cells to calcium and nicardipine. Paired control was raised from sham-operated rats. Four mg/kg calcium given intravenously (i.v.) to the control rats stimulated the release of calcitonin up to 15-times the basal level at 1 minute examined. The same dose of calcium induced 30-fold increase of serum calcitonin from the basal level in the PT rats. Nicardipine in a dose of 1mg/kg injected i.v. 3 minutes prior to calcium stimulation suppressed the calcium-induced calcitonin release to 50% of its peak value at 1 minute in the control rats. In the PT rats, the nicardipine-priming suppressed the calcium-induced calcitonin release to a greater extent, to 37% of the peak value. The results suggest that the PT rats have altered calcium signal transduction in the thyroid C cells.