Zur Blutdruckwirkung von Aludrin und Adrenalin

Summary The depressor action of small doses of adrenaline on the blood pressure (B.P.) of the decapitated cat may be abolished by pretreatment with pilocarpine; atropine restores the original depressor action. The fall in B.P. due to adrenaline after ergotamine once more becomes an increase when pilocarpine has been given earlier. After atropine a fall in B.P. again occurs. This effect of pilocarpine and atropine on a depressor response has already been described in the case of Aludrine (N-isopropyl-noradrenaline) byFromherz.     

Über ein Chromoplastin aus reifenden Tomaten

Summary (1) By precipitation with ammonium sulfate, streptomycin, or calcium salts, we obtained from the pulp of tomatoes a substance containing carotinoids. The behaviour of this substance was analogous to that of chloroplst-substance and to that of animal cytoplasmatic nucleoproteins. Like these it contains proteins, lipids, and very probably nucleic acids. We regard this substance as achromoplastine.(2) Experiments with slices of green tomatoes show that the changing over of the chlorophyll content into the carotinoid content is inhibited by the presence of streptomycin.(3) Streptomycin inhibits the formation of chlorophyll in etiolated separated cabbage leafs, just as this drug inhibits the formation of chlorophyll in growing seeds.(4) The development of anthocyanides is not influenced by streptomycin.     

Zur Entstehung des Lungenödems

Ohne Zusammenfassung     

Overcompensation and population cycles in an ungulate.

Although theoretical studies show that overcompensatory density-dependent mechanisms can potentially generate regular or chaotic fluctuations in animal numbers, the majority of realistic single-species models of invertebrate populations are not overcompensatory enough to cause sustained population cycles. The possibility that overcompensation may generate cycles or chaos in vertebrate populations has seldom been considered. Here we show that highly overcompensatng density-dependent mortality can generate recurrent population crashes consistent with those observed in a naturally limited population of Soay sheep. The observed interval of three or more years between crashes points to sharp 'focusing' of mortality over a narrow range of population density.     

Ca2+ release induced by inositol 1,4,5-trisphosphate is a steady-state phenomenon controlled by luminal Ca2+ in permeabilized cells.

Low concentrations of inositol 1,4,5-trisphosphate (InsP3) evoke a very rapid mobilization of intracellular Ca2+ stores in many cell types, which can be followed by a further, much slower efflux. Two explanations have been suggested for this biphasic release. The first proposes that the Ca2+ stores vary in their sensitivity to InsP3, and each store releases either its entire contents or nothing (all-or-none release); the second proposes instead that the stores are uniformly sensitive to the effects of InsP3, but that they can release only a fraction of their Ca2+ before their sensitivity is somehow attenuated (steady-state release). Experiments using purified InsP3 receptor molecules reconstituted into lipid vesicles have shown heterogeneity of the receptors in their response to InsP3 under conditions in which the total Ca2+ level at both sides of the receptor is held constant. We now report that in permeabilized A7r5 smooth-muscle cells incubated in Ca(2+)-free medium, the amount of 45Ca2+ remaining in the stores after the rapid transient phase of release is independent of their initial Ca2+ levels, indicating that partially depleted stores are less sensitive to InsP3. Moreover, if the stores are reloaded with 40Ca2+ after the first stimulus, reapplication of the same low concentration of InsP3 will release further 45Ca2+. This recovery of InsP3 sensitivity is almost complete. Under these conditions, Ca2+ release must thus occur by a steady-state mechanism, in which the decreasing Ca2+ content of the stores slows down further release.