Adaptation of pulmonary receptors in the spontaneously breathing anaesthetized rat.

It has been suggested that species with high breathing frequencies have pulmonary stretch receptors which adapt more rapidly than species with low breathing frequencies. This has proved not to be so. Our hypothesis is that this theory is in fact correct if modified so that overall rate of adaptation of afferent vagal activity, i.e. the sum of stretch and rapidly adapting receptors, is considered. A rapidly breathing species, such as the rat, would thus have a greater proportion of rapidly adapting receptors, than a more slowly breathing species. To test this hypothesis, we measured the proportion of rapidly adapting pulmonary mechanoreceptors in spontaneously breathing rats for comparison with existing results from more slowly breathing species. We found there to be one rapidly adapting receptor for every three slowly adapting receptors present. This measurement has not previously been made in spontaneously breathing rats. The ratio of rapidly to slowly adapting pulmonary receptors in the species sequence cat-rabbit-rat is the same as the ratio of their breathing frequencies (3:4:10). We propose that the difference in proportion of slowly to rapidly adapting pulmonary receptors in different species may be related to their eupnoeic breathing frequency.

The effect of etidocaine on spontaneous and evoked release of norepinephrine from rat brain synaptosomes.

Local anesthetics have been shown to have an effect on neurotransmission. In this study we examined the effect of a local anesthetic, etidocaine, on the uptake, efflux, and release of norepinephrine (NE) from central nerve terminals. The studies were performed on synaptosomes and vesicles prepared from rat brains. Etidocaine 10(-4) M inhibited synaptosomal accumulation of [3H]NE and did not significantly effect vesicular accumulation of this neurotransmitter. This concentration of etidocaine also augmented efflux of norepinephrine from synaptosomal preparations. This augmented efflux was primarily due to an increase in the deaminated metabolite 3,4-dihydroxyphenylglycol (DOPEG). The presence of etidocaine did not significantly alter the release of NE from synaptosomes superfused with high potassium (40 mM), a calcium-dependent exocytotic release process. These results indicate that in the central nervous system, as previously demonstrated in the peripheral nervous system, high concentrations of etidocaine alter vesicular storage of NE, resulting in more NE leaking into the cytoplasm where it is metabolized to an inactive metabolite.