No abstract

When the right vagus nerve of anesthetized cats was stimulated with repetitive bursts of pulses, decelerated heart rate became synchronized to the rhythm of the vagal bursts. Each burst applied to the vagus was followed by a single heart contraction. Within defined limits an increase in the frequency of vagal bursts evoked a proportional acceleration of the heart, whereas a decreased frequency diminished the heart rate. Therefore, over the range of synchronization the heart rate was precisely controlled by changing the vagal stimulation rate. We concluded that the chronotropic effect evoked by vagal bursts was composed of two functionally different types of influence, namely, inhibitory tonic and synchronizing. The vagotropic influence of intravenously injected regulatory peptides was found to be selective for either the tonic or synchronizing component. For instance, dalargin (D-Ala2-Leu5-Arg6-enkephalin) and neokyotorphin selectively diminished the inhibitory tonic vagal influence, whereas delta sleep inducing peptide and neurotensin potentiated it. The magnitude of synchronizing vagal influence was not modified by these peptides. In contrast, secretin selectively inhibited the synchronizing vagal effect, but the tonic one was not affected. Somatostatin potentiated the synchronizing effect but diminished the tonic one. These data support the hypothesis that certain regulatory peptides can modulate the effects of repetitive vagal bursts on pacemaker activity.

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A main issue in pharmacology is the seek for effective agents for the correction of ED. To study the endothelioprotective effects of 2-ethyl-3-hydroxy-6-methylpyridinium (2e3h6m) nicotinate under conditions of L-NAME-induced oxidation. The L-NAME pattern of induced oxide efficiency (25 mg/g) for one week was used. The endothelial and cardioprotective effect of 2e3h6m nicotinate at an amount of 3.75 mg/kg compared to picamilon 10 mg/kg was examined via the coefficient of ED (QED) and a number of exercise tests. Nicotinate 2e3h6m and picamilon exerted a pronounced endothelioprotective impact on the pattern of L-NAME-induced NO deficiency, which manifested itself in a decrease in the coefficient of endothelial dysfunction (ED). At the same time, 2e3h6m nicotinate (7.6 mg/kg) was 2.1 times more effective than picamilon (10 mg/kg). So, 2e3h6m nicotinate was produced itself as an endothelio and cardioprotector.