| Abstrakt: |
The strength of action of the parasympathetic innervation of the heart was tested, in anaesthetized dogs, by regular delivery of bursts of supramaximal electrical pulses at low frequency to the cut, cardiac end of the vagus nerve. Periods of 'conditioning' stimulation of the same nerve at relatively high frequencies (15-30 Hz, for 15-300 s) were found to cause a slowly developing potentiation (up to 280% increase in the vagally induced prolongation of pulse interval) of the cardiac action of the low-frequency stimulation. This potentiation lasted for periods of up to 30 min after the conditioning period. Similar potentiation could be elicited for the action of one vagus nerve by conditioning the vagus on the other side. Potentiation of vagal action was not associated with an enhancement of the response of the heart to injected methacholine. Several neuropeptides, reported to be present in cardiac autonomic nerves, were tested for ability to mimic this effect when administered by intravenous injection. Vasoactive intestinal polypeptide, neurotensin, somatostatin and substance P all failed to do so at the doses tested. Vasopressin did induce an enhancement of cardiac vagal efficacy, but effective pharmacological blockade of its action did not block the potentiation caused by conditioning stimulation. In the absence of any evidence of neuromodulation of vagal action by these neuropeptides, it was presumed that the effect could be attributed to a classical homosynaptic post-tetanic potentiation mechanism involving intracellular accumulation of calcium ions in prejunctional nerve terminals. |
