Abstract
In spinal cats, we studied the effects of nicotinic and non-nicotinic ganglionic stimulants on two groups of stellate ganglion cells: the adrenergic neurons which mediate cardioacceleration and the cholinergic ones which mediate sweat secretion in the front foot pads. The stimulant drugs were administered close i.a. toward the right stellate ganglion and were compared in terms of: 1) their threshold doses for producing ganglionically mediated cardioacceleration and sweat secretion and 2) the maximal response of each type which the drugs were able to produce. Nicotine was equally potent and effective in stimulating each group of ganglion cells, as were 1, 1-dimethyl-4-phenyl-piperazinium iodide, KC1 and preganglionic electrical stimulation. However, 5-hydroxy-tryptamine was a much more potent and effectivestimulant of the cholinergic than of the adrenergic neurons, whereas the opposite was true for the other substances studied. Acetyl-choline and histamine each stimulated the adrenergic neurons more potently and effectively than the cholinergic neurons, while 4-(m-chlorophenylcarbamoyloxy)-2-butynyltrimethyl-ammonium chloride (McN-A343), angiotensin and bradykinin each stimulated only the adrenergic ones. Supramaximal preganglionic stimulation at high frequency enhanced the responsiveness of both groups of ganglion cells to acetyicholine, 5-hydroxytryptamine and histamine but not to KCI or the nicotinic substances, nicotine and 1, 1-dimethyl-4-phenyl-piperazinium iodide. After blocking the nicotinic gangliomc receptors with chiorisondamine or hexamethothum, transmission of preganglionic impulses to the cholinergic neurons no longer occurred, although it still took place to the adrenergic neurons via muscarinic mechanisms. These results indicate that the cell population of the stellate ganglion is pharmaco-logically as well as functionally heterogeneous.
Footnotes
- Received April 1, 1969.
- Accepted June 18, 1969.
- © 1969, by The Williams & Wilkins Co.
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