Abstract
Vascular effects of benzyltrimethylammonium bromide (BTM) were investigated in the perfused dog hindlimb, mesentery, hindpaw, isolated rabbit heart and dog kidney since previous work indicated that BTM could depress smooth muscle reactivity. BTM was found to produce a nonspecific antagonism to responses of norepinephrine, nerve stimulation, isoproterenol and nitroglycerin. This antagonism was found to be reversed by pretreatment with atropine. Similar nonspecific antagonism was produced with high doses of mecholyl and carbachol. BTM and other muscarinic stimulants were able to reduce responses of the isolated heart to isoproterenol but not to calcium stimulation. Renal blood flow and sodium excretion were increased by intrarenal infusions of BTM without concomitant increases in glomerular filtration rate. These effects could be antagonized by atropine and reproduced by acetylcholine. Nonspecific antagonism to various agonists that affect renal blood flow could not be produced even at high concentrations of BTM. Depression of vascular reactivity by BTM appeared to be related to its ability to act as a muscarinie agonist. These data suggest that BTM-induced changes in vascular reactivity closely correlate with the phenomenon of desensitization.
Footnotes
- Received April 5, 1971.
- Accepted August 26, 1971.
- © 1972, by The Williams & Wilkins Company
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