Mechanism of action of angiotensin and bradykinin on smooth muscle in situ

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Abstract
Atropine inhibited the contractile response of isolated guinea pig ileum to angiotensin by 60–70%. This inhibition could be reversed with neostigmine. Morphine, which is known to prevent the release of acetylcholine from the nerve endings, also inhibited the response to angiotensin. The response to bradykinin under the same circumstances was not altered, nor was the response of the uterus to angiotensin and bradykinin. Except for tetraethylammonium chloride (TEAC), the quaternary nitrogen blocking agents had no effect on the ileal response to angiotensin. TEAC potentiated the response of the ileum to both angiotensin and bradykinin, even after the administration of atropine. Depolarizing doses of nicotine and tetramethylammonium chloride inhibited the response of the ileum to angiotensin without altering the response to bradykinin. Results thus suggest that angiotensin acted both by stimulating ganglion cells and smooth muscle. In the intestines, the ganglion stimulating effect was preponderant. Bradykinin, on the other hand, acted on smooth muscle cells only. TEAC potentiation of the response to the polypeptides was by direct action on the smooth muscle independent of its ganglion blocking effect.