Abstract
The hypotensive response to tetraethylammonium chloride (TEAC) and pentamethonium iodide (C6) is greatly increased in dogs with neurogenic hypertension and to a lesser extent in chronic expts. after section of only the carotid sinuses when compared with normal or renal hypertensive animals. Repeated doses do not lessen their hypotensive effect as they do in normal dogs. Augmentation of other pressor-depressor substances usually occurs only to a small extent in the presence of increased resistance to TEAC blockade."Total" sympathectomy and spinal cord section at C6 abolish the hypotensive response. The response pattern persists to a certain degree despite ablation of both sympathetic chains except for the stellate ganglia. Neither sympathetic denervation of the heart or adrenals alone abolishes the chronic TEAC vasodepressor response but the combined operations do so. Blockade at the periphery by Priscoline and Benodaine in dogs exhibiting the response pattern reverse epinephrine and norepinephrine responses. For a short time the hypotensive response to TEAC is also partially blocked but it reappears well before the control response to epinephrine and norepinephrine. Atropine, Benadryl, pituitrin, Prostigmin and ACTH failed to influence the hypersensitive depressor response to TEAC. Some hypertensive patients exhibit reaction patterns similar to those in neurogenic hypertensive dogs. Probably the phenomenon is best viewed as a result of loss of the influence of the buffer nerves on the sympathetic ganglia such that blockade by TEAC or pentamethonium iodide of the heightened vasomotor activity is only transient.