TY - JOUR T1 - MECHANISMS OF SINUS BRADYCARDIA INDUCED BY VERATRUM ALKALOIDS—PROTOVERATRINE A JF - Journal of Pharmacology and Experimental Therapeutics JO - J Pharmacol Exp Ther SP - 546 LP - 557 VL - 154 IS - 3 AU - C. Y. Chai AU - S. C. Wang Y1 - 1966/12/01 UR - http://jpet.aspetjournals.org/content/154/3/546.abstract N2 - In cats anesthetized with chloralose and urethane, protoveratrine A (1.5-3 µg/kg injected intravenously, or 2-5 µg injected into the carotid artery) produced moderate to marked bradycardia and hypotension. On the other hand, injection of 2 to 5 µg into the vertebral artery produced either no cardiac slowing or slight hypertension concomitant with cardio-acceleration. The degree of bradycardia and, to a certain extent, of the hypotension following intracarotid injection was directly related to the amount of protoveratrine entering the occipital artery. Occlusion of that vessel during injection or surgical interruption of the blood supply to the nodose ganglion area markedly reduced the bradycardia and hypotension. When these procedures were carried out on both sides, the bradycardia and hypotension induced by intravenous injection of protoveratrine were markedly reduced or abolished. Unilateral sectioning of the vagus nerve, either above or below the nodose ganglion, eliminated the bradycardia following intracarotid injection on the homolateral side while the hypotensive response was only minimally affected. Unilateral sectioning of the carotid sinus nerve without vagotomy, on the other hand, did not affect the cardiac slowing or hypotension following the same injection. It is concluded that receptors in the nodose ganglion itself or its neighboring structures play an important role in the reflex activation of sinus bradycardia induced by protoveratrine, whereas the carotid sinus baroceptors are primarily responsible for the reflex hypotension induced by the same agent. © 1966 by The Williams & Wilkins Co. ER -