Release of norepinephrine from sympathetic nerve efferents by bilateral carotid occlusion.
To investigate the response of the efferent sympathetic nervous system to carotid sinus hypotension, norepinephrine and epinephrine were measured in the dog during control and following bilateral carotid occlusion in arterial, coronary sinus, renal vein, hepatic vein, femoral vein, and pulmonary artery plasma. Mean arterial pressure increased from 109 mmHg during control to 144 and 143 at 1 and 5 min after carotid occlusion, respectively (P less than 0.01). This was associated with an increase in arterial norepinephrine, which could be prevented by the ganglionic blocking agent mecamylamine. While the concentration of norepinephrine rose in all venous effluents, the venous minus arterial norepinephrine difference increased only in the coronary and renal circulations. The results indicate that bilateral carotid occlusion increases the arterial norepinephrine concentration and the overflow of this neurotransmitter from the heart and kidney. The data thus suggest that norepinephrine release from sympathetic axon terminals in the heart and kidney is increased by carotid sinus hypotension. The magnitude of the increase in sympathetic activity evoked by carotid occlusion may have little effect on renal hemodynamics but may have a significant influence on cardiac contractility and coronary blood flow.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002346:Carotid Sinus / Q000502:physiology*; D004285:Dogs; D004525:Efferent Pathways / Q000378:metabolism*; D005260:Female; D005268:Femoral Vein / Q000502:physiology; D006503:Hepatic Veins / Q000502:physiology; D008297:Male; D008464:Mecamylamine / Q000494:pharmacology; D009638:Norepinephrine / Q000097:blood / Q000378:metabolism*; D011651:Pulmonary Artery / Q000502:physiology; D012082:Renal Veins / Q000502:physiology; D013564:Sympathetic Nervous System / Q000378:metabolism*
D008464:Mecamylamine; D009638:Norepinephrine