Extracellular recordings were made from 127 neurons, identified by antidromic activation from the supraoptic nucleus, in the A1 area of urethan- anesthetized rabbits. The median axonal conduction velocity was 0.7 m/s, and the median discharge rate was 3.9 spikes/s. Raising arterial pressure decreased the discharge rate in 94 of 101 neurons tested. Lowering arterial pressure increased the discharge rate in 50 of 64 neurons tested. Of 70 neurons inhibited by baroreceptor activation, 40 were excited and 25 inhibited by hypercapnic hypoxia. Of 23 neurons excited by hypercapnic hypoxia, all were excited by hypoxia but only 2 were affected by hypercapnia. Of 16 neurons inhibited by hypercapnic hypoxia, 15 were inhibited by hypoxia and 1 was inhibited by hypercapnia. Of 14 neurons excited by hypoxia, 13 were excited by injection of sodium cyanide into the common carotid artery. Of five neurons inhibited by hypoxia, four were inhibited by sodium cyanide. Our results provide electrophysiological evidence that neurons projecting from the A1 area to the supraoptic nucleus increase their discharge rate in response to baroreceptor unloading and decrease their discharge rate in response to baroreceptor activation. These neurons may form part of the central pathway mediating secretion of vasopressin in response to hemorrhage. A high proportion of the neurons also receive peripheral chemoreceptor inputs, and these A1 cells may also be part of the central pathway whereby chemoreceptor stimulation modifies the secretion of vasopressin.
|Number of pages||8|
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|Publication status||Published - 1 Aug 1992|
- blood pressure
- catecholamine neurons
- extracellular recording
- ventrolateral medulla