ADMINISTRATION OF AVP TO THE AREA POSTREMA ALTERS RESPONSE OF NTS NEURONS TO AFFERENT INPUTS

Authors
Citation
L. Qu et al., ADMINISTRATION OF AVP TO THE AREA POSTREMA ALTERS RESPONSE OF NTS NEURONS TO AFFERENT INPUTS, American journal of physiology. Regulatory, integrative and comparative physiology, 41(2), 1997, pp. 519-525
Citations number
31
Categorie Soggetti
Physiology
ISSN journal
03636119
Volume
41
Issue
2
Year of publication
1997
Pages
519 - 525
Database
ISI
SICI code
0363-6119(1997)41:2<519:AOATTA>2.0.ZU;2-F
Abstract
This study was designed to determine if arginine vasopressin (AVP) fac ilitates the response of nucleus of the solitary tract (NTS) neurons t o baroreceptor input. In anesthetized sinoaortic-denervated vagotomize d rabbits, AVP was intravenously infused (15 mu g . kg(-1) . min(-1), 1 min) or microinjected into the area postrema (AP; 1 ng/nl, 10 nl). E xtracellular recordings of evoked NTS neuronal responses to electrical stimulation of the aortic depressor nerve (ADN) or vagus nerve (1 Hz, 2-20 V, 0.05-0.6 ms) were evaluated before and after AVP administrati on. In neurons receiving input from the ADN (n = 19), 58% of them incr eased their responses after AVP (40.3 +/- 5.0 to 71.5 +/- 4,8%, P < 0. 001). Similarly, in neurons activated by vagal stimulation (n = 22), 5 5% of them were facilitated during AVP administration (59.7 +/- 12.8 t o 90.8 +/- 10.7%, P < 0.01). This action of AVP was independent of the mode of AVP administration, since either microinjection or venous inf usion was effective in augmenting responses of NTS neurons to aortic/v agal stimulation. In an additional 37 spontaneous NTS neurons, AVP sho wed no effect on the mean baseline firing rate (8.9 +/- 1.3 vs. 9.6 +/ - 1.3 spikes/s, P > 0.05), but increased neuronal activity in 54% of n eurons (6.9 +/- 1.3 vs. 13.1 +/- 1.7 spikes/s, P < 0.01). In two rabbi ts pretreated with vasopressin antagonist (15 mu g/kg iv), AVP failed to produce facilitatory effects (n = 8). The results of this study pro vide evidence in support of the hypothesis that circulating peptides m odulate the arterial baroreflex via activation of neurons in the AP.