Cardiovascular change induced by central hypertonic saline are accompanied by GABA release in awake rats.
- Author:
Xiao-Lei GAO
1
;
Gui-Dong YIN
;
Yan-Hua BING
;
Yuan-Zhe JIN
;
Qing-Hua JIN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Blood Pressure; drug effects; physiology; Male; Microdialysis; methods; Paraventricular Hypothalamic Nucleus; metabolism; physiology; Pressoreceptors; drug effects; Rats; Rats, Wistar; Saline Solution, Hypertonic; administration & dosage; pharmacology; gamma-Aminobutyric Acid; metabolism
- From: Chinese Journal of Applied Physiology 2009;25(4):462-466
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo investigate the possible involvement of gamma-aminobutyric acid (GABA) in the paraventricular nucleus (PVN) in cardiovascular responses induced by central salt loading.
METHODSDirect perfusion into PVN region with hypertonic saline (0.6 mol/L) was performed in conscious rats by using an in vivo brain microdialysis technique. Then, the extracellular concentration of GABA in the PVN region was measured by microdialysis and high performance liquid chromatography (HPLC) techniques, and the blood pressure (BP) and heart rate (HR) were with recorded simultaneously. Bicuculline (an antagonist of GABAA receptor) or saclofen (an antagonist of GABAB receptor) were coperfused hypertonic saline into PVN region, then the cardiovascular responses were examined.
RESULTS(1) The local perfusion of 0.6 mol/L saline elicited significant increases on BP and HR (P < 0.01). In addition, perfusion of 0.6 mol/L saline increased the extracellular GABA levels in the PVN region, which reached 561.96% +/- 173.96% (P < 0.05) of the basal level. (2) Bicuculline or salcofen significantly attenuated the in-response of BP (P < 0.01, respectively), whereas the antagonists did not influence the response of HR induced by hypertonic saline.
CONCLUSIONLocal perfusion of hypertonic saline in the PVN region elicits a local release of GABA, which may act via GABA(A) and GABA(B) receptors to produce pressor response.