Possible involvement of nitric oxide in the central salt-loading-induced cardiovascular responses in conscious rats

• Published in: Brain research Vol. 963; no. 1; pp. 224 - 231
• Main Authors: Jin, Qing-Hua, Kunitake, Takato, Chu, Chun-Ping, Qiu, De-Lai, Kato, Kazuo, Ishizuka, Yuta, Kannan, Hiroshi
• Format: Journal Article
• Language: English
• Published: London Elsevier B.V 14.02.2003; Amsterdam Elsevier; New York, NY
• Subjects: Animals; Biological and medical sciences; Blood pressure; Blood Pressure - physiology; Enzyme Inhibitors - pharmacology; Extracellular Space - metabolism; Fundamental and applied biological sciences. Psychology; Heart rate; Heart Rate - physiology; Hemodynamics - drug effects; Hemodynamics - physiology; Male; Microdialysis; Molsidomine - analogs & derivatives; Molsidomine - pharmacology; Motor control and motor pathways. Reflexes. Control centers of vegetative functions. Vestibular system and equilibration; Nitric oxide; Nitric Oxide - metabolism; Nitric Oxide - physiology; Nitric Oxide Donors - pharmacology; Nitric Oxide Synthase - antagonists & inhibitors; omega-N-Methylarginine - pharmacology; Paraventricular Hypothalamic Nucleus - drug effects; Paraventricular nucleus; Rats; Rats, Wistar; Saline Solution, Hypertonic - pharmacology; Vertebrates: nervous system and sense organs; Heart rate; Endocrine and autonomic regulation; Blood pressure; Paraventricular nucleus; Nitric oxide; Cardiovascular control; Rat; Rodentia; Central nervous system; Salt; Vertebrata; Mammalia; Hemodynamics; Brain (vertebrata)
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(02)03982-3

The objective of this study was to elucidate the possible involvement of nitric oxide (NO) in the cardiovascular responses induced by central salt loading. Direct perfusion of the hypothalamic paraventricular nucleus (PVN) region with hypertonic saline (0.3 or 0.45 M) was performed in conscious rats by using an in vivo brain microdialysis technique. The extracellular concentration of NO metabolites in the PVN region was measured, as were the blood pressure (BP) and heart rate (HR). Perfusion of 0.45 M saline increased the BP, HR, and NO metabolite levels in the PVN region; however, perfusion of 0.3 M saline enhanced only the level of NO metabolites but did not induce changes in the BP and HR. Next, we determined whether the NO was involved in the cardiovascular responses induced by hypertonic saline. Pretreatment with N G-methyl- l-arginine ( l-NMMA), an inhibitor of NO synthase, attenuated the increases in the BP and HR induced by direct perfusion of 0.45 M saline, while direct infusion of 3-morpholinosyndnonimine (SIN-1, a NO donor) in the PVN region induced increases in the BP and HR. These results suggest that local perfusion of the PVN region with hypertonic saline elicits a local release of NO, which may be carried out by activating nitric oxide synthase to produce cardiovascular responses.