Role of the autonomic nervous system in the acute blood pressure elevation during repetitive hypoxic and hypercapnic breathing in rats

• Published in: Blood pressure Vol. 5; no. 6; p. 371
• Main Authors: Bakehe, M, Hedner, J, Dang, T, Chambille, B, Gaultier, C L, Escourrou, P
• Format: Journal Article
• Language: English
• Published: England 1996
• Subjects: Animals; Autonomic Nervous System - physiopathology; Blood Pressure; Hypercapnia - physiopathology; Hypoxia - physiopathology; Male; Rats; Rats, Wistar
• ISSN: 0803-7051
• DOI: 10.3109/08037059609078077

Acute intermittent repetitive hypoxia simulating sleep apnoea syndrome is responsible for acute rises in blood pressure (BP). In the rat, the BP rises are enhanced by added hypercapnia. To investigate the role of the autonomic nervous system (ANS) in acute hypertension during repetitive hypoxia alone, FiO2 (inspiratory fractional concentration of oxygen) 2 to 5%, or combined with hypercapnia FiCO2 (inspiratory fractional concentration of carbon dioxide) 2 to 5%, we used autonomic blockade by atropine (1 mg kg-1) + propranolol (1 mg kg-1)-phentolamine (1 mg kg-1). Seven Wistar male rats were chronically instrumented with two aortic and venous catheters. Repetitive administration of N2 and N2 + CO2 for 10s followed by 20s compressed air was repeated for 4-5 min before (control) and after autonomic blockade. After autonomic blockade there was no significant difference in mean blood pressure (MBP) during severe hypoxia (SHO) (14.9 +/- 0.5 mmHg) compared to control (10.5 +/- 0.9 mmHg), while MBP was significantly decreased in severe hypoxia + hypercapnia (SHOHC) (14.1 +/- 0.4 mmHg) compared to control (26.8 +/- 0.3 mmHg) (p < 0.001). We conclude that the acute BP rise observed during hypoxic breathing is not due to the activation of ANS, but when hypercapnia is added to the hypoxic stimulus about half of pressor response is caused by ANS.