THE PERIPHERAL SYMPATHETIC NERVOUS-SYSTEM AND THE INCREASE IN SYSTEMIC BLOOD-PRESSURE IN RESPONSE TO INTERMITTENT HYPOXIA

We have described a rat model which responds to repetitive episodic hy poxia mimicking sleep apnea (3-5% lowest ambient oxygen, every 30 s fo r 7 h/day for 35 days) with a chronic increase in arterial blood press ure 9!. Denervation of the peripheral chemoreceptors prevents the inc rease in blood pressure 7, 21!. The purpose of the current study was to determine whether the peripheral sympathetic nervous system is inst rumental in producing persistent blood pressure elevation in this mode l. Chemical sympathetic denervation was achieved and maintained by 3 i ntraperitoneal injections of 100 mg/kg of 6-OH dopamine on days 2, 4, and 28 of a 49-day experiment in two groups of male Wistar rats (320-4 10 g). One 6-OH dopamine-treated group was subjected to intermittent h ypoxia (for 40 days, begin at day 8) and the other 6-OH dopamine-injec ted group remained unhandled in their usual cages. A third group was i njected with placebo only and subjected to the same hypoxia while a fo urth remained unhandled for 40 days. Measurement of catecholamines in cardiac muscle homogenate using HPLC confirmed denervation in 6-OH dop amine animals. There were no significant differences among the 4 group s at baseline. The placebo-treated, episodic hypoxia-exposed group sho wed a 7.7 mmHg increase in mean arterial blood pressure (conscious, un restrained) over the 40-day period, whereas all other groups showed a decrease in mean arterial pressure. The left ventricle-septum/total bo dy weight ratio was - like in all other animals with more than 35 days of treatment with intermittent hypoxia 7, 9, 21! - higher in the hyp oxia treated groups at the end of the study. These results indicate th at an intact peripheral sympathetic nervous system is a prerequisite f or the persistent increase in blood pressure in response to intermitte nt hypoxia 8!.