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Division of Respiratory, Critical Care, and Environmental Medicine, Department of Medicine, Louisville Veterans Affairs Medical Center and University of Louisville School of Medicine, Louisville, Kentucky 40292; and Section on Hypertension and Clinical Pharmacology, Baylor College of Medicine, Houston, Texas 77030
Received 7 October 1996; accepted in final form 14 February 1997.
Bao, Gang, Naira Metreveli, Rena Li, Addison Taylor, and
Eugene C. Fletcher. Blood pressure response to chronic episodic hypoxia: role of the sympathetic nervous system. J. Appl. Physiol. 83(1): 95-101, 1997.
Previous
studies in several strains of rats have demonstrated that 35 consecutive days of recurrent episodic hypoxia (7 h/day) cause an 8- to
13-mmHg persistent increase in diurnal systemic blood pressure (BP).
Carotid chemoreceptors and the sympathetic nervous system have been
shown to be necessary for development of this BP increase. The present
study was undertaken to further define the role of renal artery
sympathetic nerves and the adrenal medulla in this BP
increase. Male Sprague-Dawley rats had either adrenal
medullectomy, bilateral renal artery denervation, or sham surgery. Rats
from each of these groups were subjected to episodic hypoxia for 35 days. Control groups received either compressed air or were left
unhandled. Adrenal demedullation or renal artery denervation eliminated
the chronic diurnal mean BP response (measured intra-arterially) to
episodic hypoxia, whereas sham-operated controls continued to showed
persistent elevation of systemic BP. Plasma and renal tissue
catecholamine levels at the end of the experiment confirmed successful
adrenal demedullation or renal denervation in the respective
animals. The chronic episodic hypoxia-mediated increase in
diurnal BP requires both intact renal artery nerves as well as an
intact adrenal medulla.
adrenal demedullation; renal denervation; hypertension
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