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Am J Physiol Regul Integr Comp Physiol 278: R1125-R1133, 2000;
0363-6119/00 $5.00
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Vol. 278, Issue 5, R1125-R1133, May 2000

Angiotensin stimulates respiration in spontaneously hypertensive rats

Donald B. Jennings and Heather J. Lockett

Department of Physiology, Queen's University, Kingston, Ontario, Canada K7L 3N6

Spontaneously hypertensive rats (SHR) have an activated brain angiotensin system. We hypothesized 1) that ventilation (V) would be greater in conscious SHR than in control Wistar-Kyoto (WKY) rats and 2) that intravenous infusion of the ANG II-receptor blocker saralasin would depress respiration in SHR, but not in WKY. Respiration and oxygen consumption (VO2) were measured in conscious aged-matched groups (n = 16) of adult female SHR and WKY. For protocol 1, rats were habituated to a plethysmograph and measurements obtained over 60-75 min. After installation of chronic intravenous catheters, protocol 2 consisted of 30 min of saline infusion (~14 µl · kg-1 · min-1) followed by 40 min of saralasin (1.3 µg · kg-1 · min-1). V, tidal volume (VT), inspiratory flow [VT/inspiratory time (TI)], breath expiratory time, and VO2 were higher, and breath TI was lower in "continuously quiet" SHR. In SHR, but not in WKY rats, ANG II-receptor block decreased V, VT, and VT/TI and increased breath TI. During ANG II-receptor block, an average decrease in VO2 in SHR was not significant. About one-half of the higher V in SHR appears to be accounted for by an ANG II mechanism acting either via peripheral arterial receptors or circumventricular organs.

angiotensin II-receptor block; breath timing and drive; respiratory pattern; respiratory control; behavioral state; sleep


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