Angiotensin stimulates respiration in spontaneously hypertensive rats

Spontaneously hypertensive rats (SHR) have an activated brain angiotensin system. We hypothesized 1) that ventilation ((V) over dot) 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 ((V) over dot O-2) 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 (similar to 14 mu l.kg(-1).min(-1)) followed by 30 min of saralasin (1.3 mu g.kg(-1).min(-1)). (V) over dot, tidal volume (VT), inspiratory flow [VT/inspiratory time (TI)], breath expiratory time, and (V) over O-2 were higher, and breath TI was lower in "continuously quiet" SHR. In SHR, but not in WKY rats, ANG II-receptor block decreased (V) over dot, VT, and VT/TI and increased breath TI. During ANG II-receptor block, an average decrease in (V) over dot O-2 in SHR was not significant. About one-half of the higher (V) over dot in SHR appears to be accounted for by an ANG II mechanism acting either via peripheral arterial receptors or circumventricular organs.