Angiotensin stimulates respiration in spontaneously hypertensive rats

Spontaneously hypertensive rats (SHR) have an activated brain angiotensin s ystem. We hypothesized 1) that ventilation ((V) over dot) would be greater in conscious SHR than in control Wistar-Kyoto (WKY) rats and 2) that intrav enous infusion of the ANG II-receptor blocker saralasin would depress respi ration 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 plethysmograp h and measurements obtained over 60-75 min. After installation of chronic i ntravenous catheters, protocol 2 consisted of 30 min of saline infusion (si milar 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/insp iratory time (TI)], breath expiratory time, and (V) over O-2 were higher, a nd 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 incre ased breath TI. During ANG II-receptor block, an average decrease in (V) ov er dot O-2 in SHR was not significant. About one-half of the higher (V) ove r dot in SHR appears to be accounted for by an ANG II mechanism acting eith er via peripheral arterial receptors or circumventricular organs.