Angiotensin stimulates respiration in spontaneously hypertensive rats

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Abstract
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 (V˙o2) 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 2consisted 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 V˙o2were higher, and breath Ti was lower in “continuously quiet” SHR. In SHR, but not in WKY rats, ANG II-receptor block decreasedV˙, VT, and VT/Ti and increased breath Ti. During ANG II-receptor block, an average decrease in V˙o2in SHR was not significant. About one-half of the higherV˙ in SHR appears to be accounted for by an ANG II mechanism acting either via peripheral arterial receptors or circumventricular organs.