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. 2006 May 8;103(20):7807–7812. doi: 10.1073/pnas.0600875103

Fig. 2.

Fig. 2.

Cardiovascular responses to AVP. (A) Representative hemodynamic measurements of BP and HR in V1a+/+ (Upper) and V1a−/− (Lower) mice after stimulation with AVP (≈0.1–100 μg/kg). (B) The concentration-response curve for the AVP-induced pressor (Left) and HR (Right) response. The changes in MAP (in mmHg) and HR (bpm) are shown. The concentration–response curves of MAP and HR for AVP in V1a−/− mice (filled circles) were significantly (P < 0.05) different from those in V1a+/+ mice (open circles). Data points are the means ± SEM from analyses of 8–10 mice. (C) Representative hemodynamic measurements of BP for V1a−/− mice in the absence (Upper) or presence (Lower) of the V2 receptor antagonist, [adamantaneacetyl1, O-ethyl-d-Tyr-2, Val-4, aminobutyryl6, Arg-8,9]-vasopressin (100 μg/kg per min i.v.) 10 min before AVP injection (≈10–100 μg/kg). (D) Representative hemodynamic measurements of BP and HR in V1a−/− mice in the presence (Right) or absence (Left) of the NO inhibitor l-NNA (200 μg/kg per min i.v.) 60 min before AVP injection (100 μg/kg).