Figure 6.

(A) Cardiovascular responses to naloxone – methiodide (3 nmol) or vehicle (aCSF) bilaterally injected into the PVN of conscious rats, in the absence (n=12 for both central injections) or presence (n=12 for naloxone – methiodide; n=11 for aCSF) of intravenous treatment with a vasopressin V₁-receptor antagonist (10 μg kg⁻¹, i.v. bolus, 10 kg⁻¹ h⁻¹, infusion). (B) Cardiovascular responses to β-FNA (0.5 nmol) or vehicle (aCSF) bilaterally injected into the PVN of conscious rats, in the absence (n=15 for both central injections) or presence (n=9 for both central injections) of intravenous treatment with the vasopressin V₁-receptor antagonist. Values are means±s.e.mean shown by vertical lines. (A) A significant interaction between treatment and time was found for all measured cardiovascular variables; (B) A significant interaction between treatment and time was found for ΔHR, ΔMAP and ΔRenal and Hindquarter Doppler Shift. ^*P<0.05 when the cardiovascular responses to naloxone – methiodide or β-FNA in the absence or presence of the vasopressin V₁-receptor antagonist are compared with their respective untreated or intravenously treated control (aCSF) group. †P<0.05, when the cardiovascular responses to naloxone – methiodide or β-FNA in the presence of the vasopressin V₁-receptor antagonist are compared with those elicited in the absence of the vasopressin V₁-receptor antagonist. No significant interaction was observed for ΔMesenteric Doppler Shift, the comparison between β-FNA and the control (aCSF) (in the absence or presence of the vasopressin V1 receptor antagonist) was done averaging over time.