It has been demonstrated that opioids modulate the renin-angiotensin and sympathetic nervous systems. To clarify the interaction of central angiotensin II (Ang II) and endogenous opioids, we studied the effects of naloxone, an opioid antagonist, on cardiovascular and sympathetic responses to intracerebroventricular (ICV) Ang II in conscious rabbits. ICV Ang II (20 ng/min) significantly increased mean arterial pressure (MAP), plasma epinephrine, and arginine vasopressin (AVP) levels, with no significant change in renal sympathetic nerve activity (RSNA) or heart rate. Pretreatment with intravenous naloxone (0.1 mg/kg) failed to alter the cardiovascular and neurohormonal responses to ICV Ang II. To eliminate the effect of AVP on cardiovascular and sympathetic responses, [d(CH2)5Thy(Me)]AVP, a vasopressin V1-receptor antagonist, was given intravenously. Pretreatment with intravenous injection of the V1-receptor antagonist (30 μg/kg) augmented the maximum increase in RSNA caused by ICV Ang II (8.9±2.2 vs. 16.2±0.7%, P<0.05). Combined pretreatment with naloxone and V1-receptor antagonist further increased MAP and RSNA in response to ICV Ang II (20±1 vs. 16±2 mmHg, p<0.05, and 30.9±3.7 vs. 16.2±0.7%, p<0.01, respectively). These results suggest that opioids and AVP synergistically modulate sympathetic outflow so as to suppress the central presser action of Ang II in conscious rabbits.
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