L-Arginine reverses the abolition of hypovolaemic decompensation by N-nitro-L-arginine methyl ester and naloxone in conscious rabbits.

Graded caval occlusion in conscious rabbits caused a biphasic haemodynamic response. Phase I was characterized by a fall in systemic vascular conductance so that arterial pressure was maintained. When cardiac output had fallen to 65 +/- 2% of its baseline level, phase II supervened. During phase II, conductance rose abruptly and arterial pressure fell to a life-threatening level (< or = 40 mm Hg). Fourth ventricular administration of either N-nitro-L-arginine methyl ester or naloxone prevented the occurrence of phase II. Fourth ventricular administration of L-arginine had no effect on the response to graded caval occlusion but was able to reverse the phase II blocking action of N-nitro-L-arginine methyl ester and naloxone. It is concluded that central nitrergic and opioid mechanisms interact to cause the vasodilatation characteristic of the decompensatory phase II of the cardiovascular response to acute hypovolaemia.