Activation of spinal opioid receptors contributes to hypotension after hemorrhage in conscious rats

• Published in: American journal of physiology. Heart and circulatory physiology 1999-05, Vol.276 (5), p.H1552-H1558
• Main Authors: Ang, Kooi K, McRitchie, Robert J, Minson, Jane B, Llewellyn-Smith, Ida J, Pilowsky, Paul M, Chalmers, John P, Arnolda, Leonard F
• Format: Article
• Language: English
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.1999.276.5.h1552

1  Cardiovascular Neuroscience Group, Cardiovascular Medicine and Centre for Neuroscience, Flinders University, Bedford Park, SA 5042; and 2  Royal North Shore Hospital, St. Leonards, NSW 2065, Australia Opioid receptors are activated during severe hemorrhage, resulting in sympathoinhibition and a profound fall in blood pressure. This study examined the location and subtypes of opioid receptors that might contribute to hypotension after hemorrhage. Intrathecal naloxone methiodide (100 nmol) abolished the fall in blood pressure after hemorrhage (1.5% of body wt; mean arterial pressure 122   ± 8 mmHg after naloxone methiodide vs. 46 ± 5 mmHg in controls, P  1600-fold. Comparisons of the minimum effective doses of these antagonists in relation to their binding affinities provides strong evidence for the participation of -receptors in mediating hypotension after hemorrhage. In contrast, the dose at which nor-BNI was effective suggests an effect at -receptors but not -receptors. The efficacy of CTOP, albeit at a high dose, also suggests an effect at µ-receptors. sympathoinhibition; sympathetic nervous system; naloxone; enkephalin