Hypothalamic opioid peptide regulation of catecholamine secretion.
We compared the plasma catecholamine responses to intracisternal beta-endorphin with those to two mu receptor agonists. Morphine was less potent and [D-Ala2, MePhe4, Gly5-ol]enkephalin (DAGO) was more potent in stimulating catecholamine secretion. Since the hypothalamic paraventricular nucleus (PVN) contains a high level of opioid binding sites and is important for sympathoadrenal regulation, we examined the effects on catecholamine secretion of DAGO infusion into the PVN. DAGO infused into the PVN produced dose-related increases in plasma catecholamine concentrations, with an effective dose as low as 10pmol. This DAGO effect was blocked by the prior systemic administration of naloxone, and DAGO was ineffective when infused into frontoparietal cortex. Thus, endogenous opioid peptides appear to increase central sympathetic outflow and catecholamine secretion by stimulating mu receptors in the PVN.
D000818:Animals; D001921:Brain / Q000187:drug effects; D002395:Catecholamines / Q000378:metabolism*; D004723:Endorphins / Q000494:pharmacology*; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; D004745:Enkephalins / Q000494:pharmacology; D008297:Male; D009020:Morphine / Q000494:pharmacology; D010286:Paraventricular Hypothalamic Nucleus / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains; D011957:Receptors, Opioid / Q000187:drug effects; D001615:beta-Endorphin
D002395:Catecholamines; D004723:Endorphins; D004745:Enkephalins; D011957:Receptors, Opioid; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; D001615:beta-Endorphin; D009020:Morphine