On the mechanisms of k‐opioid‐induced diuresis

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Abstract
1 In conscious saline loaded rats, the k-opioid agonists tifluadom, U50488, and ethylketocyclazocine, given subcutaneously, induced a characteristic diuresis which could be antagonized by naloxone. 2 Bilateral adrenal demedullation significantly reduced adrenal gland catecholamine content and plasma adrenaline levels, but did not significantly affect plasma corticosterone levels, indicating that the adrenal cortex remained both intact and functional. 3 Seven days following bilateral adrenal demedullation, the subcutaneous administration of the k-agonists no longer induced diuresis. However, demedullation did not affect the diuretic response to frusemide or clonidine, nor did it affect the antidiuretic response induced by the μ-opioid agonists morphine and buprenorphine. 4 Adrenal catecholamines do not appear to be involved in k-opioid-induced diuresis, since pretreatment with propranolol, prazosin and idazoxan did not affect the diuretic response in intact animals. 6 The results indicate a link between the adrenal medulla and k-opioid-induced diuresis and suggest that a peripheral mechanism may also be involved in mediating this effect.