RESPONSES OF PLASMA OXYTOCIN AND ARGININE VASOPRESSIN TO NAUSEA INDUCED BY APOMORPHINE AND IPECACUANHA

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Abstract
SUMMARY: Apomorphine, a centrally‐acting emetic, was administered subcutaneously (50 /μg/kg) to nine normal subjects (four male, five female; aged 22‐36 years) and four patients with idiopathic diabetes insipidus (DI) (one male, three female; aged 24‐49 years). In the normal subjects this stimulus caused nausea (and vomiting in seven of nine) with a latency of 9‐5 ± 0‐9 min which was followed by a large increase in plasma arginine vasopressin (AVP) concentration (from 0‐9 ± 0‐2 pmol/1 to 249 ± 104 pmol/1 at 15 min after the onset of symptoms; mean ± SEM, PP<005). Mean arterial pressure (MAP) fell slightly (from 87±1‐9 mm Hg to 71±4‐4 mm Hg; P < 005) 15 min after the onset of nausea; there was no change in blood haematocrit or plasma osmolality and sodium concentration. In the DI patients apomorphine produced nausea (with vomiting in three of four) with a latency of 100±1 ‐4 min but failed to cause an increase in either plasma AVP or OXT. In the DI patients the fall in MAP did not reach statistical significance (83 ± 4 mm Hg to 71 ± 11 mm Hg); there was also no change in haematocrit, osmolality or sodium concentration. Ipecacuanha, an emetic with both peripheral and central actions, was administered orally to seven normal subjects (three male, four female; aged 22‐36 years) six of whom also underwent apomorphine tests. Nausea followed with a latency of 16‐9 ± 3‐2 min (with vomiting in five of seven). However, despite producing symptoms considered by the subjects to be as severe as those caused by apomorphine there was no increase in plasma AVP or OXT. In contrast to apomorphine, ipecacuanha produced a significant increase in MAP (from 82 ± 2 mm Hg to 11101+7 mm Hg; P‐1 to 76 ± 4 mm‐1; P<0‐05); there was no change in haematocrit, osmolality or sodium concentration.The results provide evidence that OXT neurones are affected by the pathological process involved in the aetiology of idiopathic DI in some patients. They indicate that while nausea (and vomiting) produce elevations of plasma OXT and AVP these sequelae are not essential to these physiological processes. Finally, we interpret the failure of ipecacuanha‐induced nausea to increase plasma AVP and OXT concentrations as evidence that the neuroendocrine response to nausea, in the human, may depend on the site of action of the emetic stimulus.