Rowe J W, Shelton R L, Helderman J H, Vestal R E, Robertson G L
Kidney Int. 1979 Dec;16(6):729-35. doi: 10.1038/ki.1979.189.
The mechanisms underlying the frequent association of nausea and vomiting with elevations of plasma vasopressin(PAVP) were studied in man and rat. After oral water loads (N = 16), plasma osmolality fell in all human subjects and was associated with a decline in PAVP in 14 asymptomatic human subjects. In 2 human subjects, nausea occurred and was associated with increases in PAVP, without changes in blood pressure. During ethanol infusion (N = 28), PAVP was suppressed unless nausea supervened. In 4 nauseated human subjects, PAVP escaped from ethanol inhibition and rose to levels 10 times basal, despite the absence of hemodynamic changes. Apomorphine, a potent dopamine agonist and emetic agent, was administered to human volunteers in doses of 7 to 24 microgram/kg. There was no increase in PAVP in 3 human subjects who remained asymptomatic (7 to 16 microgram/kg). Ten human subjects experienced nausea after 16 microgram/kg, which was followed shortly by marked increases in PAVP. Emesis occurred in 5 human subjects given 16 to 24 microgram/kg, and was followed by PAVP levels similar to those seen with nausea alone. In 7 human subjects from the nausea group, the repeat study (16 microgram/kg) after pretreatment with dopamine antagonist (haloperidol, N = 4; fluphenazine, N = 3) resulted in complete blockage of apomorphine-induced AVP release. In rats, which lack an emetic reflex, apomorphine doses of 200 microgram/kg induced only slight increases in PAVP when compared to the response to 16 microgram/kg in man. These studies indicate that stimulation of the emetic reflex results in AVP-release in man. Nausea-mediated AVP release supervenes over concomitant osmolar or pharmacologic (ethanol) inhibition.
在人和大鼠身上研究了恶心和呕吐与血浆血管加压素（PAVP）升高频繁相关的潜在机制。口服水负荷后（N = 16），所有人类受试者的血浆渗透压均下降，14名无症状的人类受试者的PAVP也随之下降。在2名人类受试者中，出现了恶心，且与PAVP升高相关，血压无变化。在乙醇输注期间（N = 28），PAVP受到抑制，除非出现恶心。在4名恶心的人类受试者中，尽管没有血流动力学变化，但PAVP摆脱了乙醇抑制，升至基础水平的10倍。向人类志愿者注射7至24微克/千克剂量的阿扑吗啡，一种强效多巴胺激动剂和催吐剂。3名无症状的人类受试者（7至16微克/千克）的PAVP没有增加。10名人类受试者在接受16微克/千克剂量后出现恶心，随后PAVP显著增加。5名接受16至24微克/千克剂量的人类受试者发生呕吐，随后PAVP水平与仅出现恶心时相似。在恶心组的7名人类受试者中，用多巴胺拮抗剂（氟哌啶醇，N = 4；氟奋乃静，N = 3）预处理后重复研究（16微克/千克），导致阿扑吗啡诱导的抗利尿激素释放完全受阻。在缺乏呕吐反射的大鼠中，与人类16微克/千克剂量的反应相比，200微克/千克剂量的阿扑吗啡仅引起PAVP轻微增加。这些研究表明，催吐反射的刺激导致人类抗利尿激素释放。恶心介导的抗利尿激素释放超越了同时存在的渗透压或药理学（乙醇）抑制作用。
