Burrell L M, Lambert H J, Baylis P H
Department of Medicine, Medical School, Newcastle upon Tyne, UK.
Clin Endocrinol (Oxf). 1991 Sep;35(3):229-34. doi: 10.1111/j.1365-2265.1991.tb03527.x.
To assess whether drinking and oropharyngeal stimuli mediate the release of plasma atrial natriuretic peptide (ANP) in man.
Hypertonic saline was infused into male volunteers to stimulate thirst. In order to avoid any effect of volume change on ANP release, the studies were performed with the subject in the seated position.
Seated normal male volunteers (n = 6) were infused with hypertonic saline at a rate of 0.06 ml/kg/min for 90 min on two separate occasions. After a 15-min equilibrium period, subjects were allowed to drink for the following 45-min period on one occasion, but no drinking was permitted on the other occasion.
Aliquots of blood were withdrawn at 30-min intervals for 90 min during hypertonic saline infusion, and +3, 6, 9, 12, 15, 30 and 45 min during the drinking/control period for the measurement of plasma ANP, plasma vasopressin, plasma osmolality, serum sodium and haematocrit; thirst was assessed at the same time points using a visual analogue scale. Blood pressure was measured at 15-min intervals.
Hypertonic saline infusion induces increases in plasma vasopressin, plasma osmolality, serum sodium and thirst appreciation (P less than 0.005), and blood volume (P less than 0.05) on both study days; there was no increase in plasma ANP during hypertonic saline infusion. During the drinking period there was the expected decrease in plasma vasopressin (P less than 0.01), plasma osmolality (P less than 0.05), serum sodium (P less than 0.05) and thirst appreciation (P less than 0.01); no significant changes occurred in plasma atrial natriuretic peptide, mean arterial blood pressure or haematocrit during either the drinking or the control period.
The drinking-mediated inhibition of thirst appreciation and plasma vasopressin is not associated with any change in plasma ANP concentrations; it does not appear that oropharyngeal stimuli contribute to the release of ANP in man.
评估饮水和口咽刺激是否介导人体血浆心钠素(ANP)的释放。
向男性志愿者输注高渗盐水以刺激口渴感。为避免容量变化对ANP释放产生任何影响,研究在受试者坐位时进行。
坐位正常男性志愿者(n = 6),在两个不同时间段以0.06 ml/kg/分钟的速率输注高渗盐水,持续90分钟。在15分钟的平衡期后,其中一次在接下来的45分钟内允许受试者饮水,另一次则不允许饮水。
在输注高渗盐水期间,每隔30分钟抽取血样,共90分钟;在饮水/对照期的+3、6、9、12、15、30和45分钟抽取血样,用于测量血浆ANP、血浆血管加压素、血浆渗透压、血清钠和血细胞比容;使用视觉模拟量表在相同时间点评估口渴感。每隔15分钟测量血压。
在两个研究日,输注高渗盐水均导致血浆血管加压素、血浆渗透压、血清钠和口渴感增加(P < 0.005),以及血容量增加(P < 0.05);输注高渗盐水期间血浆ANP无增加。在饮水期,血浆血管加压素(P < 0.01)、血浆渗透压(P < 0.05)、血清钠(P < 0.05)和口渴感(P < 0.01)如预期下降;在饮水期或对照期,血浆心钠素、平均动脉血压或血细胞比容均无显著变化。
饮水介导的口渴感和血浆血管加压素抑制与血浆ANP浓度的任何变化均无关;口咽刺激似乎并未促使人体释放ANP。