Knapp M F, Hicks M N, Linden R J, Mary D A
J Endocrinol. 1986 May;109(2):R5-8. doi: 10.1677/joe.0.109r005.
To determine whether natriuresis attributable to atrial natriuretic peptides (ANP) is obtained in response to atrial stretch after blockade of the afferent input and reflex diuresis from atrial receptors, urine flow and sodium excretion were measured in response to distension of a balloon in the left atrium with the vagi at 37 and 9 degrees C. It is known that during such a distension ANP plasma concentration is increased by the same amount whether or not the afferent vagal fibres are intact. In 11 chloralose anaesthetized dogs 22 distensions with the vagi at 37 degrees C increased urine flow 117.5% and increased sodium excretion 28.7%. In 11 distensions with the vagi at 9 degrees C, urine flow did not change but sodium excretion decreased significantly (-20.9%). Thus natriuresis could not be demonstrated in response to atrial stretch in anaesthetised dogs after blockade of the atrial receptor reflex. These results imply that under these conditions, in which ANP is reportedly released into plasma, ANP is not acting as a hormone. The results must call into question the suggestion that ANP is released into plasma in a concentration capable of causing a natriuresis as its normal physiological function.
为了确定在阻断心房受体的传入输入和反射性利尿后，心房拉伸是否会引起心房利钠肽（ANP）介导的利钠作用，在37℃和9℃下，测量了11只氯醛糖麻醉犬在左心房球囊扩张时的尿流量和钠排泄量，同时测量了迷走神经的反应。已知在这种扩张过程中，无论传入迷走神经纤维是否完整，ANP血浆浓度的增加量是相同的。在37℃下对11只氯醛糖麻醉犬进行22次迷走神经完整的球囊扩张，尿流量增加了117.5%，钠排泄量增加了28.7%。在9℃下进行11次球囊扩张，尿流量没有变化，但钠排泄量显著下降（-20.9%）。因此，在阻断心房受体反射后，麻醉犬对心房拉伸没有出现利钠作用。这些结果表明，在据报道ANP释放到血浆中的这些条件下，ANP并没有起到激素的作用。这些结果必然会让人质疑ANP以能够引起利钠作用的浓度释放到血浆中作为其正常生理功能的这一观点。
