Arterial pulse pressure and vasopressin release during graded water immersion in humans

Abstract

Previous results indicate that arterial pulse pressure modulates release of arginine vasopressin (AVP) in humans. The hypothesis was therefore tested that an increase in arterial pulse pressure is the stimulus for suppression of AVP release during central blood volume expansion by water immersion. A two-step immersion model ( n = 8) to the xiphoid process and neck, respectively, was used to attain two different levels of augmented cardiac distension. Left atrial diameter (echocardiography) increased from 28 ± 1 to 34 ± 1 mm ( P < 0.05) during immersion to the xiphoid process and more so ( P < 0.05), to 36 ± 1 mm, during immersion to the neck. During immersion to the xiphoid process, arterial pulse pressure (invasively measured in a brachial artery) increased ( P < 0.05) from 44 ± 1 to 51 ± 2 mmHg and to the same extent from 42 ± 1 to 52 ± 2 mmHg during immersion to the neck. Mean arterial pressure was unchanged during immersion to the xiphoid process and increased during immersion to the neck by 7 ± 1 mmHg ( P < 0.05). Arterial plasma AVP decreased from 2.5 ± 0.7 to 1.8 ± 0.5 pg/ml ( P < 0.05) during immersion to the xiphoid process and significantly more so ( P < 0.05), to 1.4 ± 0.5 pg/ml, during immersion to the neck. In conclusion, other factors besides the increase in arterial pulse pressure must have participated in the graded suppression of AVP release, comparing immersion to the xiphoid process with immersion to the neck. We suggest that when arterial pulse pressure is increased, graded distension of cardiopulmonary receptors modulate AVP release.