Arterial pulse pressure and vasopressin release during graded water immersion in humans
1 Danish Aerospace Medical Centre of Research, National University Hospital, Rigshospitalet, Copenhagen; and 2 Department of Medical Physiology, Panum Institute, University of Copenhagen, Copenhagen; and 3 Department of Internal Medicine and Endocrinology, Herlev Hospital, University of Copenhage...
Saved in:
Published in | American journal of physiology. Regulatory, integrative and comparative physiology Vol. 278; no. 6; pp. 1583 - R1588 |
---|---|
Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
01.06.2000
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | 1 Danish Aerospace Medical Centre of Research,
National University Hospital, Rigshospitalet, Copenhagen; and
2 Department of Medical Physiology, Panum
Institute, University of Copenhagen, Copenhagen; and
3 Department of Internal Medicine and
Endocrinology, Herlev Hospital, University of Copenhagen, Herlev,
Denmark
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.
blood pressure; sympathetic nervous system; baroreceptors; cardiac
output |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0363-6119 1522-1490 |
DOI: | 10.1152/ajpregu.2000.278.6.r1583 |