AJP - Heart and Circulatory Physiology, Vol 243, Issue 6 970-H973, Copyright © 1982 by American Physiological Society
Response of vasopressin and norepinephrine to lower body negative pressure in humans
S. R. Goldsmith, G. S. Francis, A. W. Cowley and J. N. Cohn
To examine the contributions of cardiopulmonary and sinoaortic
baroreceptors to the nonosmotic release of arginine vasopressin (AVP) in
normal humans, we subjected nine individuals without evidence of
hypertension or heart disease to graded, lower body negative pressure
(LBNP). We also studied the effects of this maneuver on sympathetic nervous
system activity using plasma norepinephrine (NE) as an index. Heart rate
(HR), mean arterial pressure (MAP), pulse pressure (PP), and central venous
pressure (CVP) were measured in the control state and during two
consecutive levels of increasingly intense LBNP. At each stage blood was
sampled for AVP and NE. AVP was analyzed by radioimmunoassay, NE by a
radioenzymatic method. During the first level of LBNP, CVP decreased with
no change in HR, MAP, or PP. NE increased from 147 +/- 47 to 212 +/- 53
(SD) pg/ml, P less than 0.01, whereas AVP (5.0 +/- 1.0 pg/ml) did not
change. With increased suction CVP fell further, HR increased, and PP
narrowed, but MAP did not change. NE further increased to 291 +/- 58 pg/ml
(P less than 0.01), but AVP still did not change significantly. One subject
became markedly hypotensive, and his AVP increased from 2.6 to 81 pg/ml. A
fall in CVP that results in sympathetic activation presumably via
cardiopulmonary receptors does not therefore increase AVP levels; a further
fall in CVP that leads to modest unloading of the sinoaortic baroreceptor
and further increased sympathetic activity also fails to stimulate AVP.
Hypotension, however, is accompanied by a rapid and profound increase in
circulating AVP.
