The venous system contains similar to 70% of the blood volume. The sympathe
tic nervous system is by far the most important vasopressor system in the c
ontrol of venous capacitance. The baroreflex system responds to acute hypot
ension by concurrently increasing sympathetic tone to resistance, as well a
s capacitance vessels, to increase blood pressure and venous return, respec
tively. Studies in experimental animals have shown that interference of sym
pathetic activity by an alpha (1)- or alpha (2)-adrenoceptor antagonist or
a ganglionic blocker reduces mean circulatory filling pressure and venous r
esistance and increases unstressed volume. An alpha (1)- or alpha (2)-adren
oceptor agonist, on the other hand, increases mean circulatory filling pres
sure and venous resistance and reduces unstressed volume. In humans, drugs
that interfere with sympathetic tone can cause the pooling of blood in limb
as well as splanchnic veins; the reduction of cardiac output; and orthosta
tic intolerance. Other perturbations that can cause postural hypotension in
clude autonomic failure, as in dysautonomia, diabetes mellitus, and vasovag
al syncope; increased venous compliance, as in hemodialysis; and reduced bl
ood volume, as with space flight and prolonged bed rest. Several alpha -adr
enoceptor agonists are used to increase venous return in orthostatic intole
rance; however, there is insufficient data to show that these drugs are mor
e efficacious than placebo. Clearly, more basic science and clinical studie
s are needed to increase our knowledge and understanding of the venous syst
em. (C) 2001 Elsevier Science Inc. All rights reserved.