The main difference between Rothe's and our points of view seemsto be in the extent to which we regard the likely effect ofthe reduction in capacitance caused by venous constriction inhumans to be of physiological importance. We both agree thatveins are the major reservoir of blood and that passive changesin volume, caused by external compression or by changes in flowinto them, are probably more important than changes due to venoconstriction.We also agree that, in humans, it is likely that it is the liverthat forms the major active reservoir. There is, however, astatement at the start of Rothe's article that we would question.He states that "we bipeds... .have evolved active venoconstriction."This may be so, but, as he points out in the same paragraph,"proof of active venoconstriction in humans is sparse." Thisreally is the nub of the problem. A major limitation to ourknowledge of the importance of active venoconstriction in humansis that virtually all the research has been done in animals,mainly dogs (2, 3). In dogs, the largest controllable reservoiris the spleen and this is very much smaller in humans. In absenceof evidence to the contrary, we have worked on the assumptionthat humans behave in the same way as splenectomized dogs, andthis leads us to the conclusion that active venoconstrictionis unlikely to be of major physiological importance (4, 5).In addition, we know that active venoconstriction occurs atlow levels of sympathetic activity (6), which would suggestthat, in supine resting humans, 50% of the response would alreadybe engaged (1), leaving little reserve. However, if Rothe iscorrect and humans have indeed evolved differently from dogs,to facilitate maintenance of their upright posture, active venoconstrictioncould be of more importance. The problem, however, is that atpresent there is no evidence for this and until such evidenceis forthcoming we feel we have to hold to the view that activevenoconstriction is unlikely to have a major role in cardiovascularcontrol.
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