Hypotension produced by vagal block in primates

In many species, the vagus has been reported to contain afferents that inhibit sympathetic tone. Vagal block (VB) increases blood pressure in both the intact and sinoaortic-denervated (SAD) dog. In the present study, VB was produced in intact and SAD monkeys by infiltrating the vagi with a local anesthetic. This was done in conjunction with blood volume expansion or head-out water immersion. The cardiovascular parameters monitored were heart rate (HR), blood pressure (BP), and left atrial pressure (LAP). VB decreased BP (-13 ± 2.8 mmHg) in the control group and the SAD animals (-47 ± 6.7 mmHg) without changing HR. Volume expansion decreased BP in the SAD animals (-6 ± 3.4) but not in the intact monkeys (1.8 ± 2.27), whereas HR did not change. Volume expansion after VB increased BP in both the SAD and the intact animals while producing a decrease in HR. Volume expansion caused LAP to increase in all groups (SAD 13.9 ± 6.3; control VB 11.6 ± 1.8, control 9.3 ± 0.89, SAD VB 7.66 ± 3.46). Immersion in the VB SAD animals increased BP to a greater extent than volume expansion. VB in the monkey must be removing input from peripheral receptors, which maintain sympathetic tone. Because immersion with VB increases BP more than volume expansion with VB, it is concluded that VB causes predominantly venous pooling. Because cardiopulmonary receptors generally inhibit sympathetic tone, it is concluded that those receptors responsible for the observed hypotension are located in the venous system, probably in the chest or the abdominal cavity.