We tested the hypothesis that arterial baroreceptor discharge remains constant during nonhypotensive hemorrhage. Aortic baroreceptor activity was recorded from anesthetized dogs during slow, continuous hemorrhage until 24 ml blood/kg body wt had been removed. The relationship between simultaneously recorded hemodynamic variables and single-unit aortic baroreceptor activity was evaluated by a unique computer program that sampled all variables 500 times/s and analyzed data from each consecutive cardiac cycle throughout the entire experiment. In three hemorrhages performed on three dogs, aortic blood pressure did not decrease during the experiment (nonhypotensive hemorrhage), but aortic nerve activity decreased progressively when data from individual cardiac cycles having identical mean aortic pressures were compared. Reduced baroreceptor activity correlated closely with progressive reductions in pulse pressure. In other hemorrhages, mean aortic pressure decreased by a variable amount; decreases in recorded single-unit baroreceptor activity occurred during each of these hemorrhages also. In summary, hemorrhage consistently caused decreases in the activity of aortic baroreceptors regardless of whether mean aortic pressure decreased or remained constant during hemorrhage. We conclude that experimental techniques employing nonhypotensive hemorrhage do not provide an effective method for selectively studying reflexes from cardiopulmonary receptors in the absence of changes in arterial baroreceptor input.

Hemodynamic responses to varying intravenous infusion rates of vasopressin were studied in two groups of dogs; one group was cardiac denervated and the other sham operated. Vasopressin given at 200, 1,000, and 5,000 fmol X kg-1 X min-1 produced increases in aortic pressure that were significantly greater in cardiac-denervated dogs than in sham-operated dogs. The augmented pressor response in cardiac-denervated dogs was associated with greater increases in total peripheral resistance in this group; decreases in cardiac output were similar in the two groups of dogs. Vasopressin decreased heart rate significantly in each group, but the magnitude of the decrease was significantly smaller in cardiac-denervated dogs. In contrast to these results, the intravenous infusion of phenylephrine or angiotensin II in other experiments on the same dogs produced comparable increases in aortic pressure in each group. These results are consistent with earlier evidence indicating that vasopressin elicits more effective reflex mechanisms to attenuate the increases in blood pressure caused by its direct vasoconstrictor action than do other vasoconstrictor agents, such as angiotensin II and phenylephrine. Since the infusion of vasopressin produced a greater increase in arterial blood pressure in cardiac-denervated dogs than it did in sham-operated control dogs, it appears that at least part of the unique action of vasopressin may be mediated by the potentiation of a peripheral vasodepressor reflex arising from cardiac receptors.