We measured plasma arginine vasopressin (AVP) and plasma renin activity (PRA) during continuous hemorrhage in cardiac-denervated and sham-operated conscious dogs. Hemorrhage produced comparable decreases in aortic pressure, cardiac output, stroke volume, pulmonary arterial pressure, and left and right atrial pressures in each group of dogs. After 10 ml blood/kg body wt had been removed, AVP was increased in sham-operated dogs (P less than 0.05) but not in cardiac-denervated dogs. After 20 and 30 ml blood/kg body wt had been removed, AVP was increased in all dogs, but the response was markedly attenuated in cardiac-denervated dogs. Hemorrhage at 10 and 20 ml/kg caused comparable increases in PRA in each group of dogs. However, at 30 ml/kg hemorrhage the increase in PRA was significantly higher in cardiac-denervated dogs than in sham-operated dogs. Our results suggest that cardiac receptors play a dominant role in mediating the release of AVP during hemorrhage in conscious dogs. In contrast, we found no evidence for a dominant role of cardiac receptors in mediating renin secretion during hemorrhage.

We monitored cardiovascular and renal function in conscious dogs with surgically denervated hearts during two experimental procedures: 1) inflation of a balloon in the left atrium and 2) intravascular volume expansion. The results obtained were compared with results from identical experiments on sham-operated control dogs. Left atrial balloon inflation in the sham-operated dogs produced an increase in left atrial pressure, heart rate, urine flow, and sodium excretion; central venous pressure decreased. These changes were absent in the cardiac-denervated dogs. Infusion of 6% dextran in isotonic saline (16% of estimated blood volume) increased the heart rate significantly in the control dogs but not in the cardiac-denervated dogs; other hemodynamic measurements were comparable in the two groups. Urine flow and sodium excretion increased significantly in both the cardiac-denervated and control dogs; the responses did not differ significantly between the two groups. These experiments demonstrate that inflation of a balloon in the left atrium of a conscious dog elicits diuretic and natriuretic responses that are dependent on intact cardiac neural pathways, presumably specifically dependent on afferent neural impulses from left atrial receptors. On the other hand, an increase in circulating blood volume induced by the intravenous infusion of an isotonic, isoncotic solution elicits diuretic and natriuretic responses in the cardiac-denervated dog that are similar to the renal responses produced in a control dog. Thus, although cardiac receptors are capable of eliciting reflex changes in both hemodynamics and renal function, it is not clear what role they play in mediating the renal responses evoked by increases in blood volume.

We measured hemodynamics and renal function in conscious dogs while partially obstructing blood flow at various sites within the thorax. Inflation of a balloon in the left atrium increased left atrial pressure (LAP) by 9 mmHg and caused a parallel increase in pulmonary arterial pressure (PAP); heart rate, arterial pressure, and total peripheral resistance increased; stroke volume and right atrial pressure decreased; and cardiac output remained unchanged. The increase in LAP was accompanied by a fourfold increase in urine flow and a threefold increase in sodium excretion. Plasma vasopressin (AVP) and renin activity (PRA) decreased. On the other hand, partial occlusion of the pulmonary veins or the main pulmonary artery produced similar increases in PAP without affecting LAP, systemic hemodynamics, renal function, or plasma AVP. Similarly, inflation of a balloon in the right atrium failed to alter renal function, plasma AVP, or PRA. Finally, constriction of the thoracic inferior vena cava decreased LAP and increased PRA. In summary, these data emphasize that inflation of a balloon in the left atrium of the conscious dog produces a composite response consisting of alterations in cardiovascular function, renal function, and circulating hormones. Moreover, our data indicate that the response is mediated by a reflex initiated from receptors located in the left atrium; we detected no evidence that receptors located in the pulmonary vasculature or right heart contribute to this response.

Hypoxia and hypercapnia have been shown to cause an increase in the concentration of vasopressin in plasma, but their effects on vasopressin in cerebrospinal fluid (CSF) are not known. In addition, the effect of metabolic acidosis on plasma and CSF vasopressin has not been reported. In this study, plasma and CSF vasopressin levels were measured in anesthetized dogs subjected to either hypoxia, hypercapnia, or metabolic acidosis. Rate and depth of respiration were closely regulated with the aid of muscle paralysis and mechanical ventilation. Vasopressin increased markedly in both plasma and CSF during severe hypoxia (10% O2) and during hypercapnia (10% CO2) but did not change during either mild (15% O2) or moderate (12.5% O2) hypoxia. Although mild hypoxia by itself did not affect either plasma or CSF vasopressin, it did potentiate the increase in plasma and CSF vasopressin that was induced by severe hypercapnia, thus suggesting that hypoxia and hypercapnia may exert synergistic effects on vasopressin secretion. Metabolic acidosis produced by slow intravenous infusion of 1 N hydrochloric acid decreased arterial pH to values comparable to those induced by hypercapnia and increased vasopressin in plasma; CSF vasopressin was unchanged. These results are consistent with the concept that the source of vasopressin secreted into plasma may be different from that secreted into CSF.

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.