Vasoconstriction and hypersensitivity to vasoactive substances after acute volume expansion in dogs.

Abstract

SUMMARY In a search for factors contributing to the sustained Mood pressure (BP) elevation in acutely volume-loaded animals, dextran dissolved in lactated Ringer's solution (20 ml/kg) was infused into 34 mongrel dogs over a period of 1 hour under pentobarbital anesthesia and changes in bemodynamic and humoral variables were monitored during its infusion and for 3 hours after its infusion. BP elevation during volume loading (from 114 ± 3 to 128 ± 3 [SEM] mm Hg) was attributed to an increase in cardiac output. After volume loading, some dogs maintained BP elevation whereas others did not. The former group showed an increase in total peripheral resistance, demonstrating a transformation of cardiac output to total peripheral resistance as a responsible factor in maintenance of the elevated BP. The plasma levels of norepinephrine, vasopressin, and plasma renin activity were not elevated, indicating that these vasoactive factors were not responsible for elevation of the BP or total peripheral resistance. The changes in the hematocrit, atrial natriuretk factor, urine volume, and urinary sodium excretion were identical in the two groups, and natrluresis was not prominent when total peripheral resistance was high. Pressor responses to norepinephrine and angiotensm n were potentiated 3 hours after stopping Infusion in both groups, but this potentiation was not correlated with the Increase hi total peripheral resistance or mean BP. Thus, acute volume expansion produced resistance-dependent hypertension following the initial volume-dependent hypertension. It is unlikely that a vascular sensitizing natriuretk factor plays a role in the resistance-dependent BP elevation. The mechanism and physiological importance of hypersensitivity to vasoactive substances remain to be elucidated.

Contribution of the baroreflex afferent nerves to the production of vasoconstricted hypertension in volume-expanded dogs.

“…In a previous study on acute volume expansion, 11 we found that all dogs showed cardiac outputdependent hypertension during volume expansion and that blood pressure 3 hours after infusion was stopped was attributed to increase in the TPR. Peripheral sympathetic activity, the reninangiotensin system, and vasopressin did not seem to contribute to this vasoconstriction, and our results provided no evidence against the systemic autoregulation theory.…”

“…This destruction of the barorefiex was confirmed by the complete lack of bradycardia during volume expansion in groups II and IV. Decrease in the TPR may be partly due to decreases in the renin-angiotensin system 11 ' 19 and vasopressin, 11 which would contribute to vascular relaxation. Decrease in viscosity resulting from decrease in the hematocrit 11 would also cause reduction of the calculated TPR.…”

“…These three sham groups were not subjected to volume expansion. The studies on groups I and V were reported previously, 11 but here we include the results with additional data for better understanding of the hemodynamic changes in groups II and IV.…”

Exogenous insulin augments in healthy volunteers the cardiovascular reactivity to noradrenaline but not to angiotensin II.

“…Volume expansion itself is an unlikely explanation for the increase in vascular responsiveness to NA (24). To correct for any change in pressor response during the clamp as a consequence of the infusion of dextrose 20% to maintain euglycemia, all subjects received corresponding amounts of water orally on the day of the control experiment.…”

“…To correct for any change in pressor response during the clamp as a consequence of the infusion of dextrose 20% to maintain euglycemia, all subjects received corresponding amounts of water orally on the day of the control experiment. Moreover, any change in cardiovascular reactivity would have been expected to affect the pressor response to NA and All equally (24). The (43,44).…”