Why the study?
Does vasopressin antagonism or captopril alter hemodynamics in a rat model of high output heart failure?
Does vasopressin antagonism or captopril alter hemodynamics in a rat model of high output heart failure?
In a rat model of high output heart failure, the renin-angiotensin system and vasopressin are activated, with captopril reducing mean arterial pressure while vasopressin antagonism showed no significant hemodynamic effect.
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Cautions against acute hemodynamic benefit from vasopressin antagonism in HF; leaves open its role in human disease pending clinical trials.
We studied the hemodynamic effects of vasopressin and the renin-angiotensin system in an animal model of high output heart failure in conscious rats (aorto-caval fistula). We found significantly elevated levels of plasma renin concentration (p less than 0.025), norepinephrine (p less than 0.02), and up to 4 to 5 times higher values of vasopressin (p less than 0.002) in the rats with heart failure as compared with control animals. In contrast to the control rats that had a normally functioning osmoreceptor system, we found an inverse relationship between plasma osmolality and arginine vasopressin in the rats with heart failure in association with edema. Using a specific antagonist of the pressor activity of vasopressin, we found no significant effect on heart rate, mean arterial pressure, cardiac output (thermodilution), and peripheral vascular resistance in the control animals and in the rats with aorto-caval fistula. Captopril resulted in a significant fall of mean arterial pressure in the rats with shunt (p less than 0.001). The coincidence of high values of vasopressin and, in a number of animals, low plasma osmolalities and edema suggests a role of vasopressin in the formation of edema and in the development of "dilutional hypo-osmolality."
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Riegger et al. (1985) studied this question.
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