Why the study?
Does acute and chronic vasodilator therapy alter renin release and blood volume in dogs with heart failure?
Does acute and chronic vasodilator therapy alter renin release and blood volume in dogs with heart failure?
In a canine model of heart failure, neural feedback control of renin release is blunted, yet chronic vasodilator therapy still leads to sustained augmented renin secretion and increased blood volume.
Answers are grounded in this paper and cite their sources.
Caution against assuming blunted renin feedback nullifies vasodilator effects on volume in HF; leaves open translation from canine models to patients.
Neural control of renin secretion is an important physiologic mechanism, but alterations in the central nervous system feedback and control of renin release in heart failure have not been investigated. Accordingly we studied conscious dogs after volume overload (arteriovenous fistula) or chronic myocardial infarction. Acute infusion of nitroprusside was used to test the renin response to arterial hypotension and decreased central blood volume. Hydralazine and prazosin administration were used to test the response to chronic vasodilator administration. After 4 weeks of volume overload or 3 weeks after myocardial infarction, the renin response to a graded hypotensive stimulus was blunted. After 7 days of hydralazine or prazosin administration, plasma renin activity remained elevated and blood volume increased from baseline values. Our results indicate a decrease in the neural feedback control of renin release after chronic volume overload or myocardial infarction. However, chronic vasodilator administration still resulted in sustained augmented renin secretion and an increase in blood volume.
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Engler et al. (1982) studied this question.
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