Key result
Atrial natriuretic factor infusion blunts hypotension-induced plasma renin activity increases independent of neural stimulation.
Why the study?
The mechanism by which atrial natriuretic factor inhibits the renin response to hypotension, independent of neural stimulation, was unclear.
Does atrial natriuretic factor inhibit the renin response to hypotension independently of neural stimulation in conscious dogs?
Does atrial natriuretic factor inhibit the renin response to hypotension independently of neural stimulation in conscious dogs?
ANF inhibits the renin response to hypotension independently of neural stimulation and attenuates reflex increases in AVP and ACTH at higher doses, while inhibiting aldosterone synthesis at very low doses.
Answers are grounded in this paper and cite their sources.
ANF may blunt reflex renin activation in low-pressure states; leaves open relevance to human cardiorenal syndromes.
We have reported that infusion of atrial natriuretic factor (ANF) inhibited the rise in plasma renin activity (PRA) in response to constriction of the abdominal aorta to cause a reduction in renal perfusion pressure (RPP). To evaluate the effect of ANF on neural control of renin release, acute thoracic inferior vena caval constriction (TIVCC) was performed in conscious dogs to reduce arterial pressure by 25% of control and stimulate PRA by a reflex increase in renal nerve activity and a reduction in RPP. Propranolol was used to block neural stimulation of renin release. TIVCC caused significant increases in PRA, plasma aldosterone, arginine vasopressin (AVP), and adrenocorticotropic hormone (ACTH) concentrations. The increase in PRA was significantly reduced by the infusion of either ANF at 20 ng.kg-1.min-1 or propranolol. The combined infusion of ANF and propranolol produced an additive and complete inhibition of the renin response to TIVCC; therefore the effect of ANF is independent of neural stimulation of renin release. ANF at 20 ng.kg-1.min-1 also inhibited increases in aldosterone, AVP, and ACTH, but ANF at 5 ng.kg-1.min-1 only affected the aldosterone response to TIVCC. Therefore ANF inhibits angiotensin II-stimulated aldosterone synthesis and/or secretion at very low doses and at higher doses attenuates reflex increases in AVP and ACTH caused by hypotension.
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Scheuer et al. (1989) studied Hypotension. Atrial natriuretic factor (ANF) vs. Control (TIVCC alone) and Propranolol was evaluated on Plasma renin activity (PRA). Infusion of atrial natriuretic factor at 20 ng/kg/min significantly reduced the increase in plasma renin activity caused by hypotension, independent of neural stimulation.
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