NO and ANP both increase renal Na excretion in non-pregnant individuals by acting in the kidney tubules. They act primarily through increasing cGMP levels as a second messenger in the kidney tubules. cGMP is normally degraded by cGMP phosphodiesterases in the kidney tubules. During normal pregnancy in rats and in non-pregnant rats with chronic vasodilation, two sodium retaining changes occur in the renal collecting duct: decreased sodium reabsorption and increased potassium secretion. These changes are believed to be controlled by decreased levels of angiotensin II and aldosterone.
1 What are the actions of NO and atrial natriuretic peptide.pdf
1. 1. What are the actions of NO and atrial natriuretic peptide (ANP) on renal Na excretion by the
normal, non-pregnant individual? Where is the major site of action of ANP and NO in the kidney
tubule? What is the 2
nd
messenger system that mediates the renal tubular action of both NO and
ANP? How is this 2
nd
messenger normally degraded in the kidney tubules?
2. Describe 2 net Na retaining changes that occur in the renal medullary collecting duct of both the
normal pregnant rat and in the normal non-pregnant, chronically vasodilated rat (using nifedepine).
What is the current hypothesis on the role of angiotensin II and aldosterone in controlling each of
these changes
