Key result
Inhibition of the renin-angiotensin system, adrenergic nervous system, and renal prostaglandins left plasma renin activity 17 times normal during chronic sodium depletion in conscious dogs.
Renal prostaglandins are important for maintaining renal arteriolar tone and modulating renin release in high renin states, though other mechanisms also contribute significantly.
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No immediate clinical implications for sodium depletion; extends animal evidence for redundant renin regulatory pathways beyond three major systems.
Renal prostaglandins play a role in the control of renin release during chronic sodium depletion, during the acute phase of renovascular hypertension and in experimental low output heart failure in conscious dogs. However, with marked inhibition of the renin-angiotensin system, the adrenergic nervous system and the renal prostaglandins, PRA was still 17 times normal during chronic sodium depletion. After blockade of the adrenergic nervous system and the renal prostaglandins, PRA was 10 times normal during the acute phase of one-kidney renovascular hypertension. These findings demonstrate that other important mechanisms, possibly both the renal vascular receptor (so-called baroreceptor) and the macula densa, were involved. Both PGI2 and PGD2 given intrarenally increased renin release in both filtering and nonfiltering kidneys, but PGI2 was more potent than PGD2. Available evidence favors a role of PGI2 and it seems likely that the site of action is on the JG cells. Indomethacin produced a profound drop in CCr and CPAH during sodium depletion and in experimental heart failure which demonstrates an important role for the renal prostaglandins in the control of renal arteriolar tone. An important incidental finding is that renal denervation combined with propranolol administration decreased PRA from very high levels to normal in 50% of the dogs with experimental low output heart failure and a concurrent striking natriuresis occurred.
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Davis et al. (1980) studied High renin states (chronic sodium depletion, renovascular hypertension, low output heart failure). Prostaglandin inhibition and administration was evaluated on Plasma renin activity and renal hemodynamic function. Inhibition of the renin-angiotensin system, adrenergic nervous system, and renal prostaglandins left plasma renin activity 17 times normal during chronic sodium depletion in conscious dogs.
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