This preclinical study suggests that intrarenal angiotensin II mediates the regulation of glomerular filtration rate during nerve stimulation or pressure reduction, but is likely not involved in increased sodium reabsorption.
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Intrarenal angiotensin II may mediate GFR but not sodium reabsorption responses; leaves open translation to human cardiorenal physiology.
The renal responses to low level renal nerve stimulation and reduction in renal perfusion pressure within the autoregulatory range were measured before and after blockade of converting enzyme activity. Experiments were carried out using the unilaterally nephrectomized cat with the nerves of the remaining kidney acutely sectioned. 2. Renal nerves were stimulated to cause a 14% fall in blood flow for 15 min. Glomerular filtration rate was unchanged but sodium excretion and the ratio of sodium clearance to glomerular filtration rate fell significantly. 3. Renal nerve stimulation after blockade of converting enzyme activity was associated with a significant fall in glomerular filtration rate. The reductions in sodium excretion and in the ratio of sodium clearance to glomerular filtration rate were as large as in the absence of the blocking drug. 4. Reduction in renal perfusion pressure was associated with autoregulation of both renal blood flow and glomerular filtration rate but with large falls in sodium excretion and the ratio of sodium clearance to glomerular filtration rate. 5. After blockade of converting enzyme activity blood flow was still autoregulated in response to similar perfusion pressure reduction and glomerular filtration rate fell significantly. The ratio of sodium clearance to glomerular filtration rate, and sodium excretion, were reduced to the same extent as in the absence of the drug. 6. This information suggests that regulation of glomerular filtration rate associated with nerve stimulation or pressure reduction may be mediated by the intrarenal formation of angiotensin II, possibly acting at the efferent arteriole. They also indicate that angiotensin II is probably not involved in causing the increased sodium reabsorption.
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Edward J. Johns (1979) studied this question.
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