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No Effect of Short Term Angiotensin II Infusion on Plasma Renin Substrate Levels in Man^*

Unit of Clinical Physiology, the Minerva Foundation Institute for Medical Research (K.M., F.F., I.T.), Fourth Department of Medicine, Helsinki University Central Hospital (K.M., F.F., I. T.) Helsinki, Finland
The Deaconess Medical Centre (K.J.T.) Helsinki, Finland

Address all correspondence and requests for reprints to: Kaj Metsärinne, M.D., Minerva Institute for Medical Research, P.O. Box 819, SF-00101 Helsinki 10, Finland.

We studied the effect of angiotensin II (A-II) infusion (4 ng/kg BW·min) on plasma renin substrate (RS) levels and PRA in five normal men during normal, diureticstimulated, and enalapril-interrupted function of the renin-angiotensin system. A-II infusion increased (15–25%) both systolic and diastolic blood pressure in the normal state and during angiotensin-converting enzyme inhibition, whereas the increase during diuretic-stimulated renin-angiotensin system function was less. The plasma RS concentration was measured by both direct and indirect RIA. The mean basal plasma RS levels, measured with direct assay, were 1516 ± 150 (SE) in the normal state, 1566 ± 150 after diuretic administration, and 1650 ± 133 nmol/L after enalapril administration. The corresponding mean basal plasma RS levels measured with the indirect assay were 1073 ± 100, 1031 ± 57, and 902 ± 78 nmol/L, respectively. Plasma RS levels did not change during or after the A-II infusions, whereas PRA decreased significantly in all experimental conditions. The results suggest that A-II exerts no direct stimulatory effect on hepatic release of RS. Thus, A-II appears not to be important in the short term regulation of plasma RS levels.

^* This work was supported by grants from the Finska Läkaresällskapet, the Oskar Öflund Foundation, the Nordisk Insulinfond, and the Finnish-Norwegian Medical Foundation, Helsinki. Institutional support was received from the Sigrid Jusélius Foundation, Helsinki.

Received June 16, 1988.