Abstract

To examine the possible activation of prorenin in the circulation, recombinant rat prorenin was intravenously given to pentobarbital-anesthetized rats. Bolus injection of prorenin at the dose of 100 micrograms angiotensin I (ANG I).h-1.kg-1 into Wistar rats, leading to a 15-fold increase in plasma prorenin concentrations (from 27 +/- 6 to 393 +/- 75 ng ANG I.h-1.ml-1) at 5 min after the injection, did not affect blood pressure, heart rate, and plasma active renin concentrations throughout experiments. On the other hand, the administration of active renin at the dose of 1, 3, and 10 micrograms ANG I.h-1.kg-1 increased mean blood pressure of Wistar rats by 8 +/- 2, 15 +/- 2, and 27 +/- 4 mmHg, respectively. Similar results were obtained in Wistar rats at 18 h after bilateral nephrectomy. These results confirmed no activation of prorenin in the circulation of normotensive rats. The activation of prorenin was also examined on both stroke-prone spontaneously hypertensive rats (SHRSP) and 18 h-nephrectomized SHRSP. There was no rise in blood pressure or plasma active renin concentrations in both groups of SHRSP after injection of prorenin. Thus the elevated plasma active renin in SHRSP [Shibota, M., A. Nagaoka, A. Shino, and T. Fujita. Am. J. Physiol. 236 (Heart Circ. Physiol. 5): H409-H416, 1979] seems to be caused by the enhanced release of active renin from the kidney rather than the activation of circulating prorenin.

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