T-kininogen in rat plasma after nephrectomy and other surgical traumas.

Plasma kininogen is known to increase after nephrectomy in the rat, and we studied the type of kininogen responsible for the increase. Total kininogen in plasma was estimated by measuring the kinins released after incubation with an excess of trypsin, and expressed as micrograms bradykinin equivalents per ml of plasma (bk eq/ml). Plasma Kininogen in 24-hournephrectomized rats increased five-fold over the control values (16.4 +/- 0.8 vs 3.0 +/- 0.3 micrograms bk eq/ml; p less than 0.001). However, we found that the increase in total kininogen was not due to nephrectomy per se, but rather to surgery, since similar increases were found after 24 hours in shamnephrectomized rats (15.5 +/- 0.5 micrograms bk eq/ml), and in rats with a catheter implanted into the carotid artery (14.2 +/- 1.7 micrograms bk eq/ml). The increase in kininogen was proportional to the extent of the surgery since simple exposure of the carotid artery increased kininogen to 5.3 +/- 0.5 micrograms bk eq/ml, and sham carotid cannulation to 8.3 +/- 0.4 micrograms bk eq/ml. Anesthesia without surgery did not affect plasma kininogen concentration. To determine whether the adrenals or the pituitary glands are involved in mediating the changes, plasma kininogen was measured after adrenalectomy and hypophysectomy. Total kininogen in plasma of 24 hour-adrenalectomized rats was sevenfold higher than that of intact rats, also higher than the total kininogen in plasma of sham-adrenalectomized rats (21.6 +/- 1.7 vs. 16.5 +/- 1.1 micrograms bk eq/ml; p less than 0.05). The role of the hypophysis was studied by nephrectomizing rats 12 days after they had been hypophysectomized. Total plasma kininogen in the control group of rats was still four-fold higher than in intact rats. Twenty-four hours after nephrectomy, a further two-fold increase was obtained (12.7 +/- 1.6 vs. 25.6 +/- 2.0 micrograms bk eq/ml; p less than 0.001). Kinins released by trypsin from plasma of the various groups of rats were separated by reserve-phase (C18) high pressure liquid chromatography (HPLC), and then quantitated. Only T-kinin was found to be increased. Unknown kinins, which were partially converted to T-kinin by increasing trypsin concentration from 10 to 80 mg/ml plasma, were also found by HPLC. The results indicate that surgical trauma induces a marked increase in the concentration of T-kininogen in rat plasma. Neither the hypophysis, nor the adrenals seem to be involved in mediating the increase in T-kininogen.