Mouse plasma contains a protein antigenically related to mouse protein AA, the principal protein derived from tissue deposits of amyloid substance in mice. In this work the plasma antigen, SAA, was found mainly as a high molecular weight form (2 x 10(5)) residing for the most part in the density interval 1.063-1.21 g/cm3 (high density lipoprotein, HDL); the largest amount of SAA, absolute and relative to total protein, was found in the density interval 1.125-12.1 g/cm3 (HDL3). When apoproteins of the mouse HDL obtained by delipidation of the lipoprotein particles were chromatographed in acid/urea, the antigenic activity appeared in the 10,000- to 15,000-dalton portion of the apoprotein complex. In these characteristics mouse SAA closely resembles human SAA and the behavior of the protein related to amyloid protein AA indicates that is one of the apoproteins of the HDL complex in both species. Therefore we suggest that it be named apoSAA.

Unilateral renal artery plication in dogs reduced renal blood flow by 80% and produced a sustained elevation in arterial pressure whereas plasma renin activity increased for only 4 days. Sodium was retained for 3 days after plication, but this response is similar to that after a sham operation. Of seven dogs studied chronically, elevated arterial pressure was sustained for 27 days or longer in six animals. In three dogs hypertension continued for 2 mo before collateral vessels developed and arterial pressure fell; ligation of these collaterals restored hypertension. Arterial pressure was unaffected by an infusion of [1-sarcosine, 8-alanine] angiotensin II in chronic hypertensive dogs on a normal sodium intake. This angiotensin antagonist lowered arterial pressure after sodium depletion, but became ineffective following rapid sodium repletion. Chronic hypertensive dogs showed normal responses to deoxycorticosterone acetate. These findings suggest that the renin-angiotensin system is not critically involved in maintenace of chronic two-kidney renovascular hypertension in the dog. The data also show that the homeostatic role played by the renin-angiotensin system in the maintenance of arterial pressure remained intact in chronic hypertension.

Estrogens are known to produce sodium retention in laboratory animals (1-4) and in humans (5-7). However, most of the studies on the sodium-retaining effects of estrogens have been concerned with the effects of estrogens injected intramuscularly or subcutaneously during daily sodium balance observations. In an earlier study Dignam et a f . ( 5 ) reported an inability to observe any changes in urinary sodium excretion 60-90 min following the intravenous administration of estradiol in humans, and concluded that estradiol does not alter urinary sodium excretion when administered i.v.; it is possible, however, that the sodiumretaining effects of estrogens are slow in onset. The present study examined the acute effects (over a 4-hr period) of the intravenous administration of estradiol or estriol on the urinary excretion rates of sodium and potassium and the clearance of creatinine in adrenalectomized, ovarectomized dogs. Adrenalectomized dogs were used to prevent adrenal steroid hormones from masking the effects of the estrogens on sodium and potassium excretion rates.Materials and methods. Five female mongrel dogs, ranging from 17.3 to 20.2 kg in weight, were used in these experiments. Each dog was anesthetized with sodium pentobarbital (30 mg/kg body weight), and both adrenal glands and both ovaries were removed by sterile surgical procedures. Prior to surgery, each dog received 100 mg of cortisone orally, 50 mg of cortisone im, and 5 mg of deoxycorticosterone acetate (DOCA) im; following surgery, each dog Research Service (151). Harry S Truman Memorial V . A . Hospital, Columbia, Missouri 65201. received 50 mg of cortisone and 5 mg of DOCA im daily for at least a week, and then was maintained on 25 mg of cortisone and 2.5 mg of DOCA per day. A period of at least 3 weeks was allowed for the dogs to recover from surgery before beginning any experiments. Completeness of the adrenalectomy was verified by placing each dog in a metabolic cage, feeding it a diet of 65 mequiv of sodium per day, and stopping all steroid maintenance for 4 days; a negative sodium balance during this time was used as an indication of complete adrenalectomy .Three separate experiments were performed on each dog, and at least 10 days were allowed between experiments for each animal. The design of the three experiments was identical, except that in one experiment the dog received an acute injection of estradiol, in another experiment estriol was administered, and in the third experiment the dog received the vehicle alone. The order of these three experiments was randomized.Four days prior to an experiment, each dog was placed on a diet containing 200 mequiv of sodium and 24 mequiv of potassium per day, and steroid maintenance was reduced to 5 mg of cortisone daily with no DOCA administration; this was essentially the same assay preparation used by Liddle et al. (8). The last feeding prior to an experiment occurred exactly 10 hr before beginning the experiment. On the morning of an experiment, a catheter of polyethylene tubing (PE 50) was inserte...