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Uteri of pregnant and nonpregnant women contain enzymic activities which inactivate oxytocin. A potent enzyme, which has been partially purified from uterine homogenates, cleaves the prolyl-leucyl peptide bond of oxytocin. This findinig associates for the first time the release of the dipeptide leucylglycinamide with the degradation of neurohypophyseal hormones.

In a typical experiment sweating was induced in symmetrical forearm sites by intradermal injection of B-methylacetylcholine hydrochloride (Mecholyl), 2 mg. in 0.5 ml. of isotonic saline. The collection of sweat by a standard procedure (2) has been described previously.In brief, the unit used for collection of sweat consisted of an aluminum ring cemented to the skin and an aluminum cover assembly containing a rubber compression gasket to insure a gas-tight seal. The chamber formed when the lid was fixed into the ring had an internal diameter of 25 mm. and a height of 1 mm. The sweat was absorbed into one or more filter paper discs, its quantity determined by weight and its content of sodium and potassium by flame photometry using lithium as an internal standard.1 This work was presented in part at the Fall Meeting of the American Physiological Society, Madison, Wisconsin, 1954.In each experiment there were 5 to 20 consecutive collection periods each lasting from 10 to 30 minutes. In all, 53 experiments were completed and 557 samples of sweat collected and analyzed for sodium. Of this group, 362 samples (32 experiments, 9 subjects) were also analyzed for potassium. Most of the collections of sweat were obtained from the proximal medioventral surface of the forearm, while in a few experiments sites on the arms, thighs, abdomen and back were used. During the tests one or more samples of blood were drawn from an antecubital vein, heparinized, centrifuged immediately and the plasma analyzed for sodium and potassium in the same manner as the samples of sweat.Two experiments served to estimate the precision of the measurements: A solution containing 122 mEq. per L. of sodium and 10 mEq. per L. of potassium was delivered onto filter paper discs in 20 weighing vessels. Each of five vessels received approximately 0.2 ml. of the solution (Na 24 /sEq., K 2.0 *Eq.); five received 0.1 ml.(Na 12 ,uEq., K 1.0 /AEq.); five received 0.05 ml. (Na 6 #Eq., K. 0.5 AEq.); and the remaining five vessels received 0.025 ml. (Na 3 ,uEq., K 0.25 usEq.). In the second experiment a solution containing 33 mEq. of sodium and 10 mEq. of potassium per liter was delivered onto discs in 15 weighing vessels. Five of the vessels received 0.05 ml. (Na 1.6 AEq., K 0.5 jEq.) five received 0.025 ml. (Na 0.8 ,uEq., K 0.25 JAEq.) and five received 0.125 ml. (Na 0.4 uEq., K 0.13 uEq.). The size of each sample was measured by weight and the quantity of sodium and potassium determined by flame photometry just as in the routine procedure. The results showed that the recovery became less precise with decrease in the absolute quantities of sodium and potassium brought to analysis (Table I). The recoveries of 3 /AEq. of sodium and 0.5 uEq. of potassium averaged 101 + 3.1 per cent and 101.5. ± 5.1 per cent respectively. These are the quantities of sodium and potassium that would be encountered in 50 mg. of sweat containing 60 mEq. per L. of sodium and 10 mEq. per L. of potassium. RESULTS SodiumThe concentration of sodium, SNa, rose toward a maximum, S'Na, with inc...

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In the recent literature there has been a revived interest in the role of the kidney in congestive heart failure, particularly with reference to the mechanism of sodium retention and edema formation (1-12). In view of the contention by Blake and his associates (13) that a rise in renal venous pressure in the dog may prevent excretion of sodium without altering renal blood flow or filtration rate as measured by clearance methods, and its possible implications in man, it was felt that actual measurement of renal venous pressure in subjects with congestive heart failure was indicated. A review of the literature revealed that there were no previous measurements of renal venous pressure in normal human subjects other than the six figures cited by Bradley and Bradley (14) who, for their purposes were more concerned with comparative pressures before and during abdominal compression than with a precise set of normal values. The purpose of this communication is 1) to establish a standard technique and set of normal values for renal venous pressure measurements in man, and 2) to report on renal venous pressure in patients with congestive heart failure, discussing the significance and the hemodynamic mechanisms involved. MATERIALS AND METHODSThe control subjects were all patients in Bellevue Hospital with no evidence of cardiovascular or renal disease. Most of them had benign lesions, such as leg ulcers, or were convalescent and about to be discharged from the hospital. The subjects with congestive heart failure had such evidence of right-sided failure as ankle edema, distended liver, pulsating neck veins and increased peripheral venous pressure as measured on the ward; the degree of left-sided failure was variable.