Comparison of hypertension treatment on and off the worksite.

A survey was carried out in two plants in Haifa, Israel on the prevalence of treated and controlled hypertension. In both plants hypertension treatment was being carried out by family physicians at regular family clinics. In factory A, after screening, a programme of follow-up and treatment by the plant doctor and nurse was introduced. In factory B all hypertensives continued to be referred to their family physician for treatment and follow-up. One year later all previously detected hypertensives were reassessed. The percentage of treated hypertensives had increased from 70.9% to 100% in factory A, and from 55.0% to 62.1% in factory B. The percentage of controlled hypertensives among those treated had increased from 52.7% to 83.7% in factory A, and from 28.0% to 38.9% in factory B. Thus, the percentage of all hypertensives who were controlled increased from 37.3% to 83.7% in Factory A and from 15.4% to 24.1% in Factory B. The introduction of on-site treatment and follow-up of hypertension by a doctor-nurse team was associated with marked improvement of all aspects of hypertensive care.

The effect of main artery occlusion of one kidney on blood pressure of dogs.

Occluding the main artery of one kidney in each of six dogs resulted in an average increase in the renin concentration of the peripheral blood from the original 0.040 to 0.198 milliunit/ml of serum. During the same time (3-4 days), the occlusion also resulted in a significant rise of directly measured mean systemic blood pressure from an average basal level of 104 to 139 mm Hg.

Kinetics of renin-antirenin reaction: micromethods for the assay of renin and antirenin.

Indirect micromethods were designed for the assay of human renin (lower limit 0.25 times 10-4 U and of antirenin to human renin (lower limit 3 times 10-4 U), with the rat used for the bioassay of the angiotensin produced by the action of renin on renin substrate. This made possible the assay of unusually small amounts (0.01 mu1) of serum for antirenin. The Michaelis-Menten concept of a dissociating complex can be applied to the antireninrenin reaction: the rate constants for the formation and for the breakdown of the complex were k1 equal to 1.65 (ml/U antirenin per min) and k3 equal to 1.97 times 10-3 (U inactivated renin/U antirenin per min), respectively; the apparent Michaelis constant was 12 times 10-4 (U renin/ml). A second method of analysis was also applied by assuming the formation of a rather tight complex, with antirenin functioning as an irreversible inactivator of renin. Both methods of analysis yielded practically the same rate constant (k1 equal to 1.65 and k1 equal to 1.71), but the treatment according to the Michaelis-Menten equation affords a slightly better fit of the experimental data (accuracy equal to plus or minus 15.5 percent) than the second method of calculation (accuracy equal to plus or minus 21.6 percent).

Release of antirenin to human renin by anaphylactic shock or by antihypertensive agents.

In dogs that have had repeated intravascular injections of small doses of human renin, even for long periods, the development of antirenin to human renin in the blood has not been previously noted, and their pressor response (30 mmHg) to 1 U of human renin has remained unchanged for years. In such dogs, however, a profound, abrupt fall of the systemic blood pressure, due to an anaphylactic reaction to human renin, or to the infusion of depressor agents, such as Arfonad, histamine, or diazoxide, resulted in the appearance in the blood of an inhibitor specific for human renin. This inhibitor was suddenly released into the blood-stream from the tissues in which it presumably had been stored, and it persisted, in a relatively high concentration, in some animals for months. It did not occur in dogs that had not previously received many injections of human renin. This study has shown that the inhibitor has all of the properties of antirenin to human renin. It abolished the pressor response to hog, dog, and rat renin or to angiotensin and norepinephrine. It inactivated human renin, but not dog renin, duringits incubation with renin substrate to form angiotensin.

Prevention of malignant change in mammalian cells during prolonged culture in vitro.

Mixed cultures of epithelial cells and fibroblasts, derived from primary cultures of the skin of embryo rats, grown always in rubber-stoppered T-60 flasks, first yielded a transplantable tumor from the 52nd passage, at the end of 13 months of frequently repeated subculture. A group of subcultures, derived from the 22nd passage, grown under the same medium, with the addition of 1% oxyhemoglobin, failed to yield a tumor in 23 months of repeated subculture. A return of these cultures to the regular medium with oxyhemoglobin, yielded a tumor in 4 months, after 12 more passages. Cultures of transformed cells that had regularly yielded a transplantable tumor, for 6 years, up to the 305th passage, continued to yield transplantable tumors when 1% oxyhemoglobin was added to the medium. The cells remained highly atypical, microscopically, and there was no indication of reversal of the malignancy. Although oxyhemoglobin in the medium of cell cultures seems to have had the ability to keep malignancy in abeyance, it did not reverse the established malignant transformation of the cells.