1. Renin was measured in individual juxtaglomerular apparatuses before and after acidification in vitro. . 2. Active renin increased with delivery of extra sodium by microperfusion to the macula densa and this increase was similar to that achieved with acidification. 3. In rats pretreated with an inhibitor of protein synthesis active renin increased when extra sodium was delivered to the macula densa. 4. Salt intake changed the amount of renin present in the juxtaglomerular apparatus. In rats on a high salt intake the total renin was low and was all in an active form.
1. A total of 206 patients, elderly males with hypertension (diastolic blood pressure 95–110 mmHg) were followed for periods varying from 1 to 5 years, 107 patients with diastolic blood pressure <95 mmHg were followed over the same period, and 101 patients with diastolic blood pressure ≥110 mmHg were also followed. 2. The mortality of each group and the effect of therapy for hypertension on mortality has been compared. 3. The incidence of myocardial infarct in the group treated with thiazide diuretics is greater than in the other groups. 4. It would appear unlikely that therapy will improve the prognosis in elderly people with mild hypertension.
1. A technique was developed to measure renin concentration in nanolitre volumes of blood. 2. The renin concentration in renal venous blood was higher than in renal arterial blood. 3. The renin concentration in blood from the efferent arteriole was less than in blood from the renal artery and renal vein. 4. Renin enters the circulation distal to the efferent arteriole. 5. The release of renin into the interstitium would allow local formation of angiotensin and the system could act as an intrarenal control mechanism.