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. Males, born between 1900 and 1925, with mild hypertension have been treated for periods varying from 300 to 2000 days. 2. The life and death status of all patients (except two) was known on 1st November 1978. 3. A group of patients with mild hypertension receiving treatment based on a thiazide diuretic had a greater mortality than the other drug-treated group. 4. The increased mortality was caused by an increased number of myocardial infarcts. 5. Elderly male patients with mild hypertension probably have preexisting vascular disease and therapy should not automatically be started. If therapy is started, β-adrenoreceptor-blocking drugs may be a preferred therapy.
1. Salt intake and the incidence of hypertension correlate between populations. 2. Salt intake within a population may correlate with the incidence of hypertension. 3. Disorders that lead to retention of salt cause hypertension. 4. Modest salt restriction reduces blood pressure in many patients. 5. Reducing salt balance and preventing the compensatory rise in angiotensin II controls blood pressure in most patients. 6. Salt is the probable cause of the epidemic of hypertension in the Western world; this could be prevented by salt restriction.
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. Blood pressure was controlled to the same extent whether propranolol or pindolol was given once or three times/day. 2. The anti-hypertensive action of β-receptor-blocking drugs persisted for 36–48 h when administration ceased.
1. Prindolol and propranolol chronically cause a fall in mean blood pressure and mean plasma renin activity, but no correlation was observed between the two variables. 2. The response of blood pressure to prindolol and propranolol was not predicted by the basal plasma renin activity. 3. Propranolol administered acutely caused the plasma renin activity to fall with no acute change in blood pressure, whereas prindolol caused the blood pressure to fall with no change in plasma renin activity. 4. The effects of β-adrenergic-blocking drugs on plasma renin activity and blood pressure can be dissociated and it is unlikely that their hypotensive action is mediated through the renin-angiotensin system. 5. Basal plasma renin activity does not identify the patients who will respond to β-adrenergic-blocking drugs.