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The apparent suppression of plasma renin activity in essential hypertensive patients compared to normotensive controls prompted an examination of factors which might be responsible for this difference in people taken from a blood pressure screening survey. Plasma renin activity was lower in 89 previously untreated "hypertensive" subjects than in an equal number of age- and sex-matched "controls" from the same community. The rise in plasma renin activity on standing or after frusemide was proportional to the resting level, and it was generally less in hypertensives, but small or absent responses were also seen in those with normal blood pressure. There was no evidence for a "low renin sub-group" among the hypertensives. Plasma renin activity fell with both increasing age and increasing arterial pressure. A low renin activity is more likely to be a consequence of hypertension than to be associated with its cause.

Fifteen of 29 commercial dairy herds were given a series of anthelmintic treatments. The remaining herds were untreated to provide a measure of seasonal variation. In the treated herds all milking cows were treated once in the summer and the autumn and three times at monthly intervals in late winter and early spring. Any other animals grazing the same area were similarly treated. No herds had been treated with anthelmintics in the preceding year and mean herd lactations for that year were used as covariate corrections. This experimental design had the potential to detect differences in production of the order of 5 X 7 per cent (P = 0.05). Although levels of subclinical parasitism were low, anthelmintic treatment increased milk fat production by 10.8 kg (8.3 per cent) in heifers. Average response in mature cows was much smaller (3.1 per cent) and not significant. Apparent milk fat responses in individual herds were variable with no relationship to level of production in the previous year.

Plasma renin activity (PRA), supine, erect and post-frusemide (1 mg/kg IV) was studied in 51 patients with previously untreated essential hypertension and their age- and sex-matched normotensive controls. Supine PRA, and the rise in PRA in response to the erect posture and frusemide, were significantly less in hypertensives compared to controls. When the hypertensives were arbitrarily divided into lower, mid, and upper subgroups according to supine PRA, the renin responsiveness was similar in each subgroup but significantly less in hypertensives compared to controls, subdivided in the same way. This does not support the existence of a separate "low renin" subgroup. The low supine PRA and reduced response to stimulation appears to be a feature of patients with essential hypertension. Thirty-nine of these hypertensives entered a double-blind cross-over drug trial of oxprenolol, methyldopa and spironolactone. All three drugs were equally effective in lowering the systolic and diastolic blood pressures in all three renin subgroups. Spironolactone caused a greater fall in systolic pressure in the lower renin group than in the other groups. Oxprenolol was the best tolerated drug, with only 5% of patients withdrawing due to side-effects compared to 13% on spironolacone and 29% on methyldopa.

Nineteen seriously disabled patients were operated upon a second time (using closed-heart technique) for recurrence of symptoms of mitral stenosis. The hospital mortality rate was 10.5%; there was one late death. Ten patients (52%) were well and working six months to five years after the second operation. In considering the cause of restenosis it was noted that nine patients had inadequate opening of the mitral valve at first operation. In five cases (26%) rheumatic activity appeared to be solely responsible for restenosis. In a further four cases (21%) it was considered that rheumatic activity was a contributing cause of restenosis. The diagnosis of rheumatic activity and the place of open heart procedures in the treatment of restenosis are discussed.