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Introduction Whole body concentrations of caesium-137 are closely related to dietary intake of the isotope, [1] which has a physical half life of 30 years but a biological half life [...]

Objectives--To assess incidence of and mortality from cancer in hypertensive patients taking atenolol, comparing the findings with two control populations and with hypertensive patients taking other drugs. Design--Retrospective analysis of [...]

Hyponatraemia has been described in beer drinkers and hypokalaemia resulting from increased levels of aldosterone is well recognised in patients with cirrhosis and ascites. We have encountered episodes of hypokalaemia in alcoholics accompanied by normal or increased serum concentrations of sodium. Despite a resemblance to syndromes of mineralocorticoid excess, increased levels of aldosterone and other mineralocorticoids were not found.

Malignant hypertension with severe hyponatræmia, hypokalæmia, depletion of sodium and potassium, and elevated blood levels of renin, angiotensin I, angiotensin II, aldosterone, and arginine vasopressin developed in a woman with renal-artery occlusion. Plasma angiotensin II was disproportionately high in relation to exchangeable sodium. Captopril, by inhibiting conversion of angiotensin I to angiotensin II, further elevated the blood levels of renin and angiotensin I but corrected all other abnormalities. Unilateral nephrectomy was subsequently curative.

Although homœostatic mechanisms relate sodium balance, renin, and arterial pressure, the reduction of renin sometimes seen in essential hypertension cannot be attributed to abnormal sodium retention. It is proposed instead that renin decreases and sodium status remains normal because the pressure-natriuretic mechanism within the kidney is reset by increased filtration fraction. Neurogenic factors may raise blood-pressure and cause resetting by some other means at an early (labile) stage of essential hypertension, but, once filtration fraction is raised and remains elevated on withdrawal of the neurogenic component, essential hypertension will have a renal cause. A similar mechanism may account for the failure of secondary hypertension to fall when its cause is removed.

The converting enzyme inhibitor enalapril, in single daily doses of 10 to 40 mg, was given to 20 hypertensive patients with renal artery stenosis. The decrease in blood pressure six hours after the first dose of enalapril was significantly related to the pretreatment plasma concentrations of active renin and angiotensin II, and to the concurrent decrease in angiotensin II. Blood pressure decreased further with continued treatment; the long-term decrease was not significantly related to pretreatment plasma renin or angiotensin II levels. At three months, 24 hours after the last dose of enalapril, blood pressure, plasma angiotensin II, and converting enzyme activity remained low, and active renin and angiotensin I high; six hours after dosing, angiotensin II had, however, decreased further. The increase in active renin during long-term treatment was proportionately greater than the increase in angiotensin I; this probably reflects the diminution in renin substrate that occurs with converting enzyme inhibition. Long-term enalapril treatment increased renin secretion by more than 10-fold, and renal venous and peripheral plasma renin concentration by more than 20-fold; however, the mean renal venous renin ratio was not changed. Enalapril caused a reduction in effective renal plasma flow via the affected kidney but a marked and consistent increase on the contralateral side, where renal vascular resistance decreased. The overall increase in effective renal plasma flow was significantly related to the decrease in angiotensin II. Overall glomerular filtration rate was lowered, and serum. creatinine and urea increased. Enalapril alone caused a longterm reduction in exchangeable sodium, with slight but distinct increases in serum potassium. In five patients with bilateral renal artery lesions, enalapril given alone for three months did not cause renal function to deteriorate. Enalapril was well tolerated and provided effective long-term control of hypertension; only two of the 20 patients studied required concomitant diuretic treatment.

A case of renin-secreting renal juxtaglomerular-cell tumour is described in an 8-year-old child. Severe hypertension associated with hypokalæmia was accompanied by raised plasma concentrations of renin, angiotensin II, and aldosterone in peripheral blood. The secondary hyperaldosteronism was shown not to be due to the malignant phase or to renal-artery stenosis. The tumour was lateralised by the demonstration of higher concentrations of renin and angiotensin II in left than in right renal venous plasma, and visualised on selective renal arteriography. The patient showed much greater elevation of blood-pressure and plasmaaldosterone than normal subjects infused with angiotensin to produce comparable plasma-angiotensin-II levels. Before operation, both head-up tilting and dietary sodium restriction caused a further striking increase of peripheral renin and angiotensin II. The hypertension and biochemical abnormalities were all relieved by removal of the affected kidney. The tumour had a very high content of renin. Extreme care is necessary in interpreting minor differences in renin level in renal veins if false-positive or falsenegative diagnoses are to be avoided.