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Twenty patients suffering from primary hyperaldosteronism were studied. Sixteen had a single adenoma of the adrenal and four had bilateral hyperplasia affecting both adrenals. Cases of primary hyperaldosteronism due to a tumour were characterised by a higher degree of hypermineralocorticism than was seen in the patients with hyperplasia. Plasma aldosterone, after acute volaemic expansion, did not fall below 13 ng/100 ml in the adenoma patients whilst it was lower in the case of hyperplasia. Adrenal phlebography is a useful tool in preoperative diagnosis.

In patients with renovascular hypertension, a significant decrease in glomerular filtration rate (GFR) and in renal plasma flow (RPF) in the stenotic kidney was accompanied by a significant homolateral decrease in extraction of PAH(EPAH) and in net tubular reabsorption of sodium (RNa). There was a highly significant correlation between differences in RNa and differences in either GFR or RPF, while no correlation between differences in RNa and in EPAH was noted. It is suggested that the nature of the relationship between GFR and RNa is essentially the same in unilateral renal artery stenosis in man, as in acute constriction of the renal artery or the aorta in the experimental animal.

A study of 100 men with arterial hypertension showed that: 1) hypertension was predominantly moderate with 14% index of placebo reactivity; 2) only 3 patients had a surgically curable etiologic factor; 3) frequent associated findings were hereditary factors (60%), overweight and metabolic disorders (30 to 40%). Such results suggest that: a) hypertension could be treated, in the majority of patients, without preliminary etiologic investigations and, b) non invasive hemodynamics techniques are required to evaluate arterial and cardiac lesions which are the dominant factors in the prognosis.

Eleven cases of hypertension secondary to a renal tumour secreting renin have been described in the literature between 1967 and 1978. We report here another case which presented with severe hypertension and a cerebro-vascular accident in a 30 year old woman. Intravenous urography and renal arteriography revealed a tumour of the upper pole of the left kidney. Measurement of renin levels in the renal veins demonstrated hypersecretion on the side of the tumour. Tumorectomy was followed by normalisation of blood pressure levels. Histopathological examination confirmed the diagnosis of a tumour of the juxta-glomerular apparatus.

Six patients with permanent hypertension with renal artery stenosis were treated by conservative reparative surgery appart from one of them (unilateral nephrectomy) and were all seen again at the 8th month at the earliest in the absence of any anti-hypertensive therapy. Study of the renin-angiotensin system carried out on a normal sodium diet, after stopping all anti-hypertensive treatment for at least 15 days, was combined with the anti-hypertensive response under the influence of a beta-blocker. There were two types of response pre-operatively: firstly, with beta-blockers alone a normal blood pressure which remained normal postoperatively; the second group of patients remained hypertensive, requiring the addition of diuretics, and remained hypertensive after surgery. This response, although non-specific, would appear to represent an important element in assessing the curability of reno-vascular hypertension.

A new method to demonstrate the renal arteries is presented. It consists of taking with a Synchroplan apparatus simultaneous tomographic sections during the aortic and arterial stage of intravenous urography (IVU). Direct visualization of the vessels avoids the false negative results of IVU alone in investigations of renovascular lesions, such as bilateral stenosis of the renal artery, stenoses with few functional disorders, aneurysms and associated arterial and urinary lesions. Lesions of the infra-renal portion of the aorta and of the splanchnic arteries are also visualized. In a series of 37 patients investigated for renovascular hypertension, the new method proved more sensitive, more specific and of higher predictive value than conventional IVU. In another series of 19 patients who had undergone revascularization of the kidneys, the authors were able to obtain good visualization of the new vascular system and to establish correlations between morphological features and the effects of hypertension. The method therefore appears to be valuable in detecting renovascular lesions in arterial hypertension, monitoring renal artery lesions and following up patients with surgical revascularization.

In a single-dose crossover study Captopril (SQ 14225), 1 mg/kg body weight, and Nifedipine (Bay a 1040) 20 mg were administered orally to 12 hospitalized patients with essential hypertension (Stage 1 or 2, W.H.O.). Both drugs significantly reduced blood pressure, but each dose acted differently: the mean maximum arterial pressure reduction was faster and greater with Nifedipine than with Captopril: -23 +/- 2% at 37 +/- 15 min and -17 +/- 1% at 86 +/- 25 min, respectively. Captopril inhibited angiotensin II and aldosterone production, but did not accelerate heart rate or stimulate vasopressin release. Nifedipine stimulated vasopressin release and increased heart rate, but the renin angiotensin aldosterone system was not significantly affected. The blood pressure reduction was related to the initial level of activation of the renin angiotensin system only for Captopril. The blood pressure reduction induced by one drug was not related to that produced by the other in the same patient.

PG A1, B1, E2, F1,2alpha and PRA have been measured in 8 hypertensive patients with unilateral renal arterial stenosis, 7 hypertensive patients with unilateral renal atrophy and 20 control normotensive subjects. PRA and PGA1 were significantly increased in patients with renovascular hypertension but not in patients with atrophy. PGE2 and PGF1,2alpha were increased in both groups of patients, especially on the stenotic or atrophic side. The increase of PGA1 and PGE2, represents a secondary antihypertensive, diuretic and natriuretic mechanism, the increase of PGF1,2alpha a direct hypertensive mechanism.

The role of prostaglandin A (PG A) in the pathogenesis of renal hypertension has been studied. The concentration of endogenous PG A was measured in the peripheral plasma by radioimmunoassay in patients with chronic renal disease and in control subjects. The mean plasma concentration of PG A1 equivalents was as follows: 1. normotensive healthy volunteers (n=23): 115 +/- 15 pg/ml 2. patients in terminal renal failure on regular hemodialysis a) anephric patients (n=6): 51+/- 21 pg/ml b) patients retaining their own kidneys, all but one with hypertension (n=9): 231 +/- 51 pg/ml (P less than 0.01 versus control) 3. patients with chronic renal disease a) with hypertension (n=7): 204 +/- 60 pg/ml (P less than 0.01 versus control) b) without hypertension (n=11): 136 +/- 30 pg/ml. Renal hypertension was associated with high levels of PG A in peripheral blood. This increase is probably a secondary adaptative mechanism for the excretion of a greater fraction of the glomerular filtrate at a lower blood pressure. PG A may represent a circulating "antihypertensive hormones".

Cardiac output, cardiopulmonary (CPBV) and total (TBV) blood volumes, vascular reactivity to norepinephrine and dopamine B hydroxylase (DBH) were determined in 41 borderline hypertensives patients in comparison with 28 normal subjects. Cardiac output (P less than 0.001) and CPBV/TBV ratio (P less than 0.01) were significantly increased. The ratio was directly correlated to the pressor-response to norepinephrine (P less than 0.01) and the DBH level (P less than 0.005). The results suggest that sympathetic overactivity plays a dominant role in the cardiac output elevation of borderline hypertensive patients.

An analytical study of the renin-angiotensin-aldosterone system was made in 124 individuals with essential hypertension, aged from 25 to 55 years. The results obtained, with rigorous control to posture and sodium balance, indicate the existence of a number of subgroups of hypertensive subjects related to their renin activity and plasma aldosterone in the upright position. This classification thus makes possible comparison with patients suffering from secondary hypertension.

Eleven cases of hypertension secondary to a renal tumour secreting renin have been described in the literature between 1967 and 1978. The authors here report another case which presented with severe hypertension and a cerebrovascular accident in a 30-year-old woman. Intravenous urography and renal arteriography revealed a tumour of the upper pole of the left kidney. Estimation of renin levels in the renal veins demonstrated hypersecretion on the side of the tumour. Tumourectomy was followed by normalisation of blood pressure levels. Histological examination confirmed a diagnosis of a tumour of the juxtaglomerular apparatus.

Summary A retrospective analysis of 33 patients who had undergone nephrectomy or revascularisation procedures for renovascular hypertension was carried out in order to assess the value of divided renal function studies in the prediction of the results. The classical ischaemic criteria of Howard, Rapoport, and Guedon were proved to be in- sufficiently sensitive since, when they were not satisfied, surgery nevertheless improved hyper-tension in 36 % to 60 % of cases. Our present experience leads us to recommend a single criterion of ischaemia-an increase in urinary concentration of creatinine (ACr) of 20% or more on the diseased side (calculated by dividing the difference between the 2 kidneys by the concentration on the healthy side, not the diseased side as done by Howard). This single criterion has an excellent prognostic value (P