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Hypertension is a frequent problem in children with renal tumour, yet there are few reports from centres in the third world. A retrospective study of blood pressure in a cohort of 46 patients with renal tumours seen over a 3-year period was carried out. Fifty percent of patients presenting with Wilms' tumour were hypertensive. Serum concentrations of active renin correlated poorly with blood pressure. There was no correlation between serum concentrations of active renin and tumour mass or histology. Specific antihypertensive therapy was offered to 11 patients who had either neurological or cardiac complications of hypertension. All other patients with Wilms' tumour had their blood pressure controlled by neoadjuvant chemotherapy. Patients with mesoblastic nephroma were managed by primary surgery. Patients with asymptomatic hypertension may be monitored as hypertension will resolve with neoadjuvant chemotherapy. Those with compelling symptomatology will require additional hypertensive medication.

The objectives of this study were to assess relations between ACE gene I/D polymorphism, essential hypertension, plasma renin activity and aldosterone in white (European descent) and black (Afro-Caribbean descent) peoples. Measurements were carried out on a total of 320 subjects (210 white: 116 men, 94 women; 110 black: 65 men, 45 women); all were on their usual sodium intake; none was on anti-hypertensive therapy and none had secondary hypertension. Genomic DNA was isolated from blood cells and ACE I/D genotype was established using polymerase chain reaction. Plasma hormones were measured by radioimmunoassay and blood pressure (BP) with an ultrasound sphygmomanometer. All subjects were grouped into normotensive, borderline and hypertensive according to WHO guidelines. The distribution of the I/D genotype in the white people was approximately 1:2:1; by contrast, in the Afro-Caribbean people there was a significantly higher frequency of the D allele (chi 2P = 0.04). Within the white people there was no significant association between ACE genotype and high BP; however, within the black people there was a positive association between the frequency of the D allele and increasing BP ( chi 2 for trend P = 0.03). In either group, there were no associations between ACE I/D genotype and plasma renin activity and aldosterone suggesting that ACE genotype does not contribute to the expression of the circulating renin-angiotensin system. This study highlights differences in ACE I/D polymorphism between white and black peoples and suggests the possibility of racial differences in the association between ACE genotype and BP.

The discovery and clinical availability of ACE inhibitor drugs is a triumph of rational drug development and a land-mark in biochemical pharmacology and hypertension research. The clinical pharmacological properties and haemodynamics of the clinically available drugs, captopril and enalapril, are reviewed, as is their therapeutic efficacy in African patients with essential and renal hypertension and chronic congestive heart failure. ACE inhibitors act as balanced arteriolar vasodilators and venular dilators and do not excite a reflex tachycardia in contrast to other vasodilator drugs. Their efficacy is, at least in part, dependent on plasma renin activity, which is low in Blacks and in Africans. Consistent with this, is the poor response to ACE inhibitor monotherapy of essential hypertension in controlled studies in Africans. However, the compensatory neuroendocrine activation which occurs in malignant hypertension, renal failure and congestive heart failure and concurrent diuretic therapy appears to enhance the clinical response to ACE inhibitors in African patients.

Essential hypertension is the most important cardiovascular disease in black subjects. The types of presentation, the pattern of organ involvement and the subsequent complications are similar in black races. The response (or lack of response) to different types of treatment are also alike in blacks when compared with caucasians. Striking racial differences are observed in the plasma and intracellular electrolytes, cation transmembrane transport, salt taste threshold, plasma renin activity and urinary kallikrein activity. The similarities within the black racial groups are very likely to be genetic, although the pattern of inheritance remains controversial. Differences, however, occur in the prevalence and severity of the disease among the black racial groups. That these differences are due partly to environmental causes can not be disputed because even within the same ethnic groups changing patterns are observed in the prevalence of hypertension, in the course of urbanization of rural communities, or on moving from a previously rural to an urban environment. Consequently, genetic factors may be the only important considerations in the severity of hypertension in black subjects.

The relationship between the hypotensive effect of nitrendipine (N), 20 mg/day (n = 17), or atenolol (A), 100 mg/day (n = 17), and the erythrocyte sodium [( Na]i) and potassium [( K]i) concentrations was investigated in hypertensive African blacks during a randomized double-blind study. After 6 weeks, both treatments significantly reduced supine and standing blood pressures; however, the magnitude of the decrease in supine systolic (-22.0 +/- 2.0 vs -12.1 +/- 3.4 mm Hg) and diastolic (-14.1 +/- 1.3 vs -7.6 +/- 2.1 mm Hg) pressures and in standing diastolic pressure (-16.0 +/- 1.7 vs -9.2 +/- 2.0 mm Hg) was more pronounced (p less than 0.05) in the N-treated than in the A-treated group. Pulse rate, plasma aldosterone, and plasma renin activity were lower (p less than 0.05) in the A-treated patients. Neither treatment had significant influence on [Na]i, [K]i, or ouabain-sensitive sodium efflux. The N-induced changes in supine systolic and diastolic pressure correlated (p less than 0.05) with age (r = -0.65 and r = -0.58, respectively) and pretreatment plasma renin activity (r = 0.71). Multiple regression analysis demonstrated a negative association between pretrial [Na]i and the change in systolic pressure during N treatment that was independent of age, pretreatment blood pressure, and change in pulse rate. Age and the change in supine pulse rate were also independently correlated with the change in diastolic pressure during N treatment. The results show a greater antihypertensive efficacy of N than A in the patients entered in this study and suggest that a higher intracellular sodium concentration could predict a better hypotensive response to N.