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The combination of hydrochlorothiazide and amiloride has been used in a group of patients diagnosed as having essential hypertension. Sixty-five percent of the patients for whom dietary restrictions did not achieve a reduction in blood pressure were initially controlled with this combination; the addition of a second or third drug was required by the remaining patients. During the six-month follow-up, the control of blood pressure was satisfactory with increased drug requirements, but the diuretic had to be discontinued in 12 patients because of side effects.

In a group of 26 patients diagnosed as essential hypertensive (EH) and in a control group (CG) of 27 normotensive volunteers the urinary excretion of PGE2, plasma renin activity (PRA) and plasma aldosterone were measured. EH patients were classified into normoreninemic (NREH) (n = 21) and hyporeninemic (LREH) (n = 5) by the response of PRA to the combined stimuli of ambulation and furosemide. Urinary PGE2 excretion was higher in NREH than in CG (p less than 0.05) while LREH showed values lower than in CG (p less than 0.001). Plasma aldosterone levels were similar in the three groups. In CG and EH patients PRA and urinary PGE2 were closely related (CG r = 0.516, p less than 0.05, EH patients r = 0.674, p less than 0.001). Indomethacin administration induced a decrease of PGE2 in both CG (n = 8) and NREH (n = 8) (p less than 0.01). In contrast, indomethacin induced no changes in PGE2 excretion of LREH (n = 5). Furthermore in the group of patients with NREH indomethacin induced a significant increase in blood pressure (p less than 0.01) and body weight (p less than 0.01) while glomerular filtration rate, 24 hour natriuresis PRA and plasma aldosterone decreased (p less than 0.01). On the contrary, in LREH indomethacin did not alter any of the parameters measured. These results indicate that LREH and NREH may be regarded as two different populations distinguishable not only by different secretion of PRA but also by different excretion of PGE2 in urine and by their characteristic response to indomethacin.

Recent experimental and clinical data have suggested that angiotension converting enzyme (ACE) inhibitors may decrease glomerular proteinuria by specific effects on the glomerulus. We studied a group of 15 adult patients with chronic renal failure and proteinuria due to various glomerulopathies. These patients had mild to moderate hypertension which was effectively controlled with conventional antihypertensive therapy. We then treated the patients with captopril, maintaining a similar dietary protein and salt intake. After 6 months of study, proteinuria was reduced significantly without reduction in inulin or para-aminohippurate clearance. This supports the concept that captopril may have salutary effects on the glomerulus, independently of its effect on systemic blood pressure.

The clinical aspects and response to therapy of 130 hypertensive emergencies are reviewed in this report. According to the main features of the clinical picture, the patients were divided into neurologic, cardiac or mixed emergencies. The patients were evaluated with clinical examination, fundoscopy, routine biochemistry, ECG, and chest radiograms. According to the response of the blood pressure to the administration of hypotensive drugs, the patients were divided into two groups: group I, with good response to a single drug associated to frusemide, and group II, with good response to two or more drugs associated to frusemide. Neurologic emergencies appeared in 55 patients (42% of total), and cardiac emergencies in 45 (34%), the initial blood pressure beeing higher in the first group (p less than 0.005). The fundus showed hypertensive retinopathy degrees III-IV in 55% of the patients. Patients in group I had less elevation of the initial blood pressure, showed a better response to therapy, and had only mild side effects from the administered drugs. Group II had a mortality of 11% and, as expected, showed more complications due to side effects. The frequency of appearance of toxic side effects from the drugs given is reviewed, and a therapeutic schedule is proposed.

We studied the long-term effect of an angiotensin converting enzyme (ACE) inhibitor, captopril, on the progression of chronic renal failure and on the rate of urinary protein excretion. When compared with standard triple therapy, captopril slowed the progression of renal failure. Captopril was also able to reduce the proteinuria of non-diabetic glomerular origin. This reduction was not dependent on the presence or absence of arterial hypertension but was limited by the presence of low serum albumin levels, and only occurred in patients with proteinuria in excess of 3 g/24 h.