To study effects on pituitary-adrenocortical activity of a sustained block of angiotensin II formation, six 'drug-resistant' patients with essential hypertension were studied before and during treatment with an inhibitor of the angiotensin-converting enzyme (Captopril, SQ 14,225). The drug was given in increasing doses (100-400 mg/day) for 2 weeks whilst patients received a moderately restricted sodium intake (60-80 mmol/day). Immunoreactive ACTH, cortisol, aldosterone, plasma renin activity (PRA) and the activity of the angiotensin-converting enzyme (ACE) were measured in blood samples drawn at 0800-0900 h. Urinary excretion of cortisol and aldosterone were measured in 24-h urine collections. Further information on pituitary-adreno-cortical function was obtained by measuring serial plasma corticosteroid levels after submaximal stimulation with a synthetic ACTH preparation. ACTH and cortisol did not change an observation which does not support the hypothesis that glucocorticoid activity is influenced by a decrease in plasma angiotensin II concentrations.

The aim of the study was to evaluate whether the combination of ketanserin with captopril exerts an additive antihypertensive effect, as compared with single drug treatment. Twelve patients with uncomplicated moderate essential hypertension received, according to a randomized, double-blind, crossover design, ketanserin (40 mg twice daily), captopril (50 mg twice daily), the combination of the two drugs at these dosages, and the corresponding placebo, each treatment being given for 1 month. Both ketanserin and captopril as monotherapy similarly and significantly reduced blood pressure as compared with placebo (p less than 0.001). The combination treatment of ketanserin plus captopril further and significantly reduced blood pressure when compared with single drug treatment (p less than 0.001). Moreover, the percentage of responders and patients whose blood pressure was normalized were significantly greater under the combined treatment than under ketanserin or captopril monotherapy (p less than 0.001). These data indicate that the combination of ketanserin plus captopril exerts a clear additive antihypertensive effect when compared with each treatment as monotherapy, a finding that suggests this combination can be usefully employed in the treatment of hypertensive patients.

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The effects of quinapril (an angiotensin converting enzyme inhibitor) on cardiac hypertrophy were evaluated in a noncomparative study of 98 patients with mild to moderate hypertension over 4 months. Left ventricular hypertrophy (LVH) was diagnosed using echocardiography in 60% of patients at baseline. Combination therapy with hydrochlorothiazide (HCTZ) was initiated after I month in patients with inadequate blood pressure control to achieve a target diastolic pressure reduction from baseline (~ 10mm Hg) and/or reduction to < 90mm Hg. Left ventricular mass index (LVMI) was significantly reduced for patients of either sex with a baseline diagnosis of LVH, but not for those in whom LVH was not detected at enrolment. Systolic and diastolic blood pressures were also significantly reduced. The response rate was 83%, while 28% of patients required combination therapy with HCTZ. There was no correlation between the hypotensive effects of quinapril and change in LVMI. Furthermore, the addition of a diuretic did not appear to affect the LVMI response. Thus, the amelioration of LVH noted in this investigation appears to be attributable to quinapril.Electrocardiographically detected left ventricular hypertrophy (LVH) has been recognised as an independent risk factor for increased cardiovascular morbidity and mortality for many years. [1,2] However, diagnostic ECG signs of LVH are relatively infrequent among patients with hypertension; their prevalence ranged from 3 to 5% in adults recruited to the Framingham study[l] and the Hypertension Detection and Follow-up Program. [3] The introduction of the echocardiographic technique as a much more sensitive and accurate method for LVH detection [4,5] has significantly increased the estimated prevalence of LVH, which is currently thought to range between 25 and 30% in