ACE inhibition in diabetic patients: effect on pressor responsiveness to noradrenaline.

The pressor responsiveness to noradrenaline was assessed before and after four weeks of treatment with enalapril (20 mg/day) in eight mild-to-moderate essential hypertensives, in eight normotensive type II diabetics and in eight mild-to-moderate hypertensive type II diabetic patients. The ACE inhibitor interfered to the same extent with the renin-angiotensin system and did not alter noradrenaline kinetics in the three groups of patients, but significantly reduced the arterial responsiveness only in non-diabetic subjects. It is suggested that factors, such as an exaggerated sodium retention, might determine the lack of effect of enalapril in diabetic patients.

The effect of ace inhibition on peripheral hemodynamics in normotensive and hypertensive patients with type II diabetes.

The effect of treatment with enalapril (10 days at 10 mg/d followed by 4 weeks at 20 mg/d) on forearm hemodynamics was assessed in eight normotensive patients and eight patients with hypertension affected by Type II diabetes as well as in eight patients with essential hypertension and normal glucose tolerance. The ACE inhibitor decreased regional vascular resistances and increased the maximum arteriolar-vasodilating capacity and venous distensibility in the three groups of patients. Thus, this study shows that ACE inhibition by enalapril improves regional hemodynamics in patients with Type II diabetes.

Angiotensin converting enzyme inhibitors, thiazide diuretics and magnesium balance. A preliminary study.

Serum and mononuclear cell magnesium content were determined in a cross-sectional study performed in four groups of hypertensive patients on chronic treatment with atenolol (n = 11), enalapril (n = 10), thiazide diuretics (n = 12), or enalapril + thiazides (n = 11). Our study shows that in patients treated with the thiazides alone, in spite of normal serum potassium and magnesium levels, mononuclear cell magnesium was decreased. To the extent that mononuclear Mg content mirrors the body ion stores, our results indicate that thiazides induce a Mg depletion not detectable by monitoring serum levels.

ACE inhibition and pressor responsiveness to norepinephrine in hypertensive patients.

The pressor response to norepinephrine (NE) was assessed in normal renin essential hypertensive patients before and after they were randomly assigned to receive in parallel groups of treatment a single dose of an angiotensin converting enzyme (ACE) inhibitor (captopril or lisinopril) or a prolonged therapy with lisinopril (30-45 days) or with hydrochlorothiazide (9 days). Blood pressure was significantly reduced by all treatments. The pressor response to NE was unchanged after the single administration of the ACE inhibitors, while it was blunted after chronic administration of lisinopril and after the diuretic. On the basis of these results, it is suggested that the attenuation of the sympathetically mediated vasoconstriction may represent an additional mechanism contributing to the antihypertensive effect of ACE inhibitors administered chronically.

The incidence of cough during treatment with angiotensin converting enzyme inhibitors.

The incidence of cough during treatment with angiotensin converting enzyme (ACE) inhibitors was studied using retrospective analysis of outpatient records and a questionnaire; for a more precise evaluation, all reported cases of cough were reviewed according to criteria for the operational assessment of side effects, and those found unrelated were excluded. Cough during treatment with ACE inhibitors appears to be more frequent than previously recorded and substantial differences between patients treated with captopril or enalapril seem unlikely.

Interaction study of fenoldopam--digoxin in congestive heart failure.

The potential interaction between fenoldopam, a DA1 selective agonist, and digoxin has been studied in 10 patients with heart failure (NYHA Class II or III) on chronic digoxin treatment. Plasma levels and urinary recovery of the glycoside were monitored for 24 h before and after 9 days of treatment with fenoldopam 100 mg tid. Fenoldopam caused a small, non-significant decrease in the mean steady state plasma concentration and area under the plasma concentration curve of digoxin. As the clearance of digoxin was unchanged there does not appear to be an interaction between fenoldopam and digoxin at the level of the renal tubule.