Nifedipine in antihypertensive therapy.
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Humans↗
Biomedical subjects
M Bursztyn
Publications and source records attributed to M Bursztyn.
Effect of furosemide on urinary excretion of 4-hydroxy-3-methoxymandelic acid (VMA).
Excretion of VMA was measured in 10 healthy volunteers before and after intake of 40 mg furosemide and in 3 patients with congestive heart failure who were intermittently treated with 80 mg furosemide. In healthy volunteers furosemide caused an increase in VMA excretion from 5.0 +/- 0.5 to 7.8 +/- 0.9 mg/24 h and from 2.0 +/- 0.2 to 2.9 +/- 0.3 mg/g creatinine (mean +/- SE). Excretion of catecholamines was slightly increased in some subjects, but did not reach the upper limit of normal in any case. Furosemide induced an acute increase in urinary VMA that could have derived from inhibition of renal tubular reabsorption. Administration of furosemide might result, on occasion, in a false positive test for pheochromocytoma.
Catecholamines↗
[Treatment of refractory hypertension].
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Antihypertensive Agents↗
Bilateral renal artery stenosis.
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Angiotensin-Converting Enzyme Inhibitors↗
Long acting nifedipine in the treatment of severe hypertension.
The medication of patients receiving hydralazine, captopril and minoxidil was replaced by a new galenical form, long-acting nifedipine. An additional decrease in blood pressure was observed in most of the patients. Renal function was maintained in all of them. Adverse reactions may be reduced by the use of long-acting nifedipine, which would permit a reduction in the dosage of captopril and minoxidil.
Adult↗
Adverse interaction between clonidine and verapamil.
OBJECTIVE: To report two cases of a possible adverse interaction between clonidine and verapamil resulting in atrioventricular (AV) block in both patients and severe hypotension in one patient. CASE SUMMARIES: A 54-year-old woman with hyperaldosteronism was treated with verapamil 480 mg/d and spironolactone 100 mg/d. After the addition of a minimal dose of clonidine (0.15 mg bid), she developed complete AV block and severe hypotension, which resolved upon cessation of all medications. A 65-year-old woman was treated with extended-release verapamil 240 mg/d. After the addition of clonidine 0.15 mg bid she developed complete AV block, which resolved after all therapy was stopped. DISCUSSION: An adverse interaction between clonidine and verapamil has not been reported previously. We describe two such cases and discuss the various mechanisms that might cause such an interaction. Clinicians should be acquainted with this possibly fatal interaction between two commonly used antihypertensive drugs. CONCLUSIONS: Caution is recommended in combining clonidine and verapamil therapy, even in patients who do not have sinus or AV node dysfunction. The two drugs may act synergistically on both the AV node and the peripheral circulation.
Aged↗
Effect of combination therapy with atenolol and the angiotensin-converting enzyme inhibitor benazepril.
The purpose of this study was to determine whether patients whose blood pressure failed to normalize while receiving monotherapy with atenolol would experience further blood pressure lowering by adding the angiotensin-converting enzyme (ACE) inhibitor benazepril hydrochloride to their treatment regimen. Seventy-four of the original 127 patients treated with atenolol met the criteria for entry into the 4-week, double-blind phase of the study, in which either benazepril 10 mg twice daily (increased after 1 week, if necessary, to 20 mg twice daily) or placebo was added to atenolol. At end point, 46% of the benazepril group had achieved an excellent or good response (ie, diastolic blood pressure [DBP] < 90 mm Hg or a decrease of > or = 10 mm Hg below the baseline) compared with 14% of the placebo group (P < 0.01). The mean fall in DBP at end point was -5.6 mm Hg in the benazepril group and -3.7 mm Hg in the placebo group. Because six patients in the benazepril group experienced an increase of blood pressure that offset the fall observed in the responders, the difference in DBP response between the benazepril group and the placebo group was not statistically significant. We conclude that adding benazepril to the regimen of patients whose blood pressure is inadequately controlled while receiving atenolol monotherapy can produce an additional decrease in blood pressure in almost half the patients.
Angiotensin-Converting Enzyme Inhibitors↗
Prevalence of glucose intolerance in young male Ethiopian immigrants.
The prevalence of intolerance to glucose was compared between young immigrant Ethiopian Jews shortly after their arrival to Israel, a similar group of Ethiopians 2-3 years after their arrival to Israel, and young Israeli students. A relatively high prevalence of glucose intolerance was found in both Ethiopian groups, but we could not demonstrate any deterioration in glucose tolerance after 2-3 years of Israeli life-style in the Ethiopian groups. In spite of high blood glucose levels in response to 75 g glucose load, when compared to Israeli students the Ethiopians' fasting insulin levels and insulin response to 75 g of glucose was relatively low, suggesting a higher glucose threshold for insulin secretion. However, in the Ethiopians, impaired glucose tolerance was associated with hyperinsulinemia, suggesting that similar to some other populations glucose intolerance is associated with insulin resistance.
Adult↗
Comparison of glucose tolerance, lipids and blood pressure in young male Ethiopians from two different immigrations, 1989 and 1991.
The prevalence of glucose intolerance and hypertension was compared between a group of 87 young Ethiopian males (age 21.6 +/- 2.8 years) from the post Moses immigration of 1989 (group 1) and 89 age-matched Ethiopian males (age 21.4 +/- 3.1) from the Solomon immigration of 1991 (group 2). Both groups demonstrated a relatively high, for age, prevalence of glucose intolerance: 5% and 8% in groups 1 and 2 respectively (not significant). However, group 1 had a higher glucose level 2 h after an oral glucose tolerance test (P < 0.05) and a higher level of HbA1C (P < 0.05) and fructosamine (P = 0.07), concomitant with a lower fasting insulin (P < 0.005), when compared with group 2. Group 2 had a significant increase in both systolic and diastolic blood pressure when compared with group 1 (P < 0.05, P < 0.005 respectively). Group 2 had higher blood pressure levels and higher fasting insulin than group 1, suggesting a relationship between insulin levels and blood pressure in this population.
Adult↗