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Amlodipine besylate 5mg / Benazepril hydrochloride 10mg
Smooth muscle cell and myocardium constrictions require special ion channels to transport extracellular calcium ions into intracellular space; whereas, amlodipine is a calcium channel blocker, which inhibits calcium ions from passing through cell membranes of smooth muscle cells and myocardium. This type of inhibition is selective and has greater affects on smooth muscle cells as compared to the effects on myocardium. Additionally, serum calcium ion concentration will not be affected by amlodipine. Within the range of normal physiological pH values, amlodipine is an ionic compound (pKa=8.6), which binds to the receptors of calcium ion channels with gradual dissociation rate; therefore, the effects will also be gradual events. Amlodipine is a peripheral arterial vasodilator, which acts directly on smooth muscle cells and reduces the resistance and pressure of the peripheral vessels.
In humans and animals, benazepril and benazeprilat may inhibit the angiotensin-converting enzyme (ACE), which turns angiotensin I into angiotensin II, a vasoconstrictor; angiotensin II may stimulate adrenal cortex to secrete aldosterone. The inhibition of ACE will decrease the serum angiotensin II concentration, cause decreased activity of vasoconstriction and reduce the secretion of aldosterone; the latter event will lead to a mild increase of serum potassium ion concentration. The serum potassium ion concentration had increased to 0.2mEq/L in high blood pressure patients, who had been treated with benazepril and amlodipine for 56 weeks. If the negative feedback from angiotensin II to the secretion of renin is removed, the amount of serum renin will increase; in an animal experiment, it was found that benazepril did not inhibit the vasopressor response of angiotensin II, and benazepril also will not affect the hemodynamics of neurotransmitters, such as acetylcholine, adrenaline and norepinephrine. It is believed that the mechanism of benazepril for lowering the blood pressure is inhibiting the renin-angiotensin-aldosterone system; therefore, the blood pressure lowering effect of benazepril still exists, even in patients with high blood pressure and low renin level.
The overseas clinical trials showed that no significant difference was found in the absorption rate and extent between the combination treatment of benazepril and amlodipine and single type treatment. The drug absorption of single type treatment will not be affected by food in gastrointestinal tract; no study has yet been performed on the relationship between food and the combination treatment. After taking the drug, the maximum serum benazepril concentration could be reached after 0.5-2 hours; when ester groups are being breakdown (mainly in the liver), they will become active metabolic products (benazeprilat). The maximum serum concentration of benazeprilat metabolites will be reached after 1.5-4 hours; the extent of benazepril absorption is at least 37%. The maximum serum amlodipine concentration will be reached after 6-12 hours and the extent of absorption is approximately 64%-90%.
The volume distributions of amlodipine and benazeprilat are 21L/kg and 0.7L/kg, respectively; in the body circulation, about 93% amlodipine will bind with serum proteins, and the binding ratio of benazeprilat will be even higher. In vitro studies found that concentration, age, and liver function will not affect the protein binding extent of benazeprilat.
The inhibition effect of benazeprilat on ACE is much greater than that of benazepril, and nearly all benazepril will be metabolized to benazeprilat; very few of the prototype drug will be found in urine voided, including about 20% benazeprilat, 8% benazeprilat glucuronide, and 4% benazepril glucuronide. Amlodipine is mainly metabolized by liver; 10% of the prototype and 60% of the metabolites will be excreted in urine. Patients with liver dysfunction have low amlodipine clearance rates, and the area under the curve of serum concentration will increase 40%-60%; therefore, the dose must be appropriately lowered (please refer to [instruction, dose]). Pharmacokinetics of amlodipine will not be affected in patients with renal dysfunction.
The effective elimination half-lives of benazeprilat and amlodipine are 10-11 hours and 2 days, respectively; if patients take the drugs once per day for a week, the serum concentration of those two drugs will be stabilized in blood. The elimination of benazeprilat from serum mainly goes through the kidneys; but, in normal populations, the elimination through bile represents 11%-12% of the benazepril excretion. Patients with renal dysfunction (creatinine clearance rate < 30mL/min) will require more time to reach the maximum concentration and stabilization of benazeprilat (please refer to [instruction, dose]); whereas, pharmacokinetics of benazeprilat will not change in patients with liver dysfunction. Age will not affect the pharmacokinetics of benazepril and benazeprilat, but the elimination rate of amlodipine in elders will decrease, causing the area under the curve of maximum concentration, elimination half-life and serum concentration to increase 35-70%. Therefore, dose adjustment might be required for elderly patients.
This drug requires a prescription from physicians.
The effective doses for high blood pressure are 2.5-10mg amlodipine and 10-80mg benazepril per day. In a clinical trial of 2.5-5mg amlodipine and 10-20mg benazepril combined treatment, it was found that the efficacy of the high blood pressure treatment will improve with the increasing dose of amlodipine; in non-black race populations, the efficacy of the high blood pressure treatment will also improve with the increasing dose of benazepril, which also reduced the edema events that occurred in patients that underwent amlodipine treatment.
The harm caused by benazepril is independent of dose; the harm caused by amlodipine is usually related to the dose used (peripheral angioedema), although some events are not related. When benazepril is used in combination with amlodipine, the incident rate of edema will decrease. Some non-dose related side effects may occur with the combination treatment of amlodipine and benazepril, but the edema incident rate will decrease as compared to the treatment of amlodipine alone.
: no dose adjustment is required for patients with creatinine clearance rate > 30 mL/min/1.73m2 (equaling to serum creatinine concentration ≤3 mg/dL or 265μmol/L); the starting dose of 5mg benazepril is recommended for patients with severe renal dysfunction and Amtrel use is not recommended for those patients.
For children, the elderly, weak patients and those with liver damage, the starting dose of 2.5mg amlodipine is recommended for either single treatment or combined treatment.
Do not use the drug in pregnant women, lactating women and patients who are allergic to benazepril, ACEI or amlodipine.
Potassium ion supplement and potassium-sparing diuretics: benazepril may reduce the loss of potassium ions caused by thiazide diuretics; potassium-sparing diuretics (spironolactone, amiloride, triamterene…etc.) or potassium ion supplements will increase the risk of hyperkalemia. If the described treatments above are used in combination, the concentrations of potassium ion in the serum of the patients needs to be monitored carefully.
: If a lithium agent is used in combination with ACEI treatment, some past reports have observed an increase in serum lithium concentration and lithium toxicity in the patients; therefore, the serum lithium concentration must be carefully monitored with the necessary combination treatment program.
Low dose naltrexone therapy in multiple sclerosis Y.P. Agrawal Department of Pathology, The University of Iowa, Iowa City, USA (YP Agrawal, MD PhD) Correspondence to: Yash Pal Agrawal, MD PhD, Department of Pathology, University of Iowa Roy J. and Lucille A. Carver College of Medicine, Iowa City 52242, USA. (e-m, FAX: 319-339-7148) Abstract The use of low doses of naltrexone
Pediatr Transplantation 2004: 8: 136–144Liver transplantation for children – the RedCross Children’s Hospital experienceMillar AJW, Spearman W, McCulloch M, Goddard E, Raad J,Rode H, Kahn D, Cywes S. Liver transplantation for children – theRed Cross Children’s Hospital experience. Pediatr Transplantation 2004: 8: 136–144. Ó 2004 Blackwell MunksgaardDepartment of Paediatric Surge