Nitrendipine1is a calcium entry blocker shown to inhibit the movement of calcium through the ‘slow channel’ of cardiac and vascular smooth muscle, thus inducing peripheral vasodilation with consequent reductions in elevated blood pressure.
As evidenced by clinical trials, nitrendipine promptly lowers blood pressure in patients with mild to moderate hypertension, and sustains this effect during long term administration. Combining nitrendipine with other antihypertensive agents such as diuretics or β-blockers often results in successful treatment in patients unresponsive to nitrendipine monotherapy. Headache, oedema, flushing and palpitations commonly occurring during treatment with nitrendipine are generally mild, usually subsiding with continued therapy. Thus, although additional long term studies are required to properly assess the relative merits of the drug compared with other antihypertensives, by providing the clinician with an effective and safe alternative to traditional therapies, nitrendipine represents a step forward in the treatment of mild to moderate hypertension.
As occurs with other calcium entry blockers, nitrendipine inhibits the ‘slow’ channel inward current of calcium into cardiac and vascular tissue. Furthermore, nitrendipine has been shown to possess a high degree of selectivity for vascular smooth muscle; hence, its main effect is to decrease peripheral vascular resistance with subsequent reduction of blood pressure. In vitro investigations in animal coronary artery and aorta demonstrate that nitrendipine blocks contractions induced by potassium, barium and calcium chloride, and the calcium agonist Bay K 8644 to a similar extent as nicardipine, nisoldipine and nimodipine, and more strongly than nifedipine, verapamil and diltiazem. However, unlike the latter 3 drugs, nitrendipine does not alter conduction through the sinus or atrioventricular nodes.
In patients with mild to moderate hypertension, a single 20mg oral dose of nitrendipine has been shown to lower systolic and diastolic pressure by about 15 to 20% within 1 to 2 hours after administration. During longer term administration of nitrendipine, usually 20 to 40 mg/day, this effect is sustained. The effects of nitrendipine on resting blood pressure appear to be greater than its effects on blood pressures elevated during submaximal exercise. Although most pharmacodynamic studies have employed nitrendipine in twice daily dosage regimens, once daily dosing has also been shown to effectively maintain reductions in blood pressure.
Elderly patients and those with low baseline plasma renin activities tend to respond better to nitrendipine than their younger counterparts and those with high plasma renin activities. However, a close correlation between high pretreatment blood pressure and the degree of response to the drug has not been convincingly demonstrated. In normotensive subjects blood pressure remains the same or may decrease after nitrendipine. Conversely, nitrendipine initially increases heart rate in both normotensive and hypertensive subjects, but this effect diminishes with continued treatment.
Although nitrendipine produces significant reductions in systemic vascular resistance, alterations in cardiac output and decreases in left ventricular filling pressure have not been consistently observed. Furthermore, while cardiac output and left ventricular ejection time have increased in some short term studies, these effects are probably not significant in the long term. Some hypertensive patients have experienced diminution in left ventricular hypertrophy during nitrendipine therapy, but no correlation has been demonstrated between these reductions and decreases in blood pressure in humans as yet. In a single study, nitrendipine reduced cardiac workload during exercise and prolonged time to onset of angina pectoris.
Studies in hypertensive patients investigating the effects of nitrendipine on the peripheral vascular circulation have shown that the drug produces a significant dilatation of small and large arteries resulting in decreases of total peripheral vascular resistance of about 20%.
The renal effects of nitrendipine have not been fully elucidated, but it has been observed that the drug does not produce consistent changes in animal renal perfusion or in renal blood flow, renovascular resistance or glomerular filtration rate in humans. Diuresis seen following acute doses of nitrendipine has not persisted with long term use. Significant potassium loss is unlikely with nitrendipine, but urinary excretion of aldosterone was shown to increase during a 6-month study. Furthermore, most evidence indicates that the drug initially increases plasma renin activity, but this effect may diminish with prolonged treatment.
In animal models, nitrendipine dilates cerebral blood vessels as do some other dihydropyridine derivatives, and reduces pulmonary artery vasoconstriction with subsequent decreases in pulmonary artery pressure. A single study in patients with pulmonary hypertension demonstrated similar effects. Further studies of the effect of nitrendipine in pulmonary hypertension are needed.
In addition to its relaxant effects on vascular smooth muscle, nitrendipine inhibits tracheobronchial and uterine contractions in animal models in vitro; however, the clinical implications of these findings are uncertain. No changes have occurred in fasting blood glucose or plasma lipids in patients receiving nitrendipine.
After an oral dose of nitrendipine 20mg, peak plasma concentrations (which vary widely from 5 to 40 µg/L) are achieved within 1 to 2 hours. Proportional increases in AUC after 10, 20 and 40mg oral doses of the drug indicate that nitrendipine kinetics are linear within this dosage range; furthermore, nitrendipine does not accumulate after multiple dosing.
Nitrendipine is about 98% bound to plasma proteins; its 4 more polar inactive metabolites are bound less extensively (70 to 80%). The volume of distribution of the drug is 2 to 6 L/kg at steady-state.
Nitrendipine undergoes extensive hepatic biotransformation. Less than 0.1% of an oral dose appears as unchanged drug in the urine, while about 80% of a dose is recoverable during the first 96 hours as inactive polar metabolites.
The half-life of nitrendipine, while variable, is about 12 to 24 hours as measured by recently developed sensitive assays. Since the drug is effective as a once daily dosage regimen, it has been suggested that release from deep tissue compartments prolongs its activity. As might be expected with such an extensively metabolised compound, hepatic but not renal disease prolongs the elimination half-life and increases its bioavailability, possibly because of decreases in the ‘first-pass’ effect. Consequently, dosage modifications may be required in patients with hepatic disease. Elderly subjects in apparent good health have also demonstrated increased plasma concentrations of nitrendipine.
Open trials of 1 to 12 months’ duration have shown that nitrendipine (usually 10 to 40mg daily) reduces systolic and diastolic pressures to within normal limits in 45 to 86% of patients with mild to moderate hypertension. These response rates can be further increased by the addition of a β-blocker or a diuretic. Results from a few comparative trials indicate that nitrendipine enables significantly more patients to achieve goal blood pressures than does placebo, and is as effective as hydralazine, hydrochlorothiazide, β-blockers (atenolol, oxprenolol, acebutolol and propranolol) and nifedipine.
In addition, when nitrendipine is combined with β-blockers, a diuretic or captopril, target antihypertensive response is often attained in patients previously unresponsive to nitrendipine monotherapy. While recent evidence indicates that the antihypertensive effect of nitrendipine persists during prolonged treatment, further long term studies are needed to adequately assess the potential, if any, for development of tolerance to the drug.
The most commonly reported side effects of nitrendipine — headache, flushing, oedema and palpitations — arise from the vasodilating properties of the drug. Despite their relatively frequent occurrence, these adverse reactions are generally mild and usually disappear with continued treatment, and necessitate withdrawal from therapy in only about 5% of patients. However, some patients may require supplementary analgesics, diuretics or a β-blocker if initial headache, oedema or tachycardia persists.
Plasma concentrations of digoxin have either increased or remained unchanged during concomitant administration of nitrendipine; hence, whether downward adjustment of the digoxin dose may be required is uncertain. Plasma concentrations of nitrendipine have not been affected by the simultaneous administration of ranitidine, cimetidine, digoxin or digitoxin.
Dosage and Administration
Therapy with nitrendipine should be initiated at a dose of 10mg given once daily, and the dose titrated to individual patient responses over several weeks to a maximum of 40 mg/day in 1 or 2 doses. Elderly patients may respond to lower daily doses (5 to 10mg/day). Dosage adjustments may be necessary in the presence of hepatic but not renal insufficiency.
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