Nifedipine blood pressure

Fast DHP-induced lowering of blood pressure results in compensatory sympathetic activation and a subsequent increase in heart rate and cardiac oxygen demand. This unfavorable effect has been mainly associated with the use of short-acting DHPs, such as nonretarded formulations of nifedipine, nitrendipine, or... 

Napoli et al. [286] found that the nifedipine treatment of stroke-prone spontaneously hypertensive rats (SPSHR) suppressed the plasma and LDL oxidation and the formation of oxidation-specific epitopes and increased the survival of rats independently of blood pressure modification. Their results suggest that the protective effects of calcium blockers of dihydro-pyridine-type on cerebral ischemia and stroke may, at least in part, depend on their antioxidant activity. In vivo antioxidant effect of nilvadipine on LDL oxidation has been studied in hypertensive patients with high risk of atherosclerosis [287], It was found that there was a significant decrease in the level of LDL cholesterol oxidation in patients after nilvadipine treatment. 

Calcium Channel Blockers. The calcium channel blockers work by blocking the influx of calcium, an excitatory ion, into the cell. The first calcium channel blocker, verapamil (Calan), was introduced in the 1960s. Others, including diltiazem, nifedipine, and nimodipine, are now available. The calcium channel blockers have been used to treat a variety of medical conditions including high blood pressure, cardiac pain (angina) and arrhythmias, migraines, seizure disorders, and premature labor. 

In multidrug therapy, it is necessary to consider which agents rationally complement each other. A p-blocker (bradycardia, cardiodepression due to sympathetic blockade) can be effectively combined with nifedipine (reflex tachycardia), but obviously not with verapamil (bradycardia, cardiodepression). Monotherapy with ACE inhibitors (p. 124) produces an adequate reduction of blood pressure in 50% of patients the response rate is increased to 90% by combination with a (thiazide) diuretic. When vasodilators such as dihydralazine or minoxidil (p. 118) are given, p-blockers would serve to prevent reflex tachycardia, and diuretics to counteract fluid retention. 

Nifedipin causes relaxation of smooth musculature, dilation of coronary and peripheral arteries, and reduction of peripheral resistance and arterial blood pressure, and enhances oxygen supply to the heart. 

Patients with malignant-accelerated hypertension can usually be managed by oral therapy. Patients who are seen in a nursing home or clinic, whose BP is found to be above some arbitrary danger level like a BP of 180/120 should not automatically be given nifedipine sublingually. Indiscriminate use of nifedipine sublingually could lead to a major catastrophe like myocardial infarction or cerebrovascular episodes. Nifedipine activates sympathetic response and leads to precipitous drops of blood pressure followed by rebound hypertension. 

Answer Nifedipine, unless formulated for slow, sustained release, is characterized by relatively rapid onset of vasodUatory effects. This man s side effects reflect the rapid and intense fall in blood pressure and consequent reflex increases in sympathetic tone. The increase in anginal episodes also is a result of drug-induced periodic increases in heart rate. 

SOOl 2 Molina Cuevas, V., M.L. Arruzazabala, D. Carbajal Quintana, R. Mas Ferreiro, and S. Valdes Garcia. Effect of policosanol on arterial blood pressure in rats. Study of the pharmacological interaction with nifedipine and propranolol. Arch Med Res 1998 29(1) 21-24. 

Hypertensive crises are characterized initially by headache, but can evolve to include neck stiffness, chest discomfort, palpitations, confusion, and, ultimately, hemorrhage or stroke. Treatment of MAOI-associated hypertension may include a watch-and-wait stance by the patient if the symptoms are mild. Some patients have the ability to check and monitor their own blood pressure. Others may consult with a physician for blood pressure checks and observation, but if symptoms are severe, the patient may need to go to an emergency room or self-medicate. Standard emergency room treatment is intravenous phentolamine, an a-adrenergic blocker, continuous monitoring and management until blood pressure is normalized without medication. Some doctors will provide patients with small doses of chlorpromazine or nifedipine to treat hypertension if a problem arises. 

Self-medication of a MAOI-induced hypertensive crisis is controversial. In a hypertensive crisis the lack of access to medical services may lead to even greater complications. A small dose of medication taken as part of a larger plan to blunt the rise in blood pressure may prevent serious complications. However, headache is common, has multiple causes, and patients may not accurately identify a headache due to hypertension without a blood pressure check. In addition, selfadministration of nifedipine, especially sublingually, may result in needless and perhaps dangerous drops in blood pressure. 

If a patient s blood pressure is greatly increased, pharmacological treatment should be instituted. Treatments for MAOI-induced hypertension include administration of the calcium channel blocker nifedipine and use of drugs with a-adrenergic-blocking properties, such as phentolamine (5 mg intravenous). Because treatment with phentolamine may be associated with cardiac arrhythmias or severe hypotension, this approach should be carried out only in an emergency department setting. 

To control hypertension, phentolamine 5 mg i.v. is recommended, with repeated doses of 0.25 to 0.5 mg i.m. every 4 to 6 hours. Alternatively, chlorpromazine 50 mg i.m. is given, followed by 25 mg i.m. every 1 to 2 hours. Nifedipine is not recommended. Blood pressure should be monitored closely to avoid overcompensation and hypotensive episodes. 

Verapamil, diltiazem, and the dihydropyridine family (amlodipine, felodipine, isradipine, nicardipine, nifedipine, and nisoldipine) are all equally effective in lowering blood pressure, and many formulations are currently approved for this use in the USA. Clevidipine is a newer member of this group that is formulated for intravenous use only. 

Calcium antagonists can cause serious toxicity or death with relatively small overdoses. These channel blockers depress sinus node automaticity and slow AV node conduction (see Chapter 12). They also reduce cardiac output and blood pressure. Serious hypotension is mainly seen with nifedipine and related dihydropyridines, but in severe overdose all of the listed cardiovascular effects can occur with any of the calcium channel blockers. 

Pereira et al. (1993) evaluated postoperative pain relief and incidence of side-effects of the combination of epidural morphine (0.5 mg) and sublingual nifedipine (10 mg). In this double-blind, placebo-controlled study 36 women were submitted to elective operations (hysterectomy and colpoperineoplasty). The nifedipine-treated group showed a significant drop in blood pressure which was controlled by rehydration. The results indicate that epidural morphine-induced postoperative pain relief may be enhanced by systemic administration of nifedipine with easily controlled side-effects. 

Another group of drugs that relax heart muscle are the calcium-channel blockers. One example is nifedipine, shown in Figure 14.46. Muscle contraction is initiated as a nerve impulse signals calcium ions to enter muscle cells. As their name implies, calcium-channel blockers inhibit the flow of calcium ions into muscles, thereby inhibiting muscle contraction. The heart rate slows down, and muscles of blood vessels relax and dilate, lowering blood pressure. 

There was an increase in blood pressure throughout 24 hours in a double-bhnd, placebo-controlled, crossover study in 47 hypertensive patients who were also taking nifedipine (10). This finding differs from other studies in which melatonin had a mild hypotensive effect (11) and may indicate an interaction between melatonin and nifedipine. Tachycardia, chest pain, and cardiac dysrhythmias have also been reported, although the relation to melatonin was not clearly established (5). 

Calcium channel blockers (CCBs) prevent the flow of calcium ions through channels in heart tissue. Inhibiting calcium flow decreases the strength of contraction of the heart and decreases blood pressure. Most CCBs fall into the dihydropyridine structural class, with nifedipine (Adalat, A.132) being the prototypical example (Figure A.38). Nondihydropyridine CCBs include diltiazem (Cardizem, A.135) and verapamil (Calan, A.136). 

Mibefradil is a tetralol derivative developed as a unique CCB. Its efficacy as an antihypertensive was demonstrated in phase III trials, where doses of 50 to 100 mg were compared to other CCBs (nifedipine SR, diltiazem CD, nifedipine GITS, amlodipine). Mibefradil was shown to be equally effective as or more effective than nifedipine SR, diltiazem CD, nifedipine GITS, or amlodipine in reducing blood pressure in mild to moderate hypertension. Average reductions of diastolic blood pressure of as much as 15 mmHg were seen with the 100-mg dose. It was also found to be effective in the treatment of chronic stable angina. Thus, it was indicated for use in hypertension and stable angina at doses of 50 or 100 mg once daily (15). 

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