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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Algorithms have been developed to guide the treatment of simple hypertension. The basic algorithms are modified in the face of concurrent medical conditions, taking into account the various pharmacological effects of antihypertensive agents. This article reviews the neuropsychiatric effects of the major classes of antihypertensive agents (ganglionic blockers, centrally acting agents, diuretics, vasodilators, beta-blockers, calcium channel blockers and angiotensin converting enzyme inhibitors). The purported efficacy of some antihypertensive agents in the treatment of psychiatric conditions is also discussed. Beneficial as well as adverse neuropsychiatric effects are reviewed. In this way, guidelines for the treatment of hypertension are suggested which take into account a broad spectrum of neuropsychiatric considerations.
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PMID:Neuropsychiatric considerations in the treatment of hypertension. 195 79

Angiotensin-converting enzyme (ACE) inhibitor therapy has been reported to improve patient survival and promote recovery of renal function in the renal crisis of systemic sclerosis. In addition, an ACE inhibitor and a calcium channel blocker have been reported to control hypertension and reverse dialysis-dependent renal failure in a patient with undifferentiated connective tissue disease. We treated a patient with undifferentiated connective tissue disease who developed hypertension, pulmonary compromise, and renal failure requiring prolonged dialysis therapy. Due to allergy, the patient's hypertension could not be treated with ACE inhibitors initially, yet pulmonary function improved and renal function partially recovered with tenormin and minipress. When blood pressure became refractory to tenormin and minipress after 14 months of peritoneal dialysis, the patient was treated with lisinopril alone. Pulmonary function has remained stable and the patient has been off renal replacement therapy for 26 months, with a further substantial increase in creatinine clearance following treatment with lisinopril. The delayed and sustained recovery of renal and pulmonary function in the present case suggests undifferentiated connective tissue disease, like systemic sclerosis, may benefit from therapy with ACE inhibitors.
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PMID:Recovery of renal function in undifferentiated connective tissue disease after treatment with angiotensin-converting enzyme inhibitors. 196 60

Some calcium entry blockers seem to improve the neurological survival of anoxic comas. The early monitoring of intracranial pressure shows the frequency of intracranial hypertension. A calcium channel blocker has been shown to increase the cerebral blood flow which can potentially lead to deleterious increases of the intracranial pressure. This study presents 39 out-of-hospital cardiac arrests resuscitated with success. The intracranial pressures were registered by means of an extra dural screw set up as soon as possible. Nineteen patients received an early continuous 5 days nimodipine treatment (0.58 gamma/kg weight/min. after a 12.3 gamma/kg weight bolus). The other 20 patients did not receive any calcium entry blocker. The two groups were similar in terms of age, origin and electrical type of cardiac arrest, duration of cardiac arrest before BLS and before ACLS, principles of the treatment, initial neurological status and biological values. The maximum and mean intracranial pressures of the nimodipine group were always lower than the intracranial pressure of the control group. The cerebral perfusion pressure was never significantly different in both groups. If the nimodipine treatment proves to be efficient on neurological survival, it would be all the more interesting because it seems to limit the intracranial hypertension phenomenon which aggravates the neurological prognosis.
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PMID:Early effects of nimodipine on intracranial and cerebral perfusion pressures in cerebral anoxia after out-of-hospital cardiac arrest. 196 44

The dihydropyridine derivatives constitute a distinct subcategory of calcium channel blockers that have marked peripheral vascular effects with minimal or no electrophysiologic actions when administered to intact animals or humans. These dihydropyridine derivatives are structurally similar to nifedipine, the most widely studied dihydropyridine. The derivatives have varying affinities for different regional circulations, and there may be an important relationship between structure and activity of these compounds with respect to the predilection of the site of their action in vascular tissue. It is possible that such differences may be of clinical significance. As a class, the dihydropyridines exert reasonably distinct hemodynamic changes that may be of particular importance in the treatment of hypertension, cardiac failure, and regurgitant valvular lesions. Nicardipine hydrochloride is a newer agent that has undergone extensive evaluation in recent years. Pharmacologically and electrophysiologically, it resembles other dihydropyridines. Unlike nifedipine, however, it can be administered by both the intravenous and oral routes. There are additional differences between its properties and those of other calcium channel blockers. For example, nicardipine appears to produce a greater increase in coronary sinus blood flow than other calcium channel blockers. The clinical significance of this finding is unclear. In addition, nicardipine appears to increase myocardial contractility, even in patients with severe congestive cardiac failure. Nicardipine produces a dose-dependent decrease in blood pressure and systemic vascular resistance with increases in heart rate, left ventricular dP/dt, LV ejection fraction, cardiac output, and stroke work index, but no significant change in LV end-diastolic pressure. Clearly, the drug has negligible venodilator actions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical pharmacology, pharmacokinetics, and hemodynamic effects of nicardipine. 196 96

Vascular contractile effects of postsynaptic alpha 2-adrenergic receptor stimulation are believed to involve transmembrane calcium influx. Although the current knowledge of the alpha 2-receptor response coupling of vascular smooth muscle contractions is still limited, the fundamental mechanism(s) may involve the extracellular calcium utilization process. This is mediated via the alpha 2-receptor operated calcium channel, which can be pharmacologically distinguished from that mediated via the potential-dependent calcium channel. Therefore, vascular selective alpha 2-antagonists may produce vasorelaxation via a calcium inhibitory action that is different from that of the typical calcium channel blockers. The literature on the in vitro isolated vascular tissue models has been reviewed with emphasis on the methodology for study of alpha 2-antagonist-induced vascular relaxation via selective blockade of the alpha 2-receptor-operated calcium channel. The alpha 2-adrenergic receptors, like alpha 1-receptors on vascular smooth muscle, serve an important role in the control of the arterial, as well as the venous tone in experimental animals and humans in relationship to sympathetic and humoral adrenergic activation of the cardiovascular system. Of particular importance is the possibility that alterations in vascular control of alpha 2-adrenergic mechanisms may lead to increased intracellular free calcium concentrations, thereby causing elevated vascular resistance and high blood pressure. This view is consistent with the long held concept that disturbances of cellular calcium metabolism play a primary role in the pathogenesis of various forms of hypertension. Consequently, selective blockade of vascular alpha 2-adrenergic receptors would be a feasible approach for antihypertensive therapy. This type of antihypertensive agent would be expected to exhibit fewer side effects with efficacy, directed towards the etiology of hypertension.
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PMID:Alpha 2-adrenergic receptors and calcium: alpha 2-receptor blockade in vascular smooth muscle as an approach to the treatment of hypertension. 197 6

The four classes of first-line antihypertensive agents recommended in the 1988 report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure are reviewed here. Particular consideration is given to the effects of these agents on heart rate, atrioventricular nodal conduction, and myocardial contractility in patients with other cardiovascular diseases. Diuretics and angiotensin-converting enzyme inhibitors have no significant direct effects on cardiac function. beta-Blockers inhibit catecholamine stimulation of the heart and may be particularly beneficial in treating patients with a history of myocardial infarction. Calcium channel blockers reduce blood pressure by dilating arterial resistance vessels. They are structurally heterogeneous and highly selective in their sites of action. As a consequence, cardiac effects can be minimized by selecting a calcium channel blocker with more potent peripheral vasodilatory effects. A new calcium channel blocker, isradipine, currently undergoing clinical trials, is highly selective for arterial smooth muscle and appears to be a safe and effective antihypertensive agent.
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PMID:Cardiac contractility and conduction: a comparison of antihypertensives. 197 5

Patient 1 received carteolol and captopril for hypertension. Three days after a slow-release diltiazem preparation (300 mg) had been introduced, he developed cardiogenic shock and sinus bradycardia (heart rate: 30/mn) with acidosis and severe hyperkaliemia. He was successfully treated by temporary pacing and dobutamine. Patient 2 had received sotalol and captopril for several years. Twelve hours after slow release diltiazem had been added, he was found in cardiogenic shock and extreme bradycardia with wide QRS, acidosis and hyperkaliemia. He died one hour later despite intensive emergency treatment. Concomitant use of beta-blockers and calcium channel blockers has been reported in patients suffering of severe coronary heart disease. However, several adverse reactions similar to our cases have been described. Slow-release diltiazem should be avoided in hypertensive patients taking beta-blockers.
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PMID:[Combination of slow-release diltiazem and a beta-blocker in arterial hypertension. 2 cases of cardiogenic shock with severe bradycardia]. 197 94

The pathophysiological connections between insulin resistance, hypertension and type 2 diabetes are discussed in this review article. Increased blood pressure levels are often found in type 2 diabetic patients long before the diabetes itself is diagnosed. By contrast, in type 1 diabetes hypertension is predominantly the consequence of diabetic glomerulopathy. Non-pharmacological strategies should be favoured in the treatment of hypertension in type 2 diabetic patients before specific pharmacological intervention is started. Antihypertensive treatment with beta-blocking agents and diuretics is criticized by many experts in the field of metabolic disorders, since these drugs induce a deterioration of glycaemic control and lipid metabolism in diabetic patients. Since calcium channel blockers, ACE inhibitors and alpha 1-specific blocking agents have no influence on metabolism, these drugs are recommended for the antihypertensive treatment of diabetic patients. Further studies should be undertaken to clarify, whether ACE-inhibitors have a specific nephroprotective effect. Since most type 2 diabetic patients do not develop diabetic nephropathy, a possible nephroprotective effect of ACE inhibitors is only relevant to the antihypertensive treatment of type 1 diabetic patients.
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PMID:[Hypertension, insulin resistance and diabetes mellitus: pathophysiological interactions and therapeutic consequences]. 198 Jul 67

In a double-blind, randomized, multicenter study, the efficacy and safety of intravenous (IV) nicardipine was compared with placebo in the control of postoperative hypertension in cardiac and noncardiac surgical patients. One hundred twenty-two patients (17 cardiac and 105 noncardiac surgery) met the entry criteria (systolic BP greater than or equal to 140 mm Hg or diastolic BP greater than or equal to 95 mm Hg) and were randomized (3:2) to receive IV nicardipine (n = 71) or placebo (n = 51). Therapeutic response (greater than or equal to 15 percent reduction in BP from baseline) was achieved in 94 percent of patients treated with IV nicardipine vs 12 percent with placebo (p less than 0.001). The mean response time and infusion rate for IV nicardipine were 11.5 (+/- 0.8) minutes and 12.8 (+/- 0.3) mg/h, respectively. The magnitude of BP reduction was similar in both cardiac and noncardiac postsurgical patients. Blood pressure control was sustained with minimal dose adjustments of IV nicardipine (3.0 +/- 0.2 mg/h) during a prolonged maintenance infusion period of 6.8 +/- 0.5 h. A reflex mean increase in heart rate of 5 bpm was seen in patients treated with IV nicardipine. Sixteen patients (15 noncardiac and one cardiac surgery) had a sustained heart rate of greater than 100 bpm, with a mean increase of 24 bpm from the baseline. In all these patients except three, tachycardia was resolved while receiving nicardipine. None of these patients who had development of tachycardia during nicardipine therapy had exhibited ST segment changes indicative of ischemia. One patient with tachycardia at baseline had exhibited ST segment depression (3 to 4 mm) during nicardipine treatment, which was resolved following discontinuation of nicardipine therapy and application of nitroglycerin (Nitropaste). Hemodynamic evaluation revealed that IV nicardipine significantly decreased mean arterial pressure, systemic vascular resistance, and significantly increased cardiac index with no change in heart rate. These hemodynamic changes were similar in cardiac and noncardiac surgical patients. Adverse experiences reported with IV nicardipine included hypotension (4.5 percent), tachycardia (2.7 percent), and nausea/vomiting (4.5 percent). In the placebo group, the incidence of adverse experience was 6 percent, with an equal distribution of hypotension (2 percent), nausea/vomiting (2 percent), and headache (2 percent). No clinically important changes in laboratory variables related to IV nicardipine were reported. In conclusion, these findings indicate that nicardipine, a titratable intravenous calcium channel blocker, can rapidly and effectively control postoperative hypertension in cardiac and noncardiac surgical patients.
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PMID:Efficacy and safety of intravenous nicardipine in the control of postoperative hypertension. IV Nicardipine Study Group. 198 1

Calcium channel blockers, originally developed for the treatment of angina and supraventricular arrhythmias, have been shown to lower elevated blood pressure effectively in hypertensive patients. Verapamil, nifedipine, and diltiazem represent prototype compounds for unique chemical classes with differing pharmacologic properties. These drugs lower elevated blood pressure with efficacy comparable with other commonly used antihypertensives. Combination therapy with other agents usually results in an additive response. Side effects are usually mild and reversible and usually are an extension of the drug's pharmacologic effects. Moreover, adverse metabolic effects on lipid, glucose, or potassium levels are not common. Because of the excellent antihypertensive effects of calcium channel blockers and their potential importance in a variety of other disease states, these agents should be routinely considered for use as a first-line antihypertensive agent in appropriately selected patients with hypertension of any severity as part of a comprehensive plan to minimize cardiovascular risk.
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PMID:The role of calcium channel blockers in the treatment of essential hypertension. 199 52


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