Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 51-year-old woman with Sneddon's disease presented with transient right hemifield loss of vision and transient right-sided weakness. Over the preceding decade she had experienced a slow decline in mental function. She also had hypertension, migraine, and a mixed seizure disorder. She had skin changes typical for generalized livedo reticularis but she did not have Raynaud's phenomenon or winter ulcerations. Her disease was not understood until the stroke-related symptoms were associated with the skin abnormalities. We review the neuro-ophthalmic manifestations of Sneddon's disease and add data from our case to the growing body of fact that suggests that Sneddon's disease may be an immunologically mediated vasculopathy.
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PMID:Sneddon's disease presenting with visual loss and dementia. 297 41

The widespread use of beta-adrenoceptor antagonists against hypertension, angina pectoris and migraine or as a preventive treatment after myocardial infarction has encouraged us to investigate the effects of these drugs on platelet function. The aim of this study was to examine whether beta-blocking drugs interfere with platelet beta- adrenoceptors and whether this dependency is related to their selectivity for beta-adrenoceptor subtypes. Beta-adrenoceptor stimulation of human platelets with isoprenaline increased cyclic AMP (cAMP), which is known to inhibit platelet aggregation. Furthermore, our studies showed that cAMP formation in vitro was stimulated by non-selective and beta 2-selective agonists, but not by the predominant beta 1-agonist prenalterol. Isoprenaline- stimulated cAMP formation was blocked by the non- selective beta-adrenoceptor antagonists propranolol, timolol, and alprenolol, while the beta 1-selective antagonists atenolol and metoprolol had no influence on an isoprenaline-induced cAMP formation. Receptor binding studies using (3H)-dihydroalprenolol revealed an IC50 value for propranolol of 85 nM, while metoprolol only displaced the bound (3H)-dihydroalprenolol at far higher concentrations (IC50, 20 microM). We conclude that the human platelet beta-adrenoceptors are mainly of the beta 2- subtype and that beta-adrenoceptor antagonists, especially the non-selective antagonists interfere with platelet function assessed as platelet cAMP formation.
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PMID:Characterization of human platelet beta-adrenoceptors. 300 61

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

Relatively few studies have addressed the issue of the Minnesota Multiphasic Personality Inventory (MMPI) alexithymia scale's construct validity. In this study, the validity of the scale is supported by the finding of a significantly lower percentage of alexithymic individuals in a large sample of psychiatric inpatients than in samples of patients with a variety of physical disorders (i.e., migraine headaches, asthma bronchitis/emphysema, and hypertension). Validity of the scale is further supported through a comparison of the alexithymic and nonalexithymic psychiatric inpatients on a series of Rorschach and MMPI variables. As predicted, alexithymics were less verbally productive, displayed less ability to fantasize, and demonstrated greater defensive pseudonormality. Results suggest the measure may be of value in studies of psychiatric patients as well as those with physical disorders.
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PMID:The construct validity of the MMPI alexithymia scale with psychiatric inpatients. 321 Jan 18

One hundred and twenty-nine patients notified to the Perth Community Stroke Study in whom the final diagnosis was cerebrovascular disease were matched with controls of the same sex and 5-year age group drawn from the records of the usual general practitioner of each index case. The control subjects were interviewed and examined briefly at home, following the same protocol as that used for assessment of cases. The significant risk factors for cerebrovascular disease to emerge in the case-control comparison were previous stroke (estimated relative risk 6.6), signs of peripheral vascular disease (3.6) and current smoking (2.6). Being married (0.6) and history of migraine (0.4) were significant protective factors. There was no association between a history of hypertension and cerebrovascular disease in this series.
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PMID:A case-control study of cerebrovascular disease in Western Australia. 326 50

The calcium channel blockers initially were approved for the treatment of classical and variant angina pectoris. Recent studies indicate that these agents also are useful in such diverse conditions as pulmonary and systemic hypertension, hypertrophic cardiomyopathy, arrhythmias, asthma, Raynaud's syndrome, esophageal spasm, myometrial hyperactivity, cerebral arterial spasm, and migraine.
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PMID:Calcium channel blockers. 327 88

Propranolol is a commonly used drug; of new and refilled prescriptions, it ranked no. 1 in 1984 and no. 2 in 1985. Medical conditions for its use include angina pectoris, myocardial infarction, hypertension, cardiac dysrhythmias, hypertrophic subaortic stenosis, migraine headache, hyperthyroidism, and pheochromocytoma. Almost all dental practitioners will treat a patient receiving propranolol for one of these conditions. The following recommendations seem appropriate at this time: The patient should continue to receive propranolol during dental treatment. Sudden withdrawal of the beta-blocker will cost the patient the benefit of propranolol therapy and may lead to acute myocardial ischemia. Acute stress should be minimized, as hypertensive responses may also be caused by endogenously released epinephrine. Short appointments scheduled in the morning, possibly with conscious sedation, should be considered. The dosage of adrenergic vasoconstrictors should be limited and gingival retraction cord containing epinephrine avoided entirely. The blood pressure should be taken approximately 5 minutes after local anesthesia is administered to determine if a systemic response has occurred. In the unlikely event of a hypertensive emergency, a rapidly acting, short-duration antihypertensive drug, such as the alpha-blocker phentolamine (Regitine, 5 mg intravenously) should be administered. Sublingual nitroglycerin (Nitrostat, 0.4 mg) may be useful as a nonparenteral alternative. These recommendations apply to other nonselective beta-blockers, including nadolol (Corgard) and timolol (Blocadren). They may also apply to labetalol (Normodyne, Trandate), a nonselective beta-antagonist with some alpha-blocking activity and to pindolol (Visken), a beta-blocker with some intrinsic beta 2-agonistic activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertensive response to levonordefrin in a patient receiving propranolol: report of case. 327 28

This paper calls attention to the methodologies designed to investigate the higher cortical functions in order to elicit signis of encephalopathy in apparently normal conditions. This can be done by testing the blobal hemispheric funcionts or the interhemispheric functional balance. This shows up the clinical sequels that may precede or be the outcome both of transient pathological disorders, such as transient global anemia, migraine, TIAs and subarachnoid hemorrhage without apparent clinical consequences and of nontransient pathological conditions, such as epilepsy, occupational diseases, arterial hypertension and cerebral revascularization.
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PMID:Neurobehavioral investigation as a tool for revealing preclinical disorders. 332 25

Increasing recognition of the importance of calcium in the pathogenesis of cardiovascular disease has stimulated research into the use of calcium channel blocking agents for treatment of a variety of cardiovascular diseases. The favorable efficacy and tolerability profiles of these agents make them attractive therapeutic modalities. Clinical applications of calcium channel blockers parallel their tissue selectivity. In contrast to verapamil and diltiazem, which are roughly equipotent in their actions on the heart and vascular smooth muscle, the dihydropyridine calcium channel blockers are a group of potent peripheral vasodilator agents that exert minimal electrophysiologic effects on cardiac nodal or conduction tissue. As the first dihydropyridine available for use in the United States, nifedipine controls angina and hypertension with minimal depression of cardiac function. Additional members of this group of calcium channel blockers have been studied for a variety of indications for which they may offer advantages over current therapy. Once or twice daily dosage possible with nitrendipine and nisoldipine offers a convenient administration schedule, which encourages patient compliance in long-term therapy of hypertension. The coronary vasodilating properties of nisoldipine have led to the investigation of this agent for use in angina. Selectivity for the cerebrovascular bed makes nimodipine potentially useful in the treatment of subarachnoid hemorrhage, migraine headache, dementia, and stroke. In general, the dihydropyridine calcium channel blockers are usually well tolerated, with headache, facial flushing, palpitations, edema, nausea, anorexia, and dizziness being the more common adverse effects.
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PMID:Differential effects of 1,4-dihydropyridine calcium channel blockers: therapeutic implications. 332 59

Serotonin released from aggregating platelets can reach sufficient concentrations to affect local vascular function in a number of ways. The monoamine can cause contraction of blood vessels by its direct action on smooth muscle or by potentiating the effect of other vasoconstrictor agents. It can also induce vasodilatation by a direct relaxing effect on smooth muscle, by inhibition of adrenergic nerves, and by release of an uncharacterized relaxing factor from endothelial cells. One of its most likely physiological roles is to aid in haemostasis by promoting platelet aggregation and by causing local vasoconstriction at sites of injury. It probably has a role in some forms of vascular pathology as well: it may contribute to vasospasm of cerebral, coronary, and digital arteries, particularly if there is endothelial dysfunction or damage. Much evidence has implicated serotonin (5-hydroxytryptamine) in the pathogenesis of migraine. Serotonergic agonists, such as ergotamine, and antagonists, such as methysergide and pizotifen, are both used in therapy of migraine. Promising but conflicting early results have not yet defined a place for serotonergic antagonists in other vasospastic disorders. The antihypertensive efficacy of one serotonergic antagonist, ketanserin, raises questions about the possible involvement of serotonin in either the initiation or the maintenance of the elevated peripheral vascular resistance in several forms of hypertension, including essential hypertension.
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PMID:Serotonin and the vascular system. Role in health and disease, and implications for therapy. 351 33


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