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)

When a saccular aneurysm suddenly ruptures the intracranial pressure (ICP) abruptly rises to reach a level at about the diastolic blood pressure in 1 to 2 minutes. Unless a haematoma is formed ICP will soon fall and reach a steady level in about 10 minutes. In the days following the initial SAH several pathophysiological events take place. Regional CBF and the cerebral metabolic rate of oxygen (CMRO2) are reduced resulting in so-called luxury perfusion due to an uncoupling between flow and metabolism. The arteriovenous difference of oxygen is always reduced. CMRO2 falls parallel to increasing severity of vasospasm. CBF below 20 ml/100 g/min in cases of severe diffuse spasm inevitably result in brain tissue infarction. The development of vasospasm, which reaches a maximum between the 5th and 9th day after SAH, is accompanied by CSF lactacidosis and intracranial hypertension. The reactivity of the cerebral arteries after SAH is often impaired. Cerebral autoregulation to arterial hypotension is disturbed even in mild cases, and globally fails in severe vasospasm. On the other hand the reactivity of the cerebral vasculature to changes in arterial PCO2 is always preserved although reduced. Only in the presence of severe tissue acidosis will both modes of reactivity be damaged--so-called total vasoparalysis.
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PMID:Pathophysiology of subarachnoid haemorrhage. Experimental and clinical data. 306 37

2 cases reports are described of patients with renal artery stenosis who presented with hypertensive encephalopathy, normal blood pressures having been recorded within the previous 6 months while taking oral contraceptives (OCs). A 27-year-old woman, admitted to the hospital following 2 grand mal fits, had suffered from increasing headaches, nausea, and vomiting over the previous month. Her blood pressure had been elevated at 160/110 mmHg 1 week prior to admission but had been normal over previous 11 years while taking OCs (various formulations of combined estrogen and progestogen) which she had stopped taking 2 months previously. She was a nonsmoker. Her blood pressure was controlled with atenolol, nifedipine, and bendrofluazide, and her conscious level returned to normal with no further fits. An intravenous urogram revealed a small left kidney with a delayed nephrogram, and subsequent arteriography showed bilateral medial fibromuscular dysplasia with a narrow stenosis of the left renal artery. Attempted balloon angioplasty was unsuccessful due to arterial spasm. 4 months after presentation she became pregnant. Blood pressure was controlled with methyl dopa during pregnancy which progressed uneventfully to full term. In the 2nd case, a 19-year old girl became confused and suffered a grand mal convulsion. She had complained of headaches over the previous 3 days. Her blood pressure had been normal over the previous 6 months while taking Logynon (phased formulation of ethinylestradiol and levonorgestrel). She was a nonsmoker. On admission to the hospital, she suffered further generalized convulsions. Despite control of her convulsions with intravenous chlormethiazole, her blood pressure rose to 220/140 mmHg, and this was controlled with intravenous hydralazine and propranolol. The following day she was conscious and was changed to oral therapy. A renogram and DMSA scan showed normal sized kidneys, but there was evidence of decreased blood flow to the left kidney with an increased transit time. Renal arteriography showed a stenosis of the left renal artery, typical of intimal fibromuscular dysplasia, which was dilated by balloon angioplasty. Anti-hypertensive medication was withdrawn postoperatively, and her blood pressure has remained well controlled. In both of the cases the onset of hypertension was rapid with encephalopathy being the presenting feature. Hypertensive encephalopathy is well recognized as a presenting feature of renal transplant artery stenosis but not in cases of native renal artery stenosis. 1 of the patients had stopped using OCs 2 months before presentation, suggesting that although there may have been an association between OC use and the development of fibromuscular dysplasia, it could not be implicated in the mode of presentation.
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PMID:Encephalopathy in renovascular hypertension associated with the use of oral contraceptives. 311 27

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

Pulmonary arterial hypertension may develop in patients with systemic lupus erythematosus (SLE) in the absence of lung tissue lesion or embolism in the pulmonary circulation. Its mechanisms and prognosis are imperfectly known, although various suggestions have been made concerning the possible role of pulmonary arterial spasm, immune complex arteritis or arterial wall fibrosis. We report two cases of SLE in female patients who presented with clinical signs of pulmonary arterial hypertension. The fact that pulmonary arterial hypertension regressed completely in one patient and resulted in death in the other points to different pathogenic mechanisms. In the first patient the dramatic therapeutic effectiveness of a calcium inhibitor suggests that an arterial spasm was involved, whereas the anatomical lesions found in the second patient are in favour of a fibrotic inflammatory arteritis. This pathogenic heterogeneity of pulmonary arterial hypertension in SLE, which may correspond to different evolutive stages of the disease, is documented by a review of the literature with special attention to the frequency and to the clinical biochemical, haemodynamic and histological aspects of this complication of SLE.
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PMID:[Pulmonary arterial hypertension and systemic lupus erythematosus. Apropos of 2 cases. Review of the literature]. 328 21

The clinical use of calcium antagonist drugs in coronary artery disease preceded knowledge of the mechanism of their action. Basic research into their pharmacological actions and development of a wide range of compounds which block calcium entry into cells enabled clinicians to greatly expand the indications for their use. Thus the calcium antagonists were rediscovered and found to be potent anti-anginal drugs when used in adequate dosage for effort related angina. Knowledge of their potent relaxing action on vascular smooth muscle led to their use in coronary artery spasm. The exact trigger mechanism/s for spasm and the reason for enhanced vascular reactivity remain unclear, perhaps explaining the failure of specific antagonist therapy. Calcium antagonists acting nonspecifically inhibit both induced and spontaneous attacks of vasospastic angina. They may favourably influence the prognosis and are now drugs of first choice for this condition. The vasodilator action of these drugs has most recently been utilized to treat hypertension, with efficacy confirmed in many controlled trials. Unlike other vasodilators, the calcium antagonists reduce blood pressure without salt and water retention, and with mild or no stimulation of renin, aldosterone, or sympathetic nervous overactivity, and without postural effects. This spectrum of action makes them ideal therapeutic agents, and current guidelines are changing to include calcium antagonists as first or second line therapy.
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PMID:Calcium antagonist drugs in the treatment of coronary spasm, effort angina and hypertension. 330 67

The chemistry, pharmacology, pharmacokinetics, adverse effects, dosage, and availability of nimodipine are discussed, and the clinical use of nimodipine in preventing and treating cerebral arterial spasm in patients with subarachnoid hemorrhage is reviewed. Nimodipine is a highly lipid-soluble dihydropyridine derivative that readily crosses the blood-brain barrier. In animal studies, nimodipine has been shown to be effective in increasing cerebral blood flow; preventing vasoconstriction attributable to sympathetic stimulation, hypocapnia, and hypertension; and improving neurological outcome after cerebral ischemia. Nimodipine is reported to be 90% protein bound; its half-life is approximately 13 hours, with substantial interpatient variability. Nimodipine has been studied in the prevention and treatment of cerebral arterial spasm in patients with subarachnoid hemorrhage. In four open trials, in which nimodipine was administered orally, intravenously, topically during surgery, or by intracarotid injection, and in two double-blind, placebo-controlled trials, neurological outcomes were improved in patients receiving the drug. However, in both sets of trials nimodipine had limited effects on cerebral arterial spasm. Although nimodipine can cause hypotension, no serious adverse reactions to the drug were reported in clinical trials in patients with subarachnoid hemorrhage. Based on limited data currently available, nimodipine appears to improve neurological outcome in patients with subarachnoid hemorrhage. However, its efficacy in preventing or treating cerebral arterial spasm in these patients seems to be limited.
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PMID:Use of nimodipine for prevention and treatment of cerebral arterial spasm in patients with subarachnoid hemorrhage. 332 39

Although lipids have received most attention in relation to atherosclerosis, vessel injury also has a role in the development of atherosclerotic lesions. Thrombi that form at sites of injury can be incorporated into the wall, causing thickening, and platelets that adhere to damaged vessel walls release a growth factor (PDGF) that stimulates smooth muscle cell proliferation. The early lesions of atherosclerosis are focal and develop around vessel orifices and branches in relation to the patterns of blood flow and areas of increased permeability and endothelial cell damage. Platelets also contribute to the complications of advanced atherosclerosis caused by occlusive thrombi, thromboembolism, and spasm. The causes of vessel wall injury are not established, although there is evidence pointing to disturbed blood flow, hypertension, antigen--antibody complexes, complement, materials originating from platelets and white blood cells, bacteria, endotoxin, viruses, smoking, dietary lipids, homocystinemia, diabetes, other metabolic disorders, and stress. Platelets do not adhere to intact endothelium, but they adhere to the constituents of the subendothelium, release the contents of their granules (including PDGF), and form thromboxanes. If blood flow is disturbed, platelet--fibrin thrombi can form at sites of injury. Platelet adherence to a damaged wall does not require von Willebrand factor except under conditions of high wall shear. Repeated injury of a vessel wall leads to the development of lipid-rich atherosclerotic lesions, even in normocholesterolemic animals, but these lesions do not form if the experimental animals are made thrombocytopenic before injury is induced. Measurable changes in platelets that are associated with the clinical complications of atherosclerosis include shortened survival, release of granule contents (platelet factor 4, beta-thromboglobulin, thrombospondin), formation of thromboxanes, and decreased buoyant density. "Antiplatelet drugs" such as aspirin are proving to be beneficial in selected groups of patients, such as those with unstable angina. Thromboxane synthetase inhibitors and agents that block the thromboxane receptor on platelets are under investigation. Long term administration of "antiplatelet drugs" to affect the rate of development of atherosclerosis seems neither feasible nor desirable. Modification of dietary and smoking habits and control of hypertension are more likely to be beneficial for most individuals.
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PMID:The role of platelets in the development and complications of atherosclerosis. 351 36

In coarctation, bipedal exercise induces a pressure triad: exaggerated systolic arm hypertension, unchanging leg pressure, and markedly increased systolic gradient. Constancy of leg pressure derives from the lower body sharing the poststenotic compartment with the kidneys. Exercise-induced poststenotic hypotension stimulates the juxtaglomerular apparatus (JGA) to raise renal pressure to pre-exercise levels. Ambulation during the greater part of each day stimulates the JGA repetitively. Thereby, this chronic Single-Kidney-Goldblatt model is modified by increased plasma renin, fluid volumes, and cardiac output. It also accounts for hyper-responsive renin output after renin blockage and for mild poststenotic hypertension. Hypertension after repair which corrected the resting gradient, is almost always associated with the exercise triad, indicating that renal ischemia exists during ambulation. Thus, residual hypertension usually means residual coarctation. Mesenteric ischemia complicating postoperative paradoxic hypertension is probably due to spasm in the superior mesenteric artery and not to fixed occlusion of necrotizing arteritis.
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PMID:Coarctation hypertension is renovascular, modified by ambulation. Coarctation hypertension renovascular variant. 352 15

The epidemiology and etiology, pathophysiology, diagnosis, clinical presentation, complications, and treatment of acute myocardial infarction (AMI) are reviewed. Major risk factors for AMI include age, sex (men greater than women), family history, race, hyperlipidemia, hypertension, cigarette smoking, diabetes mellitus, and diet. AMI occurs when there is a prolonged decrease in oxygen supply to the myocardium caused by coronary thrombosis or coronary vascular spasm. Traditional drug treatment of uncomplicated AMI includes oxygen, laxatives, and analgesics. For analgesia, narcotic agonists are generally preferred, although intravenous nitroglycerin is of value for both reducing infarct size and relieving pain. Fibrinolytic therapy is also indicated in these patients. Low-dose heparin should be initiated on admission to the hospital. Beta-adrenergic blocking agents have proven useful in reducing the incidence of ventricular fibrillation and sudden death. Antiplatelet agents may also be used to decrease long-term mortality. Recent studies have focused on reduction of infarct size using agents such as beta blockers, calcium-channel blockers, nitroglycerin, and thrombolytics. Revascularization procedures are required in some patients to re-establish adequate coronary perfusion. Most patients who survive AMI initially have a relatively uncomplicated clinical course. An increasing number of therapeutic interventions are available for acute and chronic treatment of AMI.
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PMID:Current concepts in clinical therapeutics: acute myocardial infarction. 352 26

Cocaine use has increased rapidly over the past few years. This has led to an increase in the number and variety of cocaine-related conditions for which medical attention is sought. Among these have been several cases of intracranial hemorrhage. Four cases reported in the literature and 6 from our own institution are presented here. They represent different diagnoses including hemorrhage from aneurysms and arteriovenous malformations, hemorrhage into a tumor, and spontaneous hemorrhage with no underlying lesion with and without preexisting hypertension. Analysis of these cases suggests that the hypertension induced by cocaine secondary to sympathetic stimulation may be the common factor. Cocaine may also cause arterial spasm. Although the pathophysiology has not been entirely resolved, the clinical significance of this association is clear. Intracranial hemorrhage should be considered in the differential diagnosis whenever a patient presents with an acute alteration in neurologic examination associated with cocaine use.
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PMID:Intracranial hemorrhage and cocaine use. 360 97


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