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)

In a series of 27 patients with proved pheochromocytoma, differential analysis of catecholamines in blood, urine, and tumor specimens of 19 patients enabled grouping of subjects into those whose tumors produced predominantly norepinephrine (NE) (11 patients), predominantly epinephrine (E [Two patients]) and approximately equal amounts of both (six patients). Sustained hypertension was more common in the first group and pallor and tremor in the latter two groups, but no distinctive syndrome could be recognized as signifying the secretion of NE or E. Headache was a symptom in 20 of 27 patients and was related to sudden, transient elevation of the blood pressure, rather than sustained hypertension. The variable duration and intensity of the headache in different patients can be explained by the pressor and cranial vasoconstrictor effects of the secreted amines, which respectively enhance and diminish vascular headache.
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PMID:Symptoms of pheochromocytoma, with particular reference to headache, correlated with catecholamine production. 125 42

During 1989-90 there were a total of 3,475,862 prescriptions of oral contraceptives (OCs) made in Australia by general practitioners. A 2- sided insert to facilitate deciding on the proper dosage for patients with various conditions was developed containing the estrogen- progestogen doses of OC preparations, management of minor side effects (nausea, vomiting, weight gain, chloasma, breakthrough bleeding, breast tenderness, or acne), and the relative contraindications to OC use. The simple, user-friendly, and flexible flow chart contains relative contraindications: age over 35 in heavy smokers, migraine or severe vascular headache, age over 45, previous cholestasis during pregnancy, hypertension, smoking, diabetes mellitus, long term immobilization, abnormal vaginal bleeding, gallbladder disease, impaired liver function, acute infectious mononucleosis, and use of rifampin or anticonvulsants.
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PMID:Prescribing oral contraceptives and the medical record. 179 98

The authors present the problem of vascular headache at children: headaches caused by high blood pressure, aneurysm and other intracranial vascular malformations of the intracranial venous sinuses thrombosis (here, the determining factors are the infectious and inflammatory factors). Here are mentioned, one by one, the kinds of headaches, following the a/m classifications, with the clinical particularities and the therapeutical indications. There are reviewed a series of other causes of the headaches at children: headache caused by muscular contractions, the post traumatic headache, headache caused by cerebral tumours, by nasosinusal causes, ocular headache, headache caused by infections or metabolic diseases, and the psychogenic headache.
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PMID:[Clinical and therapeutic aspects of headache of vascular origin in children]. 252 90

Vascular headaches are among the most prevalent yet poorly understood problems in clinical neurology. Headaches may develop in association with hypertension, seizures, stroke or without a recognizable pathophysiology such as during migraine and cluster headaches. Cephalic blood vessels (pial and dural vessels) are implicated as the most important source for all headaches and are innervated by sensory fibers which arise from ganglia innervating the forehead, scalp and neck. Sensory fibers contain vasoactive neuropeptides which become released from peripheral (perivascular) and central terminations to mediate vasodilation and pain, respectively. The presence of vascular headache implies activation of this final common pain pathway which we have termed the trigeminovascular system. The presence of vascular headache implies activation of this final common pain pathway which we have termed the trigeminovascular system. The existence of such a system a) clarifies certain pain patterns which develop following stimulation of cephalic blood vessels, b) suggests a mechanism to explain the referral of pain to the forehead, c) provides a mechanism to explain the action of certain antimigraine drugs, d) suggests a local mechanism which enhances blood flow under certain pathological conditions. Hence, this review will update existing knowledge about the trigeminovascular system and its role in headache pathophysiology.
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PMID:Pain mechanisms underlying vascular headaches. Progress Report 1989. 266 74

Estrogen replacement therapy is effective for the prevention and treatment of postmenopausal osteoporosis and should be offered to all women at high risk for osteoporosis. Such therapy is particularly beneficial for prevention of spinal compression fractures; in addition, it alleviates menopausal symptoms (hot flushes, genitourinary symptoms, and changes in mood). In each patient, these benefits must be weighted against the potential risks of endometrial hyperplasia and carcinoma, breast tenderness, hypertension, vascular headaches, and the inconvenience of menstrual bleeding if the uterus is intact. The risk of endometrial cancer associated with estrogen replacement therapy can be considerably reduced by the addition of a progestin, and other side effects can be diminished or eliminated by use of the new transdermal estrogen preparations. Thus, estrogen replacement therapy should be considered in all women who have experienced natural or surgically induced menopause, and it is advisable in women who have osteoporosis or an increased risk for this disorder and no contra-indications to its use. Estrogen replacement therapy should be instituted as soon after menopause as possible and seems to be well tolerated until at least 75 years of age.
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PMID:Estrogen replacement therapy: current recommendations. 328 71

Headaches may occur in as many as 25% of hypertensive patients and generally bears little relationship to level of diastolic blood pressure. Previous observations, in normotensive patients, suggested that abnormalities in both potassium and ammonia metabolism might be related to the pathogenesis of these headaches. The present study was undertaken to see whether these factors also occurred in hypertensive patients with headaches. The present observations were made in thirteen hypertensive patients with vascular headaches. The major findings include potassium levels of 3.45 +/- 0.25 mEq/L; CO2, 29.85 +/- 1.21 mEq/L; blood ammonia, 41 +/- 8.40 U mol/L and an alkaline pH of the urine. The blood ammonia levels, when factored by the BUN, yielded elevated ammonia to BUN ratios (3.81 +/- 1.82). These findings are similar to those previously observed in normotensive patients with vascular headaches. The profile of hypokalemia and/or alkalosis, increased blood ammonia to BUN ratios and a relatively alkaline urine appears to be a commonly observed pattern in patients with vascular headaches. These data suggest that a biochemical basis exists for the genesis of vascular headaches in patients with hypertension.
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PMID:The pathogenesis of vascular headaches in patients with hypertension; the role of the ammonia-potassium axis. 364 6

Clinical characteristics of cerebral infarctions occurring in 15 women (aged 22-51) who had taken oral contraceptives for an average of 24.8 months are described. Aside from 5 atypical cases, the 10 remaining women suffered marked increases in headache pain for only 3 months before their strokes. The subjective severity increased progressively, and in at least 6, the duration of each headache increased. Frequency of headaches in 9 women increased noticeably during the prodrome, and in some was almost constant for a week before the infarct. However only 5 patients had or had just had headaches at the exact time of the stroke. The spatial aspects of headache locations imply etiological relationship to the infarct which follows. Upon recognition of the clinical characteristics of such headache in women taking oral contraceptives, the medication should be stopped immediately. Absolute withdrawal should be recommended for patients with increasing vascular headache and headache associated with focal neurological symptoms. Hypertension in patients with the slightest sign of increasing headache should be cause for discontinuation of the pill. Following withdrawal of the oral contraceptive, synthetic narcotics are the only therapy advised. Vasoconstrictor drugs may aggravate the vasoconstrictor phase leading to infarction.
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PMID:The clinical characteristics of headache during impending cerebral infarction in women taking oral contraceptives. 573 Jan 19

The following three unusual complications of carotid endarterectomy developed in a 64-year-old woman: vascular headaches, delayed hypertension, and seizures. beta-Blockade with propranolol hydrochloride had no beneficial effect on either the hypertension or the headaches. Peripheral alpha-blockade with prazosin hydrochloride resulted in prompt improvement in the patient's condition. Altered autonomic vascular control secondary to carotid sinus trauma is proposed as a possible causative mechanism for all three complications. The therapeutic implications are discussed. Based on this experience, we would caution against the use of unopposed beta-blockade in this setting and suggest that the role of prazosin in the initial management of postendarterectomy hypertension and vascular headache be explored.
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PMID:Hypertension, vascular headaches, and seizures after carotid endarterectomy. Case report and therapeutic considerations. 673 10

Kinins, including bradykinin and kallidin, are peptides that are produced and act at the site of tissue injury or inflammation. They induce a variety of effects via the activation of specific B1 or B2 receptors that are coupled to a number of biochemical transduction mechanisms. In the periphery the actions of kinins include vasodilatation, increased vascular permeability and the stimulation of immune cells and peptide-containing sensory neurones to induce pain and a number of neuropeptide-induced reflexes. Mechanisms for kinin synthesis are also present in the CNS where kinins are likely to initiate a similar cascade of events, including an increase in blood flow and plasma leakage. Kinins are potent stimulators of neural and neuroglial tissues to induce the synthesis and release of other pro-inflammatory mediators such as prostanoids and cytotoxins (cytokines, free radicals, nitric oxide). These events lead to neural tissue damage as well as long lasting disturbances in blood-brain barrier function. Animal models for CNS trauma and ischaemia show that increases in kinin activity can be reversed either by kinin receptor antagonists or by the inhibition of kinin production. A number of other central actions have been attributed to kinins including an effect on pain signalling, both within the brain (which may be related to vascular headache) and within the spinal dorsal horn where primary afferent nociceptors can be stimulated. Kinins also appear to play a role in cardiovascular regulation especially during chronic spontaneous hypertension. Presently, however, direct evidence is lacking for the release of kinins in pathophysiological conditions of the CNS and it is not known whether spinal or central neurones, other than afferent nerve terminals, are sensitive to kinins. A more detailed examination of the effects of kinins and their central pharmacology is necessary. It is also important to determine whether the inhibition of kinin activity will alleviate CNS inflammation and whether kinin receptor antagonists are useful in pathological conditions of the CNS.
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PMID:Kinins and kinin receptors in the nervous system. 778 59

A study was made of a total of 50 patients, 36 females and 14 males, with an average age of 51.3 +/- 11.71 years (range 19-71). The group consisted of outpatients who came to the neurology clinic suffering from vascular headache or other symptomatic complaint of vascular type. In all cases, the existence of an organic neurological pathology had been considered and rejected. All patients who were smokers or suffering from hypertension were excluded, as well as those who had abnormal lipid or glucose values or who were on drug treatment for other reasons. The basal erythrocyte deformability value was determined and the patients divided into two random homogeneous groups. One of the groups was treated with nimodipine (90 mg/d) and the other with nicardipine (60 mg/d) for a period of two months. After this treatment period a further determination of the erythrocyte deformability was carried out. In the group treated with nimodipine, the erythrocyte deformability varied from 45.5 +/- 7.4 mcl/s to 50.35 +/- 12.02 mcl/s (p = 0.07123). In the group treated with nicardipine, these values varied from 45.96 +/- 7.35 mcl/s to 56.21 +/- 12.72 mcl/s (p = 0.00079). It was concluded that in both groups of patients, after two months treatment with these calcium antagonists, there was an improvement in erythrocyte deformability and, therefore, in blood fluidity, although only the nicardipine-treated group reached statistically significant levels.
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PMID:The increase in erythrocyte deformability in patients treated with nicardipine or nimodipine. 848 98


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