Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 46-year-old man, presenting with headache, nausea, and lassitude, was diagnosed as having diabetes mellitus and hyponatremia, and admitted to Tohoku University Hospital. Insulin treatment improved the hyperglycemia but aggravated hyponatremia, which was proved to be elicited by the inappropriate secretion of antidiuretic hormone (SIADH). An acute water load failed to suppress ADH release in the supine posture but slightly increased plasma atrial natriuretic peptide (ANP). On the other hand, plasma ADH markedly increased in response to an upright posture, accompanied by a fall in blood pressure and a rise in heart rate. After treatment with droxidopa "a sympathomimetic drug", ambulatory blood pressure gradually increased and hyponatremia disappeared. However, blood pressure and ADH responses to upright posture were not improved by treatment with the drug. Moreover, plasma ADH was still not sufficiently suppressed by acute water loading in the supine position, but plasma ANP markedly increased, thereby resulting in urinary dilution and natriuresis. These results suggest that exaggerated ADH release (SIADH) was brought about by the baroreceptor reflex stimulated by the postural hypotension, and also by the impaired osmoregulation associated with diabetic neuropathy, and that droxidopa improved cardiovascular function and increased ANP release with resultant urinary dilution and natriuresis in spite of slightly increased ADH release.
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PMID:A case of syndrome of inappropriate secretion of antidiuretic hormone associated with diabetes mellitus. 179 39

The antihypertensive effects and safety of a novel neutral endopeptidase inhibitor, SCH 42495, were investigated in hypertensive patients. A multicenter, open clinical trial was conducted in 27 patients with essential hypertension, WHO Stage I or II. Mean age was 64 +/- 1 years. After 2 to 4 weeks of a placebo run-in, 50 mg twice daily, was started, with the dose increased to 100 mg twice daily, and 200 mg twice daily, every 2 weeks, if necessary, to achieve a predetermined response. Blood pressure and pulse rate were monitored every 2 weeks. Blood chemistry, plasma atrial natriuretic peptide (ANP), and plasma cGMP levels were determined before and after the 8-week treatment period. Blood pressure was significantly reduced, from 171 +/- 1/100 +/- 1 mm Hg to 146 +/- 3/84 +/- 2 mmHg (P < .001) at the end of the 8-week treatment period. No change in pulse rate was noted. Efficacy rate was evaluated in 25 patients treated for 4 weeks or more. Efficacy rate was 44% with 50 mg twice daily, 60% with 100 mg twice daily, and 80% with 200 mg twice daily. Adverse reactions such as headaches and palpitation were observed in six patients (22.2%), with treatment discontinued in five. Significant correlation was observed between increment in plasma ANP levels and blood pressure reductions (r = -0.53, P < .05). Increase in plasma cGMP was positively correlated with increments in plasma hANP (r = 0.80, P < .001). SCH 42495 has potent antihypertensive effect associated with an enhancement of endogenous hANP and may be clinically useful as a new class of antihypertensive drug.
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PMID:Antihypertensive effects of the neutral endopeptidase inhibitor SCH 42495 in essential hypertension. 784 19

Acute altitude illnesses include acute mountain sickness (AMS), a benign condition involving headache, nausea, vomiting, irritability, insomnia, dizziness, lethargy, and peripheral edema, and potentially lethal high-altitude cerebral edema and pulmonary edema (HAPE). Recent evidence is summarized that AMS is related to cerebral edema secondary at least in part to hypoxic cerebral vasodilation and elevated cerebral capillary hydrostatic pressure. This results in reduced brain compliance with compression of intracranial structures in the absence of altered global brain metabolism. It is postulated that these primary intracranial events elevate peripheral sympathetic activity that acts neurogenically in the lung possibly in concert with pulmonary capillary stress failure to cause HAPE and in the kidney to promote salt and water retention. The adrenergic responses are likely modulated by striking increases of aldosterone, vasopressin and atrial natriuretic peptide. The effects of exercise on altitude-induced illness and various therapeutic regimens (acetazolamide, CO2 breathing, dexamethasone, and alpha adrenergic inhibitors) are discussed in light of this hypothesis.
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PMID:A neurogenic basis for acute altitude illness. 816 37

The autonomic nervous function in patients with migraine was studied during headache free intervals. (I) Hemodynamic test. The following observations were made: (1) a decrease in overshoot in Valsalva's maneuver; (2) orthostatic hypotension; (3) low levels of plasma norepinephrine; (4) failure in elevation of the plasma norepinephrine level after head-up tilting; (5) dilatation of the pupils after instillation in the eyes of 1.25% epinephrine; (6) a long recovery time in test by bolus injection of l-norepinephrine. These data suggest that patients with migraine show sympathetic hypofunction together with denervation hypersensitivity of the iris and arteries. (II) Neuropeptides. Blood samples were taken after 30 minutes supine rest in a quiet room and the level of substance-P (SP), calcitonin gene-related peptide (CGRP), endothelin-1 (ET-1), and human atrial natriuretic peptide (hANP) were determined by radioimmunoassay. The level of SP, CGRP, and hANP in classic migraineurs during headache-free intervals were significantly lower than that of controls. There was no significant difference in the level of ET-1 between migraineurs and controls. These data suggest that neuropeptides such as SP, CGRP and hANP are closely related to the pathophysiology of migraine. (III) L-arginine infusion test. To examine whether or not NO is involved in the pathophysiology of migraine, L-arginine, a precursor of NO, was administered. The magnitude of blood pressure decrease in migraineurs was significantly greater than that of controls. Although plasma levels of CGRP decreased significantly in controls following L-arginine infusion, those of CGRP did not change in migraine patients. These data suggest that NO and CGRP may be involved in pathophysiology in migraine.
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PMID:[Autonomic nervous activity in migraine]. 875 90

Transcatheter closure of atrial septal defect (ASD) is associated with a high success rate and become an accepted alternative to surgical treatment. We describe here a case of a 35-year-old woman who presented with migraine attacks with aura after transcatheter closure of ASD with an Amplatzer septal occluder device. We postulate that any of the following may have been responsible for her condition: platelet activation on the surface of the device, nickel allergy, or the release of the atrial natriuretic peptide associated with the stretch of the atrial septum caused by the device. This case demonstrates that de novo migraine can occur after transcatheter closure of ASD and should be recognized as a potential complication.
J Headache Pain 2012 Aug
PMID:New-onset migraine with aura after transcatheter closure of atrial septal defect. 2262 72

The natriuretic peptides (NPs), atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP), have vasoactive functions that concern humans and most animals, but their specific effects on cerebral circulation are poorly understood. We therefore examined the responsiveness of cerebral arteries to different doses of the natriuretic peptides in animals and humans. We conducted a dose-response experiment in guinea pigs (in vitro) and a double-blind, three-way cross-over study in healthy volunteers (in vivo). In the animal experiment, we administered cumulative doses of NPs to pre-contracted segments of cerebral arteries. In the main study, six healthy volunteers were randomly allocated to receive two intravenous doses of ANP, BNP or CNP, respectively, over 20 min on three separate study days. We recorded blood flow velocity in the middle cerebral artery (VMCA) by transcranial Doppler. In addition, we measured temporal and radial artery diameters, headache response and plasma concentrations of the NPs. In guinea pigs, ANP and BNP but not CNP showed significant dose-dependent relaxation of cerebral arteries. In healthy humans, NP infusion had no effect on mean VMCA, and we found no difference in hemodynamic responses between the NPs. Furthermore, natriuretic peptides did not affect temporal and radial artery diameters or induce headache. In conclusion, natriuretic peptides in physiological and pharmacological doses do not affect blood flow velocity in the middle cerebral artery or dilate extracerebral arteries in healthy volunteers.
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PMID:Effect of natriuretic peptides on cerebral artery blood flow in healthy volunteers. 2641 35