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)

The aim of this study was to estimate the effect of Nitric Oxide synthase (NOS)-inhibition (L-NMMA) on the diameter of the middle cerebral artery (MCA) and on regional cerebral blood flow (rCBF). Furthermore, to assess the effect of L-NMMA on acetazolamide induced increases in MCA blood velocity (Vmean) and rCBF. In an open crossover design 12 healthy subjects attended the laboratory twice. The first day 6 mg/kg L-LNMMA i.v. over 15 min preceded 1 g acetazolamide i.v. over 5 min. Eight days later only acetazolamide was given. V(mean) in MCA was determined with transcranial Doppler (TCD) and rCBF with Xe-133 inhalation SPECT at baseline, after L-NMMA and 25 and 55 min after acetazolamide infusion. After L-NMMA the decrease in rCBF(MCA) was 6.8% (+/- 7.4) (P < 0.019, n = 12), whereas V(mean) was not affected (P = 0.83, n = 8). The change in MCA diameter was estimated to - 1.3% (P = 0.44, n = 8). L-NMMA did not affect acetazolamide increases in Vmean (P = 0.67, n = 8) nor rCBF (P = 0.29, n = 12). The percentage increase of V(mean) was 1.5 times that of rCBF (n = 8). Our data suggest that the basal tone of human cerebral arterioles but not of conduit arteries is NO-dependent. The action of acetazolamide in man is not NO-dependent.
Cephalalgia 2005 May
PMID:The effect of i.v. L-NG methylarginine hydrochloride (L-NMMA: 546C88) on basal and acetazolamide (Diamox) induced changes of blood velocity in cerebral arteries and regional cerebral blood flow in man. 1583 49

Nitric oxide (NO) is a marker of pulmonary inflammation. In asthma, the levels of exhaled NO are elevated and the source of this increased NO is inducible nitric oxide synthase (iNOS) within airway epithelial cells. Epimagnolin and fargesin are compounds isolated from the ethanol extract of Magnoliae flos, the seed of the Magnolia plant and are used to treat nasal congestion, headache and sinusitis in Asian countries. This study investigated whether epimagnolin and fargesin inhibit extracellular signal-regulated kinase (ERK) activation and decrease iNOS expression and NO production in stimulated human respiratory epithelial cells. An immortal Type II alveolar cell line of human origin (A549) was stimulated by cytomix (CM), composed of IL-1beta, TNF-alpha and IFN-gamma, with or without concurrent exposure to M. flos extract (epimagnolin or fargesin). CM-induced levels of NO production, iNOS expression and ERK activation were evaluated. A549 cells stimulated with CM showed increases in iNOS mRNA and protein expression, and NO synthesis. However, treatment with epimagnolin or fargesin decreased levels of iNOS mRNA and protein expression, and NO synthesis. CM stimulated a rapid increase in the activity of ERK, whereas epimagnolin and fargesin inhibited ERK phosphorylation. Epimagnolin and fargesin inhibit iNOS expression and decrease production of NO via ERK pathway in cytokine-stimulated human respiratory epithelial cells.
Nitric Oxide 2009 Mar
PMID:Extracts of Magnoliae flos inhibit inducible nitric oxide synthase via ERK in human respiratory epithelial cells. 1897 18

Neuromyelitis optica (NMO, also known as Devic syndrome or Devic disease) is a rare clinical entity. Early recognition and prompt treatment can save patients from long-term disability, especially in themonophasic variant of disease. A 24-year-old African American female presented with high-grade fever for 1 day associated with frontal headache, photophobia, and 2 episodes of nonbloody vomiting. She had a history of nonitchy vesicular rash with sudden diminution of vision in the left eye 2 weeks ago. Over the next 24 hours, she developed progressively worsening weakness and numbness in her left arm and left leg, which later involved all limbs. Left eye vision was reduced to light perception with light and accommodation reflexes intact. Lumbar puncture showed lymphocytic pleocytosis with elevated protein. On day 2, neurological examination exhibited quadriparises with hypereflexia and clonus. Magnetic resonance imaging showed diffuse hyperintense signals in the spinal cord in cervical and lumbar regions. An assessment of neuromyelitis optica was made. Anti-NMO antibodies were negative. On day 3, she was intubated because of progressive dyspnea. Plasmapheresis resulted in rapid improvement in respiratory and neurological status. She was extubated on the second day and transferred to floor on day 4. Later, the patient was discharged.
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PMID:Devic syndrome: a diagnostic dilemma. 2144 72

Migraine is a debilitating illness that has no exact bio molecule to explain its pathology. After reviewing the neurophysiological and biochemical basis of the research findings of nitric oxide and migraine, I present to the best of my knowledge the first para sinus nitric oxide mediated neurobiophysiological hypothesis for migraine of sino rhinogenic origin. The diffused paranasal sinus nitric oxide in the nasal mucosa could be the primary molecule that initiates migraine and is termed Sinus Hypoxic Nitric Oxide Theory. This hypothesis regards repetitive or intermittent activation of the trigeminal sensory nerve and blood vessels in the nasal mucosa. Production of paranasal sinus nitric oxide is mainly induced by hypoxia due to several independent factors and the diffusion of paranasal sinus nitric oxide depends on the vulnerable surface area in the nasal cavity. Apart from the known trigeminal nociceptive impulse in the migraine, two main peripheral trigeminal nerve activating mechanisms may induce migraine. First the nerve endings of the nasal mucosa which are directly stimulated by diffused paranasal sinus nitric oxide are indirectly stimulated by vasoactive substances released by antidromic activation of the nerve, parasympathetic efferent of the nerve and sterile neurogenic inflammation. Secondly, the perivascular nerve of nasal mucosal and the meningial blood vessels are directly stimulated by either diffused paranasal sinus nitric oxide or by shear stress mediation. The nerve impulses of the trigeminal sensory nerve, projected at trigeminal nucleus caudalis to the central nerve system and low plasma magnesium due to the consequence of shear stress gives rise to the symptoms of migraine. Moreover sino rhinogenic impulses may mediate to disruption of inhibitory sensitization modulated of sensory input and cause sensory hiperexcitability. In addition neuronal stimulation proposed by some migraine hypotheses could also give rise to migraine headache when the sino rhinogenic vulnerable factors induce the migraine pathophysiology. Indeed this article explains a new pathophysiological initiation between sino rhinogenic nitric oxide effects and migraine and provides an initial step for the obscured or neglected etiologically important neuro vascular impulse generating pathway. The patients who are clinically suspected of having headaches should receive comprehensive sino rhinological examination and evaluation based on the sinus hypoxic nitric oxide theory. A standard surgical and medical management of migraine that links with the sinus hypoxic nitric oxide theory may restore the hypoxic state or reduce or remove the paranasal sinus nitric oxide diffusing surface. It warrants clinical testing.
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PMID:Paranasal sinus nitric oxide and migraine: a new hypothesis on the sino rhinogenic theory. 2339 37

NO donors are compounds that release NO that can be used when the endogenous NO bioavailability is impaired. The compound cis-[Ru(bpy)2(py)(NO2)](PF6) (RuBPY) is a nitrite-ruthenium, since it has a NO2 in its molecule. The aim of the present study was to evaluate the effect of RuBPY on arterial pressure, as well as on the vascular relaxation of different vascular arteries in renal hypertensive (2K-1C) and normotensive (2K) rats. We have evaluated the arterial pressure and heart rate changes as well as the RuBPY and SNP-induced relaxation (thoracic aorta, mesenteric resistance, coronary and basilar arteries). The administration of RuBPY in awake rats evoked a smaller but long lasting hypotensive effect when compared to SNP, with no increase in heart rate. The relaxation induced by RuBPY was similar between 2K-1C and 2K rats in thoracic aorta, mesenteric resistance and coronary arteries. However, the relaxation induced by RuBPY was smaller in basilar arteries from 2K-1C than in 2K. Taken together, our results show that RuBPY presents several advantages over SNP, since it does not induce hypotensive effect in normotensive animals, the hypotensive effect is slower, with no reflex tachycardia, and it is long lasting. In addition, RuBPY induces coronary artery relaxation (useful for angina) and presented only a small effect on basilar artery (may not induce headache).
Nitric Oxide 2017 Jan 30
PMID:Hypotensive effect and vascular relaxation in different arteries induced by the nitric oxide donor RuBPY. 2784 91

Medication-overuse headaches (MOH) occur with both over-the-counter and pain-relief medicines, including paracetamol, opioids and combination analgesics. The mechanisms that lead to MOH are still uncertain. Here, we show that abnormal activation of Nav1.9 channels by Nitric Oxide (NO) is responsible for MOH induced by triptan migraine medicine. Deletion of the Scn11a gene in MOH mice abrogates NO-mediated symptoms, including cephalic and extracephalic allodynia, photophobia and phonophobia. NO strongly activates Nav1.9 in dural afferent neurons from MOH but not normal mice. Abnormal activation of Nav1.9 triggers CGRP secretion, causing artery dilatation and degranulation of mast cells. In turn, released mast cell mediators potentiates Nav1.9 in meningeal nociceptors, exacerbating inflammation and pain signal. Analysis of signaling networks indicates that PKA is downregulated in trigeminal neurons from MOH mice, relieving its inhibitory action on NO-Nav1.9 coupling. Thus, anomalous activation of Nav1.9 channels by NO, as a result of chronic medication, promotes MOH.
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PMID:Maladaptive activation of Nav1.9 channels by nitric oxide causes triptan-induced medication overuse headache. 3153 33