Disease relevance of Constriction

• Gyrate atrophy of the choroid and retina is a disease characterized by progressive constriction of visual fields, a 10-fold to 20-fold elevation in plasma ornithine, and depressed activity of L-ornithine:2 oxoacid aminotransferase [1].
• These mice showed no detectable ventricular hypertrophy in response to pressure-overload induced by aortic constriction [2].
• We found that CFKO mice develop eccentric cardiac hypertrophy (normal LV wall thickness and increased left chamber dimension) upon stimulation with angiotensin II or pressure overload by transverse aortic constriction as measured by echocardiography [3].
• Thus, NPY, a peptide found in human coronary arteries, caused constriction of primarily small coronary arteries that was severe enough to produce myocardial ischemia as determined by ECG ST-T wave changes, and decreases in intramyocardial pH and LVEF in dogs [4].
• CONCLUSIONS: L-Arginine treatment decreased superoxide generation by cNOS while increasing NO accumulation, leading to protection from constriction (microvessel area, 17.77+/-0.95 versus 11.66+/-2.21 microm2 untreated, P<.0005) and reduction of edema after reperfusion (interfiber area, 16.56+/-2.13% versus 27.68+/-7.70% untreated, P<.005) [5].

Psychiatry related information on Constriction

• At basal pressures, decanoic acid dose-dependently induced motor activity consisting of 40-60 s episodes of constrictions separated by 40-200 s periods of quiescence and lasting up to 2 h [6].

High impact information on Constriction

• We show that, in PI3KgammaKD/KD hearts, cAMP levels are normal and that PI3Kgamma-deficient mice but not PI3KgammaKD/KD mice develop dramatic myocardial damage after chronic pressure overload induced by transverse aortic constriction (TAC) [7].
• Loss of zygotic cnn expression disrupts the development of the second midgut constriction, the gastric caeca, and the nervous system [8].
• These regulatory interactions are relevant to normal development, because a transgene made with this enhancer driving a dpp transcription unit rescues the second midgut constriction and larval lethality phenotypes of dpps mutations [9].
• The degree of constriction or dilation during mental stress correlated with the response to the infusions of acetylcholine (P less than 0.0003, r = 0.58) [10].
• Normal coronary vessels had a biphasic response to intracoronary serotonin: dilation at concentrations up to 10(-5) mol per liter, but constriction at 10(-4) mol per liter [11].

Chemical compound and disease context of Constriction

• Abdominal aortic constriction (7 d) and subcutaneous norepinephrine infusion (36 h) each caused ventricular hypertrophy associated with 3.1-fold and 3.8-fold increases, respectively, in TGF-beta 1 mRNA in the myocyte fraction, but had no effect on the level of TGF-beta 1 mRNA in the nonmyocyte fraction [12].
• Indeed, Sim inhibited cardiac hypertrophy and decreased myocardial Rac1 activity and O2*- production in rats treated with AngII infusion or subjected to transaortic constriction [13].
• Alternatively, constriction of the inferior vena cava and infusion of nitroprusside changed the right atrial pressure-volume loop from that of a severe pattern of tricuspid regurgitation to a less severe type of pattern [14].
• These data indicate that platelet glycoprotein Ib-von Willebrand factor interactions are important during coronary occlusion and that aurintricarboxylic acid can inhibit coronary thrombosis associated with coronary constriction [15].
• After 15 minutes of hypertension, when coronary diameter had returned to baseline values, the constriction of the large artery to serotonin was potentiated (delta D = -89 +/- 33 microns at 5 micrograms/min; -207 +/- 45 microns at 50 micrograms/min; p less than 0.05) [16].

Biological context of Constriction

• One type of response consisted of a localised constriction near the noradrenaline source: this effect could be abolished by the alpha-antagonist phentolamine and was not associated with a change in arteriolar membrane potential [17].
• These arrays efficiently recruit UBF even to sites outside the nucleolus and, during metaphase, form novel silver stainable secondary constrictions, termed pseudo-NORs, morphologically similar to NORs [18].
• Airway constriction in normal humans produced by inhalation of leukotriene D. Potency, time course, and effect of aspirin therapy [19].
• Insulin caused no vasoconstriction in either Af- or Ef-Arts, but it reversed norepinephrine-induced constriction in Ef-Arts but not Af-Arts (suggesting a vasodilator action selective to the Ef-Art): at 200 microU/ml, insulin increased Ef-Art luminal diameter by 75.8 +/- 7.0% from the preconstricted level (n = 6; P < 0.008) [20].
• Chronic infusion of the inhibitor in dogs with thoracic inferior vena caval constriction prevented the restoration of blood pressure and suppressed the rise in plasma aldosterone; sodium retention and volume expansion were less than in control experiments [21].

Anatomical context of Constriction

• Following incubation with the Ca ionophore A23187 (refs 1-4) (a non-physiological agent which circumvents membrane calcium-gating mechanisms), eosinophils generate large amounts of sulphidopeptide leukotrienes, potent inducers of smooth muscle constriction and mucus production [22].
• The light-induced constriction of the irises of some vertebrates is mediated by photosensitive pupillary sphincter cells, which have rhodopsin molecules in their sarcolemmas [23].
• Severe constriction of the abdominal aorta and simultaneous injection of isoproterenol in rats induced depression in heart function and reductions in cardiac adenosine triphosphate and total adenine nucleotides [24].
• These observations demonstrate the importance of the vascular endothelium in opposing the constriction of coronary vessels caused by 5-hydroxytryptamine and other substances released from aggregating platelets [25].
• Notably, in mice deficient in IL-5/eotaxin the ability of CD4(+) T helper cell (Th)2 lymphocytes to produce IL-13, a critical regulator of airways smooth muscle constriction and obstruction, was significantly impaired [26].

Associations of Constriction with chemical compounds

• Most infants responded to indomethacin with ductus constriction [27].
• Residues of the constriction region, in particular histidine 182, which is conserved among all known water-specific channels, are critical in establishing water specificity [28].
• Soaking of a crystal with maltotriose revealed binding of the sugar to this hydrophobic track across the constriction, which suggests that maltose and linear oligosaccharides may be translocated across the membrane by guided diffusion along this path [29].
• Cellular mechanisms mediating rat renal microvascular constriction by angiotensin II [30].
• Neither asthmatics nor normal subjects had airway constriction or changes in BAL histamine levels in response to nonspecific challenge with cold saline [31].

Gene context of Constriction

• Heme oxygenase-1 protects against vascular constriction and proliferation [32].
• Although these Dnm1p-containing complexes are thought to trigger constriction and fission, little is known about their composition and assembly, and molecules required for their membrane recruitment have not been isolated [33].
• CONCLUSIONS: Selective ETB receptor agonists cause constriction of forearm resistance and hand capacitance vessels in vivo in humans, suggesting that both ETA and ETB receptors mediate vasoconstriction [34].
• In the wild type, the Bithorax Complex forms a weak point featuring thinner bands separated by clefts or constrictions [35].
• Taken together, these data indicate that Pbx1 is essential for the function of hematopoietic progenitors with erythropoietic potential and that its loss creates a proliferative constriction at the level of the CMP [36].

Analytical, diagnostic and therapeutic context of Constriction

• In contrast, L-NAME pretreatment had no effect on Ang II-induced constriction in Ef-Arts with either perfusion [37].
• EDRF and microvascular constriction after angioplasty [38].
• In the control group, vasomotor responses of the site where acetylcholine caused dilation were compared with the responses of the site where acetylcholine caused constriction [39].
• CONCLUSIONS: Conjugated estrogens acutely abolish abnormal CPT-induced coronary artery constriction in male cardiac allografts [40].
• Platelet aggregation and coronary artery constriction secondary to thromboxane production may contribute to the morbidity of cardiopulmonary bypass [41].

References