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At least 757 records · Page 42Linked to original sources
PubMed1999

Varying division planes of secondary constrictions in spheroidal Escherichia coli cells.

Planes of successive divisions in Escherichia coli have been proposed to be either parallel or perpendicular to each other, restricted to one or two dimensions. To test the hypothesis that divisions can occur in planes alternating in three dimensions, a method was developed to generate cells with secondary constrictions during growth in suspension. The method involves a combination of thymine limitation (to manipulate chromosome replication rate) and mecillinam treatment (to inhibit penicillin-binding protein 2). The former modifies timing of terminations, the latter results in spheroidal cells. Such cells displayed secondary constrictions after adding deoxyguanosine (accelerating replication rate), thus temporarily enhancing division signals. The successive constrictions were seen to develop in planes that were tilted relative to each other, and in positions related to those of the nucleoids, visualized by staining with DAPI (4',6-diamidino-2-phenylindole dihydrochloride hydrate). Visualizing cell envelopes with FM 4-64 by confocal scanning laser microscopy supported the conclusion that planes of successive divisions can alternate in three dimensions.

Cell Division↗
PubMed1983

Effect of nifedipine on constriction of human tracheal strips in vitro.

1 Autopsy specimens of human trachealis muscle were used to investigate the effect of the calcium channel blocker, nifedipine, on airway smooth muscle constriction. With these tracheal strips, two consecutive cumulative concentration-effect curves to histamine (0.1-100 microM) obtained at a 60 min interval were highly reproducible. 2 We examined the effects of adding nifedipine (2.9 microM) to the incubation medium before the second histamine response. The concentration-effect relationships determined after nifedipine incubation were significantly different from control: the response to 100 microM histamine was reduced by approximately one-half (to 2.53 +/- 0.6 g; P less than 0.025), and the concentration of histamine causing 40% of the maximal control contraction (EC40) increased nearly ten fold (to 36.9 +/- 10.5 microM; P less than 0.02). 3 In two additional tracheal strips submaximally constricted with 10 microM histamine, nifedipine 2.9 microM caused complete relaxation to resting tension or below. 4 These results indicate a direct inhibitory effect of nifedipine on airway smooth muscle constriction and partial dependence of human trachealis muscle on calcium ion fluxes for initiation and maintenance of contraction. In addition, the results suggest a potential mechanism for the inhibitory effects of calcium channel blocking drugs in exercise-induced asthma.

Airway Resistance↗
PubMed1991

Effects of calcium modulators on vagally-mediated constriction in the guinea-pig isolated trachea.

1. The effects of calcium modulators on tracheal constriction evoked by vagal stimulation were examined in the isolated, innervated trachea of the guinea-pig. Responses were assessed in the Krebs-filled trachea as changes in intraluminal pressure (ILP), increases and decreases reflecting constriction and dilatation, respectively. 2. Preparations had a positive resting ILP, indicating significant spontaneous tone. Verapamil and nifedipine reduced baseline ILP, whilst Bay K 8644 had mixed effects. 3. Verapamil and nifedipine attenuated vagal responses in a concentration-dependent manner. At lower concentrations attenuation was due entirely to postjunctional effects but at higher concentrations prejunctional effects may have contributed to attenuation. 4. Verapamil and nifedipine attenuated vagal responses in the absence or presence of flurbiprofen, indicating that their effects are largely independent of the generation of cyclo-oxygenase products. Nifedipine, however, was less effective in reducing responses to low frequency vagal stimulation (up to 5 Hz) when flurbiprofen was present. 5. Bay K 8644 augmented vagal responses, the degree varying widely between preparations. 6. It was concluded that influx of Ca2+ through voltage-operated Ca2+ channels contributes significantly to vagally-mediated tracheal constriction in normal trachea and in trachea where endogenous release of cyclo-oxygenase products is inhibited.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1994

Enhancement of noradrenergic constriction of large coronary arteries by inhibition of nitric oxide synthesis in anaesthetized dogs.

1. Coronary vascular responses to bilateral carotid occlusion (BCO) and the intravenous infusion of tyramine (Tyr, 20 micrograms kg-1 min-1) and noradrenaline (NA, 0.5 microgram kg-1 min-1) were examined after bilateral vagotomy and antagonism of beta-adrenoceptors. BCO, Tyr and NA decreased large coronary artery diameter and increased mean coronary resistance and systemic arterial pressure without affecting heart rate. 2. Inhibition of nitric oxide (NO) synthase with NG-nitro-L-arginine (L-NNA, 5 and 15 mg kg-1) significantly increased mean arterial pressure and decreased heart rate and large coronary artery diameter. Mean coronary resistance was unaffected by either dose of L-NNA. L-NNA significantly reduced depressor and coronary vasodilator responses to the endothelium-dependent vasodilator acetylcholine (ACh, 10 micrograms kg-1, i.v.). Systemic and coronary vasodilator responses to sodium nitroprusside (SNP, 5 micrograms kg-1) were unaffected by L-NNA with the exception that the dilatation of the large coronary artery was significantly enhanced by the higher dose. 3. L-NNA significantly enhanced constriction of the large coronary arteries caused by BCO, Tyr and NA but did not affect the increases in mean coronary resistance or systemic arterial pressure. 4. Inhibition of NO synthesis enhances adrenergic constriction of large coronary arteries caused by both neuronally released and exogenous noradrenaline. In contrast, L-NNA did not affect adrenergic constriction of coronary or systemic resistance vessels. Endothelium-derived NO may play an important role in the modulation of noradrenergic vasoconstriction in coronary conductance arteries.

Acetylcholine↗
PubMed1986

Role of arginine-vasopressin for the development of hypertension following aortic constriction.

This study concerns the role of arginine-vasopressin (AVP) for the development of hypertension after constriction of the abdominal aorta proximal to the renal arteries (PAC). The PAC was applied in AVP-deficient Brattleboro (Bb) rats and the blood pressure was recorded 3 weeks later. In untreated rats, PAC did not cause hypertension. When the rats were given AVP 0.6 or 6 nmol day-1 for 2 weeks using mini-pumps, hypertension developed both proximal and distal to the constriction. The level of the hypertension was independent of the AVP dose. When the rats were given I-deamino-4-valine-8-D-arginine-vasopressin (dVDAVP) a specific antidiuretic agonist without effect on the vascular AVP receptors, hypertension did not develop. Sham-operated rats given AVP did not develop hypertension. The PAC rats treated with AVP but not with dVDAVP had an enhanced pressor response to an i.v. bolus dose of angiotensin II. It is concluded that AVP plays an important role in the development of hypertension following aortic constriction and that the action is mediated via the vascular AVP-receptors. We suggest that the presence of AVP permits the expression of other hypertensive factors, such as angiotensin II.

Angiotensin II↗
PubMed1993

The effects of photodynamic therapy using differently substituted zinc phthalocyanines on vessel constriction, vessel leakage and tumor response.

The effects of four different zinc phthalocyanines were studied during and after photodynamic therapy (PDT). Measurements of vessel constriction, vessel leakage, tumor interstitial pressure, eicosanoid release, and tumor response of chondrosarcoma were made in Sprague-Dawley rats. Animals were injected intravenously with 1 mumol/kg of mono-, di-, or tetrasulfonated zinc phthalocyanine, or 1 mumol/kg of a zinc phthalocyanine substituted with four tertiary butyl groups. Tissues were exposed to 400 J/cm2 670 nm light 24 h after photosensitizer injection. An additional group of animals was given indomethacin before treatment. The use of the monosulfonated and tertiary butyl substituted zinc phthalocyanines in PDT caused the release of specific eicosanoids, caused vessel constriction, and induced venule leakage and increases in tumor interstitial pressure. Tumor cures of 27% and 7% were observed. Photodynamic therapy using the disulfonated zinc phthalocyanine did not induce vessel constriction or the release of eicosanoids, however, tumor cure was 43%. The use of the tetrasulfonated zinc phthalocyanine caused intermediate effects between the mono- and disulfonated compounds. The administration of indomethacin to animals completely inhibited the effects of PDT using the monosulfonated compound but had minimal effects on treatment using the disulfonated compound. This suggests that the monosulfonated and disulfonated compounds act by different mechanisms of destruction.

Animals↗
PubMed2000

Direction-dependent constriction flow in a poroelastic solid: the intervertebral disc valve.

We hypothesize that a direction-dependent flow resistance exists in the intervertebral disc due to constriction flow in the cartilage endplates. A comparison of the hydrostatic pressure in the nucleus of the healthy intervertebral disc during daily loading with the relatively low osmotic swelling pressure during rest, suggests the necessity of such direction-dependent flow resistance to ensure that all the fluid exuded from the disc during loading is recovered during rest. A physical model demonstrating the direction-dependent resistance of constriction flow in a poroelastic solid is presented. A finite element model was developed and validated against this physical model. The finite element model showed that decrease of the constriction hole area not only increases the resistance to fluid flow, but also causes the direction-dependency of flow resistance to decrease. Through this mechanism, endplate sclerosis could affect normal daily fluid exchange in the intervertebral disc, resulting in decreased mass transport and/or dehydration of the disc.

Biological Transport↗
PubMed1981

Congenital ring constrictions with entrapment neuropathies.

An eight year old boy with multiple simple congenital ring constrictions is described with peripheral nerve palsies caused by entrapment in the constrictions. It is suggested that ring constrictions should be considered in the differential diagnosis of entrapment neuropathy.

Child↗
PubMed2002

Minimal duration of oral matrix metalloproteinase inhibition to prevent constrictive arterial remodeling after balloon dilation in the pig.

PURPOSE: To determine the minimal duration of oral matrix metalloproteinase (MMP) inhibition to prevent constrictive remodeling after balloon dilation. MATERIALS AND METHODS: In 37 nonatherosclerotic pigs, balloon dilation was performed in 145 peripheral arteries. Pigs were treated with an MMP inhibitor for 2, 7, 14, 28, or 42 days, or they served as controls and were killed 42 days after intervention. Arteries were visualized with angiography and intravascular ultrasonography. RESULTS: A 69% reduction in late vessel area (VA) loss was achieved after 14 days of treatment: 1.27 mm(2) +/- 0.55 (standard error of the mean [SEM]) versus 4.04 mm(2) +/- 0.93 (SEM) in the control group (P =.1). A consistent inhibition of late VA loss was observed in the 28-day (0.89 mm(2) +/- 0.83 [SEM], P =.03) and 42-day (0.74 mm(2) +/- 0.66 [SEM], P =.02) groups treated with the MMP inhibitor. After 14 and 28 days of treatment, late lumen area loss was 65% and 55% of control values, and it decreased to 41% (P =.04) after 42 days of treatment. CONCLUSION: MMP inhibition for 14-28 days is sufficient to inhibit constrictive remodeling after balloon dilation. This implies that an essential MMP-dependent initiator of constrictive remodeling was mainly active in the first 2 weeks after intervention.

Animals↗
PubMed2006

Kv2 channels oppose myogenic constriction of rat cerebral arteries.

By hyperpolarizing arterial smooth muscle, voltage-gated, Ca2+-independent K+ (Kv) channels decrease calcium influx and thus oppose constriction. However, the molecular nature of the Kv channels function in arterial smooth muscle remains controversial. Recent investigations have emphasized a predominant role of Kv1 channels in regulating arterial tone. In this study, we tested the hypothesis Kv2 channels may also significantly regulate tone of rat cerebral arteries. We found that Kv2.1 transcript and protein are present in cerebral arterial smooth muscle. In addition, our analysis indicates that a substantial component (approximately 50%) of the voltage dependencies and kinetics of Kv currents in voltage-clamped cerebral arterial myocytes is consistent with Kv2 channels. Accordingly, we found that stromatoxin, a specific inhibitor of Kv2 channels, significantly decreased Kv currents in these cells. Furthermore, stromatoxin enhanced myogenic constriction of pressurized arterial segments. We also found that during angiotensin II-induced hypertension, Kv2 channel function was reduced in isolated myocytes and in intact arteries. This suggests that impaired Kv2 channel activity may contribute to arterial dysfunction during hypertension. On the basis of these novel observations, we propose a new model of Kv channel function in arterial smooth muscle in which Kv2 channels (in combination with Kv1 channels) contribute to membrane hyperpolarization and thus oppose constriction.

Animals↗
PubMed1994

Endothelin-1 induces direct constriction of hepatic sinusoids.

We studied the hepatic microvascular response to endothelin (ET) and the possible role of Ito cells (fat-storing cells) acting as pericytes in this response using isolated rat livers under high-power intravital microscopy. Livers were perfused in a modified pressure-controlled system with Krebs buffer plus rat erythrocytes (RBC, 10%), and sinusoids at the site of Ito cells were observed under a x 100 objective (total magnification x 2,533) before and during infusion of ET-1 (10(-9 M) alone, sodium nitroprusside (NP, 10(-5) M). plus ET-1, or phenylephrine (PE, 10(-7) M). Both ET-1 and PE decreased portal flow (25 and 51%) and increased inflow pressure (28 and 43%), respectively. PE had no effect on any sinusoidal parameters except that it decreased measured sinusoidal RBC velocity (P < 0.05); ET-1 decreased sinusoidal diameter by 25% and increased the calculated sinusoidal pressure gradient and resistance by 116 and 350%, respectively, but did not alter RBC velocity. NP significantly inhibited changes induced by ET-1. These results demonstrate that ET-1 induces a specific sinusoidal constriction that disrupts normal acinar flow dynamics, and the sinusoidal constriction colocalizes with Ito cells, suggesting that the constriction may be mediated at least in part by ET-1 action on Ito cells, which can be inhibited by a nitric oxide donor.

Animals↗
PubMed2005

Reactive oxygen species from smooth muscle mitochondria initiate cold-induced constriction of cutaneous arteries.

Cold constricts cutaneous blood vessels by selectively increasing the activity of smooth muscle alpha2-adrenoceptors (alpha2-ARs). In mouse tail arteries, alpha2-AR constriction is mediated by alpha2A-ARs at 37 degrees C, whereas the cold-induced augmentation in alpha2-AR activity is mediated entirely by alpha2C-ARs. Cold causes translocation of alpha2C-ARs from the trans-Golgi to the plasma membrane, mediated by cold-induced activation of RhoA and Rho kinase. The present experiments analyzed the mechanisms underlying these responses. Mouse tail arteries were studied in a pressure myograph. Cooling the arteries (28 degrees C) caused a rapid increase in reactive oxygen species (ROS) in smooth muscle cells, determined by confocal microscopy of arteries loaded with the ROS-sensitive probes, dichlorodihydrofluorescein or reduced Mitotracker Red. The inhibitor of mitochondrial complex I rotenone (10 micromol/l), the antioxidant N-acetylcysteine (NAC; 20 mmol/l), or the cell-permeable mimic of superoxide dismutase MnTMPyP (50 micromol/l) did not affect vasoconstriction to alpha2-AR stimulation (UK-14304) at 37 degrees C but dramatically inhibited the response at 28 degrees C. Indeed, these ROS inhibitors abolished the cold-induced increase in alpha2-AR constrictor activity. NAC (20 mmol/l) or MnTMPyP (50 micromol/l) also abolished the cold-induced activation of RhoA in human cultured vascular smooth muscle cells and the cold-induced mobilization of alpha2C-ARs to the cell surface in human embryonic kidney 293 cells transfected with the receptor. The combined results suggest that cold-induced constriction is mediated by redox signaling in smooth muscle cells, initiated by mitochondrial generation of ROS, which stimulate RhoA/Rho kinase signaling and the subsequent mobilization of alpha2C-ARs to the cell surface. Altered activity of ROS may contribute to cold-induced vasospasm occurring in Raynaud's phenomenon.

Acetylcysteine↗
PubMed1987

Effect of aortic constriction on the functional border zone.

To evaluate how aortic constriction affects nonischemic myocardium adjacent to the perfusion boundary (the "functional border zone"), we measured systolic wall thickening (dWT) with sonomicrometers in eight anesthetized, open-chest dogs. The locations of the wall thickening measurements relative to the perfusion boundary (PB) were determined with myocardial blood flow (microspheres) maps constructed from multiple, small tissue samples. In nonischemic myocardium more than 10 mm from the PB produced by circumflex coronary occlusion, dWT increased significantly from 2.57 +/- 0.62 (mean +/- SD) to 3.24 +/- 0.73 mm (P less than 0.01). Within 10 mm of the PB, however, dWT did not change significantly (2.48 +/- 0.79 to 2.38 +/- 0.66 mm, NS). When the aorta was mechanically constricted, peak systolic pressure increased approximately 50%. Wall thickening decreased to the same relative degree in nonischemic muscle less than 10 mm and more than 10 mm from the perfusion boundary. By fitting sigmoid curves to the data, we estimated the extent of nonischemic dysfunction. It averaged 26 +/- 6 degrees (6-8 mm of endocardial circumference) during coronary occlusion alone and it was not significantly different (29 +/- 11 degrees) after aortic constriction. Thus elevated afterload affects nonischemic myocardium uniformly and does not increase the size or relative severity of the functional border zone.

Animals↗
PubMed1988

Sympathetic changes during development of cardiac hypertrophy in aortic-constricted rats.

Cardiac hypertrophy is frequently associated with sympathetic changes that include increased myocardial norepinephrine turnover, depleted myocardial norepinephrine stores, decreased myocardial responses to sympathetic nerve stimulation, and elevated plasma catecholamines. To better understand these events mechanistically, the time course of each was assessed in rat hearts subjected to aortic constriction-induced pressure overload. There was no evidence of increased left ventricular norepinephrine turnover in abdominal aortic-constricted rats, when compared with sham-constricted animals, during the first 3 days postoperatively. Moreover, their turnover rate constants tended to be lower during this period, then increased significantly by day 7. Plasma catecholamines were increased and left ventricular norepinephrine stores were decreased only on day 7. Heart rate responses to maximal sympathetic nerve stimulation were significantly reduced on the third postoperative day. Thus the decrease in norepinephrine stores coincided with changes in left ventricular norepinephrine turnover and plasma catecholamines, whereas the reduction in heart rate responses did not. This pattern suggests an initial reflex decrease in myocardial sympathetic tone, followed by baroreceptor resetting, with an eventual increase in general sympathetic outflow. The period of increasing catecholamine stimulation occurred after a relative left ventricular hypertrophy had developed but before a significant increase in absolute left ventricular mass. Thus catecholamines may still importantly contribute to the hypertrophy seen in this model.

Animals↗
PubMed1989

Hemodilution causes size-dependent constriction of pial arterioles in the cat.

Cerebral blood flow (CBF) rises as hematocrit (Hct) falls. We previously attributed this rise in CBF to two independent factors of equal importance, decreased arterial O2 content and decreased blood viscosity. We hypothesized that decreased arterial O2 content would dilate cerebral arterioles and that the magnitude of the vasodilation would depend on the magnitude of the passive fall in vascular resistance attributable to decreased viscosity. The present study was designed to test the hypothesis that anemia is accompanied by cerebral vasodilation. Using a closed cranial window, we measured the diameters of 42 pial arterioles (35-305 microns) in 7 cats as serial isovolemic hemodilution lowered Hct by 44% from 31 +/- 4 to 17 +/- 3%. Hemodilution increased CBF (microsphere technique) but did not change mean arterial blood pressure or arterial blood gases. Anticipated vasodilation did not occur; instead, pial arterioles constricted as Hct fell. Maximum vasoconstriction was observed when Hct reached 65-70% of the initial value. Vasoconstriction lessened as Hct was lowered further, but arteriolar diameters at the lowest Hcts remained less than base-line levels. Constriction was greater in small (less than 100 microns) than in large (greater than or equal to 100 microns) arterioles. The initial constriction of pial arterioles may represent myogenic vasoconstriction in response to flow-induced vasodilation of more proximal portions of the cerebrovascular bed and/or to washout of an endogenous vasodilator. Arteriolar relaxation with more profound hemodilution may reflect superimposed metabolic vasodilation.

Animals↗
PubMed1991

Adenosine receptor blockade with 8-p-sulfophenyltheophylline aggravates coronary constriction.

We examined the role of adenosine in modulating the coronary constrictor effect of neuropeptide Y (NPY). Anesthetized dogs (n = 22) were instrumented to record hemodynamics and to collect arterial and coronary venous blood. In control dogs (n = 7), during the first 30 min before NPY, baseline coronary resistance fell slightly. By 10 min after NPY (42 nmol over 4 min), coronary resistance was increased by 30% and fell slowly to pre-NPY levels over the ensuing hour. Intravenous (7.5 mg/kg, n = 3) or intracoronary (to 100 microM arterial concentration, n = 12) infusion of 8-p-sulfophenyltheophylline (8-THEO) blocked the vasodilator effects of adenosine but did not alter the peak dilation seen with papaverine or reactive hyperemia. Over 30 min before NPY, infusion of 8-THEO increased baseline resistance by 31% as it reduced coronary blood flow, despite no change in other hemodynamic parameters or myocardial oxygen consumption. The coronary constrictor effect of NPY was magnified in the presence of adenosine receptor blockade. At 3 min, coronary resistance was increased by 34%, at 5 min by 52%, and at 10 min by 59%. The effect of adenosine receptor blockade on constriction due to NPY could not be attributed to a nonspecific alteration in cardiac function or oxygen consumption. In addition, the increase in baseline coronary resistance following receptor blockade correlated with the worsening of the coronary constriction following NPY (r = 0.48, P less than 0.05). Thus it appears that adenosine modulates an imposed constriction of coronary vessels and acts as a "host defense" to restore coronary tone toward normal.

Adenosine↗
PubMed1992

Effect of protein kinase C inhibitors on endothelin- and vasopressin-induced constriction of the rat basilar artery.

The goal of this study was to determine whether inhibitors of protein kinase C (PKC) attenuate constrictor responses of the basilar artery in vivo to endothelin and arginine vasopressin. In anesthetized rats, the diameter of basilar arteries was measured through a cranial window [control diameter 218 +/- 3 (SE) microns]. Vessel diameter was measured during topical application of agonists and antagonists. Sphingosine (10(-6) M), a PKC inhibitor that binds to the regulatory site of PKC, attenuated vasoconstriction in response to endothelin (10(-9), 10(-8), and 10(-7) M) and vasopressin (10(-9) and 10(-8) M). H-7 (10(-9) M), a PKC inhibitor that binds to the catalytic site of PKC, also inhibited vasoconstriction in response to endothelin and vasopressin. Sphingosine and H-7 did not affect baseline diameter and did not attenuate vasoconstriction in response to prostaglandin (PG) F2 alpha. The V1 antagonist [d(CH2)5Tyr(Me)]arginine vasopressin (10(-8) M) significantly inhibited constriction in response to vasopressin (10(-9) and 10(-8) M) but not PGF2 alpha (10(-6) M). These observations suggest that activation of PKC may contribute to endothelin-induced constriction of the basilar artery in vivo and that PKC may also be a mediator of V1-receptor-mediated constriction of the basilar artery in response to vasopressin.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1992

Alpha 2-adrenoceptors mediate norepinephrine constriction of porcine pial veins.

The adrenergic innervation and alpha-adrenoceptor agonist-induced constrictions in isolated medium-size pial veins (OD 734 +/- 18 microns) of the pig were investigated. Using in vitro tissue bath techniques, we noted exogenously applied norepinephrine (10(-9) to 10(-5) M) induced venoconstriction with EC50 values of 1.71 x 10(-7) M, where EC50 is the concentration that produced 50% of (non-KCl) agonist-induced maximum constriction. The constriction was mimicked by clonidine but not by phenylephrine and was more effectively blocked by yohimbine than by prazosin. Results from histochemical studies demonstrated that porcine pial veins received a denser plexus of catecholamine fluorescence fibers than do pial arteries with similar outer diameter. These results suggest that norepinephrine-induced pial venoconstriction is mediated predominantly by alpha 2-adrenoceptors and that porcine pial veins have significantly greater sensitivity to the alpha-action of norepinephrine than that reported in pial arteries. These results add further support for adrenergic innervation in pial veins being of importance in regulating cerebral blood volume and intracranial pressure.

Adrenergic alpha-Agonists↗