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PubMed2006

Constrictive pericarditis: A reminder of a not so rare disease.

Constrictive pericarditis is a rare condition characterized by clinical signs of right heart failure subsequent to loss of pericardial compliance. The etiology of constrictive pericarditis has changed during the last decades in developed countries. While, in the past, tuberculosis and idiopathic pericardial constriction were the prevalent causes of the disease, cardiac surgery has become one of the main reasons for its development in recent years. However, cases defined as idiopathic constrictive pericarditis are still observed. In addition to the classical chronic and subacute forms, new presentations, such as effusive-constrictive, localized, transient, occult, and constrictive pericarditis with normal pericardial thickness, have been described. Although conservative treatment may alleviate the patient's symptoms, pericardiectomy remains the only definitive treatment for the disease. It is worth noting that the sooner the diagnosis of pericardial constriction is established, the better the outcome is. The pathophysiological features, clinical findings, diagnostic tools, and therapeutic approach to constrictive pericarditis are detailed in this review.

Journal Article↗
PubMed2005

Effects of oxygen tension and normalization pressure on endothelin-induced constriction of human placental chorionic plate arteries.

OBJECTIVES: Fetoplacental blood vessels constrict in response to endothelin (ET-1) or reduced oxygen tension in the placental cotyledon perfused in vitro. In nonplacental resistance arteries, hypoxia and ET-1 induce constriction by promoting Ca2+ influx into smooth muscle through membrane ion channels, which include voltage-gated Ca2+ channels (VGCCs). We hypothesized that VGCCs are involved in ET-1-induced constriction of fetoplacental resistance vessels and that their contribution to constriction is enhanced at low oxygen tension. METHODS: Chorionic plate small arteries from term placentas were studied using parallel wire myography. Arteries were normalized at 0.9 of L(5.1 kPa) ("low stretch" approximately 25 mm Hg; approximating physiologic vascular pressure) or 0.9 of L(13.3 kPa) ("high stretch" approximately 42 mm Hg) and experiments performed at oxygen tensions of 156, 38, and 15 mm Hg. RESULTS: When chorionic plate arteries were normalized at low stretch, oxygen tension did not affect constriction to ET-1. Nifedipine (10(-4) M), a blocker of L-type VGCCs, inhibited ET-1 (EC80)-induced constriction to a similar extent at each oxygen tension (52% to 64% inhibition). In contrast, when arteries were normalized at high stretch, constriction to ET-1 was greater at 38 than at 156 or 15 mm Hg oxygen and nifedipine inhibition of ET-1-induced constriction was greater at 38 and 15 mm Hg than at 156 mm Hg oxygen. CONCLUSIONS: VGCCs and nifedipine-insensitive processes underlie the contractile response of chorionic plate arteries to ET-1 and their relative contribution to vasoconstriction is modulated by oxygen tension when vessels are normalized at high stretch. However, contrary to our hypothesis, the response of chorionic plate arteries to ET-1 is not modulated by oxygen when vessels are normalized at physiologic pressure.

Arteries↗
PubMed2005

Vascular endothelial growth factor-C promotes vasculogenesis, angiogenesis, and collagen constriction in three-dimensional collagen gels.

OBJECTIVE: Neovascularization, angiogenesis, and collagen constriction are essential for wound healing. We tested whether vascular endothelial growth factor-C (VEGF-C) can promote collagen constriction, capillary sprouting (angiogenesis), and invasion/migration of bone marrow-derived endothelial progenitor cells into collagen (vasculogenesis). METHODS: We used a recently characterized three-dimensional collagen matrix assay with either monolayers of human dermal microvascular endothelial cells (HMVECs) or bone marrow-derived endothelial progenitor cells (BMD EPCs), obtained from Tie-2 LacZ transgenic mice, overlaid with an acellular layer and then a cellular layer of collagen embedded with fibroblasts, that were nontransduced or transduced with either LacZ adenoviral vector (Ad5) or VEGF-C/Ad5. The ability of VEGF-C to enhance fibroblast-mediated collagen constriction was measured, and gels overlying HMVECs or BMD EPCs were co-cultured, harvested, and assayed for HMVEC migration, sprouting, and capillary-like formation; gels containing BMD EPCs were assayed for EPC invasion/migration into the collagen extracellular matrix. RESULTS: VEGF-C significantly increased collagen constriction and formation of capillary-like structures with true lumina (P < .05) assessed by von Willebrand factor and VEGF receptor-2 immunoassaying. VEGF-C induced a significant increase in HMVEC migration, tubular polarization, and branching sprouts associated with a significant up-regulation of membrane type 1 matrix metalloproteinase (MT1-MMP) ( P < .05). Fibroblasts were necessary to support BMD-EPC invasion/migration from the monolayer into the collagen. Moreover, fibroblasts overexpressing VEGF-C significantly enhanced EPC invasion/migration ( P < .05) into the extracellular matrix by two-fold, and this effect could not be achieved with equivalent levels of exogenous VEGF-C in the absence of fibroblasts. The addition of a soluble VEGF-C competitor protein only partially inhibited these responses, reducing the EPCs by three-fold, but significant numbers of EPCs still invaded/migrated into the extracellular matrix, suggesting that other fibroblast-specific signals also contribute to the vasculogenic response. CONCLUSION: Fibroblast-specific expression of VEGF-C promotes collagen constriction by fibroblasts and enhances microvascular endothelial cell migration, branching, and capillary sprouting in association with up-regulating MT1-MMP expression. Fibroblasts are necessary for BMD EPC invasion/migration into collagen, and their overexpression of VEGF-C enhances this fibroblast-mediated vasculogenic effect. Collectively, these findings suggest a role for VEGF-C in multiple biologic steps required for wound healing (angiogenesis, vasculogenesis, and collagen constriction). CLINICAL RELEVANCE: Ischemic wound healing remains an unsolved problem with no previously identified molecular target for therapeutic intervention. This study demonstrates that VEGF-C overexpression by fibroblasts stimulates multiple biologic processes known to impact wound healing, such as collagen constriction, capillary sprouting, and EPC invasion and migration through extracellular matrix. Most ischemic wounds fail to heal and frequently lead to major limb amputation. Available cytokine ointments are ineffective, and revascularization is often not technically feasible. Even when these procedures are accomplished, many ischemic wounds frequently still do not heal because of multifactorial tissue level impairments in the fibroblastic and neovascularization responses at the wound base. Our findings identify an important role for two novel tissue level targets, dermis-derived fibroblasts and VEGF-C, in collagen constriction, angiogenesis, and postnatal vasculogenesis from BMD EPCs. Thus the findings are particularly relevant to the unsolved clinical problem of ischemic wound healing.

Animals↗
PubMed1997

The effect of indomethacin tocolysis on fetal ductus arteriosus constriction with advancing gestational age.

OBJECTIVE: Our purpose was to determine whether continuing exposure to indomethacin tocolysis is associated with an increased incidence of constriction of the human fetal ductus arteriosus with advancing gestational age. STUDY DESIGN: Fetal echocardiograms were reviewed in 61 cases in which the pregnant women were treated for preterm labor with indomethacin (25 mg orally every 6 hours). Density function analysis and regression analysis were used to assess the effect of indomethacin tocolysis on ductal constriction with advancing gestational age. RESULTS: A total of 193 fetal echocardiograms were obtained for 72 fetuses. Ductal constriction developed in 50% of the fetuses ranging from 24.7 to 35.0 weeks' gestation. Fetuses with indomethacin-induced ductal constriction demonstrated a greater increase in systolic flow velocities with advancing gestational age compared with the nonconstricted group (p < 0.05). Constriction was detected at a mean gestational age of 30.9 +/- 2.3 weeks at an average of 5.1 +/- 6.0 days after initiation of therapy. Ductal constriction occurred by 31 weeks' gestation in 70% of the affected fetuses. After discontinuation of indomethacin therapy, all follow-up echocardiograms demonstrated a return to nonconstricted ductal flow velocities. No significant adverse neonatal outcomes were attributed to indomethacin use. CONCLUSIONS: A dramatic yet reversible increase in the incidence of indomethacin-induced ductal constriction occurs at 31 weeks' gestation. However, ductal constriction can occur at any gestational age. With indomethacin tocolysis, weekly fetal echocardiography is warranted for the duration of therapy.

Ductus Arteriosus↗
PubMed1998

Endothelin ET(B) receptor-mediated constriction in the rabbit basilar artery.

The present study tests whether endothelin ET(B) receptor activation can mediate endothelin-1 constriction in the rabbit basilar artery in situ. Endothelin-1 (30 nM) induced 27% constriction of vessels pretreated with 1 microM BQ610 (homopiperidenyl-CO-Leu-DTrp (CHO)-D-Trp-OH), an endothelin ET(A) receptor antagonist, and the resulting constriction was completely relaxed by BQ788 (N-cis-2,6-dimethylpiperidinocarbonyl L-gamma-MeLeu-D-Trp (COOCH3)-Nle), an endothelin ET(B) receptor antagonist. Similarly, 30 nM endothelin-1 induced 30% constriction of vessels pretreated with 1 microM BQ788, and the resulting constriction was completely relaxed by BQ610. In contrast, sarafotoxin S6c, an endothelin ET(B) receptor agonist, did not induce constriction. This study suggests that in the basilar artery (1) endothelin ET(B) receptor activation can result in constriction and (2) the ability to elicit constriction is in some way dependent upon the agonist that activates the endothelin ET(B) receptor.

Animals↗
PubMed1996

Role of chloride channels in afferent arteriolar constriction.

The effects of IAA-94, a chloride channel blocker and/or low chloride perfusate on afferent arteriolar (AA) constriction by angiotensin II (Ang II), norepinephrine (NE) and increasing pressure (80 to 160 mm Hg) were assessed using isolated perfused hydronephrotic kidneys. In the first series of experiments, Ang II (0.3 nM) constricted AAs by 33 +/- 3% (N = 5, P < 0.01). Subsequent addition of diltiazem (10 microM) restored the decrements in the AA diameters. In the presence of diltiazem (10 microM), increasing pressure did not constrict AAs. In the second series of experiments. elevation of pressure constricted AAs by 20 +/- 2% (N = 7. P < 0.01). Subsequent addition of IAA-94 (30 microM) failed to alter the basal AA diameter and myogenic responsiveness. However, Ang II-induced AA constriction was abolished by IAA-94. In the third series of experiments, decreasing extracellular chloride exaggerated AA constriction by 0.1 nM of Ang II (from 13 +/- 2 to 20 +/- 3%, N = 6, P < 0.05). Similarly, low chloride perfusate enhanced NE (0.1 microM)-induced AA constriction (from 14 +/- 2 to 19 +/- 2%, N = 6, P < 0.05). In contrast, myogenic responsiveness was not influenced by reducing chloride concentrations. The present data provide evidence that both Ang II and NE induce AA constriction by opening chloride channels and subsequent activation of voltage-dependent calcium channels, and suggest that the myogenic response is mediated by activating voltage-dependent calcium channels independently of chloride channels.

Adrenergic beta-Antagonists↗
PubMed1998

Amniotic band syndrome: the association between rare facial clefts and limb ring constrictions.

The pathologic cause of both rare craniofacial clefts and congenital limb ring constrictions is the subject of some debate. Uncommon though these two conditions are, they have often been anecdotally reported in association. This study sought to determine the frequency of congenital limb anomalies in general and limb ring constrictions in particular amongst a population of patients with rare craniofacial clefts. Eighty-five cases of nonsyndromal, rare, craniofacial cleft were identified from a population of 280 patients assessed at the Women's and Children's Hospital, North Adelaide, with a diagnosis of rare craniofacial cleft classifiable by the Tessier system. Twenty-two patients (25.9 percent) displayed congenital limb anomalies. Eleven of these (12.9 percent) showed evidence of limb ring constrictions, a frequency much greater than in the general population. The group with limb ring constrictions demonstrated a significantly greater complexity of involvement with craniofacial clefting than the non-limb ring constriction group (4.27 clefts/patient versus 2.3 clefts/patient, p < 0.01). The distribution of craniofacial cleft locations in patients with evidence of limb ring constrictions was found to differ significantly from those with other or no limb anomalies (p < 0.01). The clefts in cases in which limb ring constrictions coexist are largely restricted to the paramedian 2-12, 3-11, 412 axes. This study confirms an association between rare craniofacial clefts and limb ring constrictions. The two conditions may therefore possess common etiology.

Abnormalities, Multiple↗
PubMed2004

Phenylpropanolamine constricts mouse and human blood vessels by preferentially activating alpha2-adrenoceptors.

Phenylpropanolamine (dl-norephedrine) was one of the most widely used therapeutic agents to act on the sympathetic nervous system. Because of concerns regarding incidents of stroke, its use as a nasal decongestant was discontinued. Although considered an alpha1-adrenergic agonist, the vascular adrenergic pharmacology of phenylpropanolamine was not fully characterized. Unlike most other circulations, the vasculature of the nasal mucosa is highly enriched with constrictor alpha2-adrenoceptors. Therefore, experiments were performed to determine whether phenylpropanolamine activates vascular alpha2-adrenoceptors. Mouse tail and mesenteric small arteries and human small dermal veins were isolated and analyzed in a perfusion myograph. The selective alpha1-adrenergic agonist phenylephrine caused constriction of tail and mesenteric arteries and human veins. The selective alpha2-adrenergic agonist UK14,304 [5-bromo-N-(4,5-dihydro-1H-imidazol-2-yl)-6-quinoxalinamine] caused constriction in tail arteries and in human veins, but not mesenteric arteries. The lack of constriction to UK14,304 was also observed in endothelium-denuded mesenteric arteries. Phenylpropanolamine constricted both types of artery but was 62-fold more potent in tail arteries. In mesenteric arteries, constriction to phenylpropanolamine was not affected by the selective alpha2-adrenergic antagonist, rauwolscine (10(-7) M) but was abolished by the selective alpha1-adrenergic antagonist, prazosin (3 x 10(-7) M). In contrast, constriction to phenylpropanolamine in tail arteries and in human veins was inhibited by rauwolscine but not prazosin. Therefore, phenylpropanolamine is a preferential alpha2-adrenergic agonist. At low concentrations, it constricts blood vessels that express functional alpha2-adrenoceptors, whereas at much higher concentrations, phenylpropanolamine also activates vascular alpha1-adrenoceptors. This action likely contributed to phenylpropanolamine's therapeutic activity, namely constriction of the nasal vasculature.

Adrenergic alpha-1 Receptor Agonists↗
PubMed1991

Effects of phorbol esters on canine coronary artery constriction and dilation in vitro.

The influence of protein kinase C (PKC) activation on canine coronary vasoreactivity was assessed in vitro. Activation of PKC by phorbol 12,13-dibutyrate (PDBu) or phorbol 12-myristate 13-acetate (PMA) caused slow sustained constriction of isolated coronary artery rings. PDBu was a more potent and efficacious constrictor than PMA (169 +/- 21 vs. 81 +/- 7% of maximum KCl constriction). Constriction to PDBu was reduced slightly by deendothelialization and by meclofenamate. Pretreatment with threshold concentrations of PDBu increased constriction to serotonin from 3 +/- 1 to 48 +/- 4% of maximum KCl constriction whether or not the endothelium was present but had no effect on response to the thromboxane analogue U-46619. In addition, in arteries constricted with PDBu, dilations to ADP, thrombin, acetylcholine, and sodium nitroprusside were impaired when compared with arteries constricted with U-46619. These results suggest that activation of PKC in coronary arteries 1) produces potent constriction mediated only in small part by the endothelium and by cyclooxygenase products, 2) potentiates markedly the constrictor response to serotonin by an endothelium-independent mechanism, and 3) attenuates both endothelium-dependent and endothelium-independent vasodilation.

6-Ketoprostaglandin F1 alpha↗
PubMed1995

Endogenous adenosine modulates alpha 2- but not alpha 1-adrenergic constriction of coronary arterioles.

In the coronary circulation alpha-adrenergic constriction competes with metabolic vasodilation. Because adenosine is produced by the working myocardium and metabolic stimulation results in arteriolar dilation, we tested the hypothesis that coronary arteriolar alpha-adrenergic constriction is attenuated by the endogenous production of adenosine. To test this hypothesis, using fluorescence microscopy during stroboscopic epi-illumination of the epicardial microvasculature, we measured the diameter of coronary arterioles in anesthetized open-chest dogs. Measurements were made in the presence of beta-blockade during selective alpha 1- or alpha 2-adrenoceptor activation (phenylephrine or B-HT-933, respectively) before and in the presence of the nonselective adenosine receptor antagonist 8-p-sulfophenyltheophylline (8-pSPT) and expressed as a percent change in microvascular diameter relative to baseline. alpha 1-Activation produced constriction of coronary arterioles under control conditions, which was not augmented after adenosine antagonism (-12 +/- 2 vs. -7 +/- 3%). In contrast, alpha 2-activation did not constrict coronary arterioles under control conditions; however, blockade of adenosine receptors unmasked a significant constriction (0 +/- 2 vs. -7 +/- 2%, P < 0.05). Also adenosine antagonism did not significantly alter the baseline diameter of coronary arterioles. These results demonstrate that endogenously produced adenosine modulates alpha 2-adrenergic constriction of coronary arterioles but not alpha 1-adrenergic constriction, and therefore we speculate that the competition between alpha-adrenergic constriction and metabolic vasodilation is mediated by the alpha 1-adrenoceptor.

Adenosine↗
PubMed1999

Integrin signaling, free radicals, and tyrosine kinase mediate flow constriction in isolated cerebral arteries.

Isolated, cannulated, and pressurized (100 mmHg) middle cerebral arteries from adult cats were perfused intraluminally at rates from 0 to 4 ml/min with heated and gassed physiological saline solution. An electronic system held pressure constant by changing outflow resistance. The arteries constricted 18.1 +/- 0.95% in response to flow and depolarized from -54 +/- 0.51 to -40 +/- 1.26 mV (P < 0.05). Constriction was independent of a functional endothelium but was eliminated by superoxide dismutase or tyrosine kinase inhibitors. Luminal perfusion with a synthetic extracellular matrix Arg-Gly-ASP (RGD) peptide that binds with integrin significantly reduced constriction to flow. Neither reducing intraluminal pressure nor increasing tone or shear stresses altered constriction to flow. Flow-induced constriction did not impede the ability of the arteries to dilate to hypercapnia, and inhibiting flow-induced constriction did not alter contractile responses to other agonists. These data suggest that, in vitro, middle cerebral arteries constrict to flow through a mechanism involving free radicals and tyrosine kinase and that flow shear stresses resulting in constriction are transduced by integrin signaling.

Animals↗
PubMed2004

Vanilloid receptor TRPV1, sensory C-fibers, and vascular autoregulation: a novel mechanism involved in myogenic constriction.

Myogenic constriction describes the innate ability of resistance arteries to constrict in response to elevations in intraluminal pressure and is a fundamental determinant of peripheral resistance and, hence, organ perfusion and systemic blood pressure. However, the receptor/cell-type that senses changes in pressure on the blood vessel wall and the pathway that couples this to constriction of vascular smooth muscle remain unclear. In this study, we show that elevation of intraluminal transmural pressure of mesenteric small arteries in vitro results in a myogenic response that is profoundly suppressed following ablation of sensory C-fiber activity (using in vitro capsaicin desensitization resulted in 72.8+/-10.3% inhibition, n=8; P<0.05). Activation of C-fiber nerve endings by pressure was attributable to stimulation of neuronal vanilloid receptor, TRPV1, because blockers of this channel, capsazepine (71.9+/-11.1% inhibition, n=9; P<0.001) and ruthenium red (46.1+/-11.7% inhibition, n=4; P<0.05), suppressed the myogenic constriction. In addition, this C-fiber dependency is likely related to neuropeptide substance P release and activity because blockade of tachykinin NK1 receptors (66.3+/-13.7% inhibition, n=6; P<0.001), and not NK2 receptors (n=4, NS), almost abolished the myogenic response. Previous studies support a role for 20-hydroxyeicosatetraenoic acid (20-HETE) in myogenic constriction responses; herein, we show that 20-HETE-induced constriction of mesenteric resistance arteries is blocked by capsazepine. Together, these results suggest that elevation of intraluminal pressure is associated with generation of 20-HETE that, in turn, activates TRPV1 on C-fiber nerve endings resulting in depolarization of nerves and consequent vasoactive neuropeptide release. These findings identify a novel mechanism contributing to Bayliss' myogenic constriction and highlights an alternative pathway that may be targeted in the therapeutics of vascular disease, such as hypertension, where enhanced myogenic constriction plays a role in the pathogenesis.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1977

Mechanism of renin release during acute ureteral constriction in dogs.

The relationship between renal arterial pressure and renin release was examined in anesthetized dogs during complete or partial ureteral constriction. During complete ureteral occlusion ureteral pressure rose to 95+/-4 mm Hg and renin release increased from 1.7+/-0.7 to 22.3+/-3.1 mug/min; renal blood flow (RBF) was not significantly changed. Renin release was not further increased during subsequent renal arterial constriction; RBF fell in proportion to perfusion pressure, indicating maximum autoregulated arteriolar dilation. During partial ureteral constriction to a ureteral pressure of 65+/-6 mm Hg, renin release was moderately raised but release mechanisms became fully stimulated when renal arterial pressure was reduced to 104+/-3 mm Hg. By further constricted of the renal artery, RBF fell in proportion to perfusion pressure and renin release remained high and constant. In control experiments without ureteral constriction, renal arterial pressure had to be reduced to below 65+/-8 mm Hg to fully stimulate renin release (22.0+/-3.8 mug/ml which is not different from 22.3+/-3.1 mug/min during ureteral occlusion). During partial ureteral constriction, saline infusion (0.9% NaCl at 40 ml/min) raised urine flow, sodium excretion, renal pelvic pressure, and renin release. Thus, the stimulatory effect on renin release of a rise in ureteral pressure exceeded the inhibitory effect of increased sodium excretion. This observation, together with maximum renin release coinciding with complete arteriolar dilation during various combinations of renal arterial and ureteral constriction, is compatible with the conclusion that arteriolar dilation is predominating stimulus to renin release during ureteral constriction.

Animals↗
PubMed1988

Endothelium-dependent constriction demonstrated in vivo in mouse cerebral arterioles.

Endothelium-dependent constriction in mouse pial arterioles was demonstrated by testing contractile responses before and after endothelial injury. All responses were monitored at the same site as the injury. Injury was produced in vivo by exposing an arteriole on the brain surface to the beam of a 6-mW helium-neon laser after first sensitizing the microvascular bed to the laser energy by injecting Evans blue intravenously. The contractile response to serotonin creatinine sulfate (20 micrograms/ml) and to sodium arachidonate (30 micrograms/ml) was monitored in vivo with an image splitter and TV microscope. The responses before laser injury were always constriction; the responses after laser injury were always relaxation. After laser injury, acetylcholine chloride (80 micrograms/ml) constricted every vessel tested at the injured site. Thus, the injured segment had not lost the capacity to constrict even though neither serotonin nor arachidonate remained able to induce a constriction. The endothelium-dependent constrictions to serotonin or arachidonate were also blocked by pretreatment of the mouse with cyclooxygenase inhibitors, acetylsalicylic acid (100 mg/kg i.p.) or indomethacin (5 mg/kg). The data suggests that endothelium-dependent constriction to serotonin is mediated by release of arachidonate from the endothelial cell and conversion of that arachidonate by cyclooxygenase to some constricting prostanoid.

Animals↗
PubMed2001

Role of endothelium in shear stress-induced constrictions in rat middle cerebral artery.

BACKGROUND AND PURPOSE: Luminal shear stress has been reported to constrict cerebral arteries and arterioles of several species. Although the endothelium is not required for this response, it is not known whether the endothelium enhances or attenuates shear stress-induced constrictions. METHODS: Middle cerebral arteries (MCAs) were isolated from male Long-Evans rats, mounted in a tissue bath, and pressurized to 80 mm Hg in the absence of luminal flow. In some MCAs, the endothelium was selectively loaded with fura 2 for the measurement of endothelial Ca(2+) concentration. Luminal shear stress was increased by adjusting luminal flow while maintaining a constant intraluminal pressure. RESULTS: After the development of spontaneous tone in MCAs without luminal flow, inside diameters were approximately 190 microm. MCAs constricted approximately 15% when luminal flow was increased to produce a shear stress of 50 dyne/cm(2). The shear stress-induced constrictions were more pronounced in vessels without intact endothelium. Scavenging reactive oxygen species with 4,5-dihydroxy-1,3-benzene disulfonic acid (Tiron) or superoxide dismutase/catalase significantly inhibited the shear stress-induced constrictions in vessels with intact endothelium and in vessels in which the endothelium had been removed. In intact vessels, endothelial Ca(2+) increased 33 nmol/L (from 133+/-11 to 166+/-12 nmol/L) when shear stress was increased to 50 dyne/cm(2). The presence of N(G)-nitro-L-arginine methyl ester (L-NAME), L-NAME+indomethacin, or L-NAME+indomethacin+charybdotoxin had no significant effect on the shear stress-induced constrictions in MCAs with intact endothelium. CONCLUSIONS: We conclude that the endothelium plays a role in attenuating the shear stress-induced constrictions in rat MCAS: The attenuation does not appear to be by release of NO, prostacyclin, or endothelium-derived hyperpolarizing factor. The endothelium apparently attenuates the constriction by an unknown dilating factor, by a dilating process, or simply by attenuating the mechanical force of the shear stress as it is transmitted to the abluminal side of the vessel.

1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium ↗
PubMed1976

Variations of Bender-Gestalt constriction and depression in adult psychiatric patients.

The present study explored variations of Bender-Gestalt constriction and their relation to depression. 20 Ss showing constriction of drawings on the upper half-page and 20 Ss showing constriction of drawings on the left half-page were compared with regard to MMPI Depression scores. No significant difference was found between these groups. However, when the constricted groups were combined and then compared with 40 Ss who did not show constriction of Bender drawings, the constricted group had significantly higher (p less than .05) MMPI Depression scores. Thus, variations in Bender constriction are not differently related to depression, but presence of constriction is an indicator. However, its rate of occurrence is so infrequent, appearing in only 5% of the records examined, that its clinical usefulness in the detection of depression is quite limited.

Adolescent↗
PubMed1999

Relaxation of endothelin-1-induced pulmonary arterial constriction by niflumic acid and NPPB: mechanism(s) independent of chloride channel block.

We investigated the effects of the Cl- channel blockers niflumic acid, 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB) and 4, 4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS) on endothelin-1 (ET-1)-induced constriction of rat small pulmonary arteries (diameter 100-400 microm) in vitro, following endothelium removal. ET-1 (30 nM) induced a sustained constriction of rat pulmonary arteries in physiological salt solution. Arteries preconstricted with ET-1 were relaxed by niflumic acid (IC50: 35.8 microM) and NPPB (IC50: 21.1 microM) in a reversible and concentration-dependent manner. However, at concentrations known to block Ca++-activated Cl- channels, DIDS (</=500 microM) had no effect on the ET-1-induced constriction. Similar results were obtained when pulmonary arteries were preincubated with these Cl- channel blockers. When L-type Ca++ channels were blocked by nifedipine (10 microM), the ET-1-induced (30 nM) constriction was inhibited by only 5.8%. However, niflumic acid (30 microM) and NPPB (30 microM) inhibited the ET-1-induced constriction by approximately 53% and approximately 60%, respectively, both in the continued presence of nifedipine and in Ca++-free physiological salt solution. The Ca++ ionophore A23187 (10 microM) also evoked a sustained constriction of pulmonary arteries. Surprisingly, the A23187-induced constriction was also inhibited in a reversible and concentration-dependent manner by niflumic acid (IC50: 18.0 microM) and NPPB (IC50: 8.8 microM), but not by DIDS (</= 500 microM). Our data suggest that the primary mechanism by which niflumic acid and NPPB inhibit pulmonary artery constriction is independent of Cl- channel blockade. One possibility is that these compounds may block the Ca++-dependent contractile processes.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2000

Nociceptin inhibits electric field stimulation-induced cholinergic constrictions in rat airways.

AIM: To study the effect of nociceptin (orphanin FQ), a newly discovered heptadecapeptide, on cholinergic constrictions in isolated trachea and bronchus of rat. METHODS: The electric field stimulation (EFS) induced a monophasic constriction, which was due to an activation of the cholinergic nerves. RESULTS: Nociceptin 0.001-0.1 mumol/L inhibited cholinergic constriction in a concentration-dependent manner. IC50 (95% of confidence limits) were 0.06 (0.04-0.08) mumol/L and 0.07 (0.05-0.1) mumol/L in tracheae and bronchi respectively. The constrictions inhibited by nociceptin 0.01 mumol/L in traheae and bronchi were (58 +/- 32)% and (60 +/- 26)% respectively compared with the control, in which nociceptin was not applied. After pretreatment with naloxone 0.1 mumol/L, the constrictions were (60 +/- 19)% and (54 +/- 20)% (P > 0.05 vs the above figures). However, the constrictions induced by exogenous acetylcholine were unaffected by nociceptin 0.01 mumol/L. kappa-Opioid receptor agonist, U-50488H (0.01-1 mumol/L) did not affect the EFS-induced cholinergic constrictions in rat airways. CONCLUSION: Nociceptin inhibits EFS-induced cholinergic constriction, which is not affected by naloxone in rat airways.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗