bluuebunny/crossref_metadata_2025_split huggingface dataset:
Investigation of the contributions of nitric oxide and prostaglandins to the actions of endothelins and sarafotoxin 6c in rat isolated perfused lungs
Authors: Lal H. , Woodward B. , Williams K.I. 
Published: July 2012

The aims of the study were to assess the contribution of prostaglandins and nitric oxide (NO) to the effects of endothelin (ETs) and sarafotoxin 6c (SX6c) in perfused rat lungs. This was carried out by using indomethacin, a cyclo‐oxygenase inhibitor and NG‐nitro‐L‐arginine (L‐NOARG), a NO synthase inhibitor. Responses were studied under basal perfusion conditions and in other experiments after the elevation of vascular tone with the thromboxane‐mimetic, U46619. The sub‐types of ET receptors involved were characterized by use of ET receptor antagonists and cross‐tachyphylaxis.
Pulmonary perfusion pressure (PPP), lung weight and pulmonary inflation pressure (PIP), were continuously recorded. Although L‐NOARG (100 μm) did not alter basal parameters it markedly augmented the vasoconstriction and lung weight increases induced by ET‐1 (50–400 pmol) or SX6C (25–200 pmol) while vasoconstrictor responses to phenylephrine were not affected by L‐NOARG.
L‐NOARG markedly potentiated the bronchoconstriction induced by ET‐1 or SX6C whereas it had no effect on responses to carbachol.
When vascular tone was elevated, low doses (1.25–40 pmol) of ET‐1, ET‐3 and SX6C produced falls in PPP. The vasodilator potencies were SX6C > ET‐1 = ET‐3. The ETA receptor antagonist, BQ123, did not affect these depressor responses, whereas the mixed ETA/ETB antagonist, bosentan, blocked them.
Indomethacin (10 μm) partially inhibited vasodilator response to ET‐1, whereas it had no effect on SX6C‐induced vasodilatation.
L‐NOARG plus indomethacin completely blocked ET‐1 induced vasodilatation, whereas responses to SX6C were blocked by L‐NOARG alone.
Repeated injections of submaximal doses of ET‐1 or SX6C caused tachyphylaxis to vasodilator responses. Subsequent injections of SX6C or ET‐1 did not elicit depressor responses showing cross tachyphylaxis had occurred.
These findings indicate that under basal conditions the pulmonary vasoconstrictor, lung weight and bronchoconstrictor responses to ET‐1 and SX6C are attenuated by evoked release of nitric oxide (NO). When vascular tone was elevated, lower doses of ETs and SX6C produced vasodilatation. These vasodilator responses are indirect, those to SX6C being mediated via NO production, whereas those to ET‐1 involve both NO and prostanoid(s). Tachyphylaxis and ET antagonist experiments indicate that the same receptor subtype is involved in mediating the vasodilatation and that this is of the ETB type located on the endothelium. However the post‐receptor vasodilator events triggered by ET‐1 or SX6C appear to be different.
Agmatine, an endogenous modulator of noradrenergic neurotransmission in the rat tail artery
Authors: González C. , Regunathan S. , Reis D.J. , Estrada C. 
Published: July 2012

We investigated the vascular effects of agmatine (decarboxylated arginine), an endogenous ligand for α2‐adrenoceptors and non‐adrenoceptor imidazoline (I‐) receptors, present in endothelium, smooth muscle and plasma, using the rat tail artery as a model.
While by itself agmatine (10 nM‐1 mM) was without effect on isolated arterial rings, at the highest concentration used (1 mM) it slightly increased EC50 values for contractions elicited respectively by the α1‐ and α2‐adrenoceptor agonists methoxamine and clonidine.
Agmatine (0.03‐1 mM) produced a concentration‐dependent transient inhibition of the contractions induced by transmural nerve stimulation (TNS; 200 mA, 0.2 ms, 1 Hz, 10 s). This effect was abolished by the α2‐adrenoceptor antagonists, rawolscine and idazoxan.
In the presence of rawolscine or idazoxan, agmatine produced a concentration‐dependent delayed facilitation of TNS‐induced contractions, which was prevented by cocaine.
Neither inhibitory nor potentiating actions were produced by agmatine on contractions induced by noradrenaline (NA) administration.
Agmatine did not directly affect [3H]‐NA uptake in bovine cultured chromaffin cells.
Agmatine can regulate vascular function by two opposing actions at sympathetic nerve terminals, with different latencies: a transient inhibition of NA release mediated by prejunctional α2‐adrenoceptors and a cocaine‐sensitive delayed facilitation the mechanism of which is undetermined at present.
The results reveal the existence of a novel endogenous amine modulating NA release in the perivascular sympathetic terminals.
Some evidence against the involvement of arachidonic acid in muscarinic suppression of voltage‐gated calcium channel current in guinea‐pig ileal smooth muscle cells
Authors: Unno T. , Komori S. , Ohashi H. 
Published: July 2012

To see if arachidonic acid (AA) plays a role in the sustained suppression of voltage‐gated calcium channel currents produced by muscarinic receptor stimulation by carbachol (CCh), the effects of AA on membrane currents were examined in whole‐cell voltage‐clamped smooth muscle cells of the guinea‐pig ileum.
In cells bathed in Ba2+ PSS and dialysed with Cs+‐based low EGTA (0.05 mM) pipette solution, and in which Ba2+ current (IBa) flowing through voltage‐gated calcium channels was evoked repeatedly by stepping to 0 mV from the holding potential of −60 mV, AA (1–30 μm), applied extracellularly, gradually suppressed IBa in a concentration‐dependent manner. The IBa suppression was observed even with 20 mM EGTA in the pipette.
AA (3 μm) and CCh (10 μm) shifted the voltage‐dependent inactivation curve of IBa in the negative potential direction, but the effect of AA differed from that of CCh in that an accompanying appreciable decrease in the slope was observed.
The sustained suppression of IBa induced by CCh (10 μm) remained almost unaltered after pretreatment with 4‐bromophenacyl bromide (10 μm), an inhibitor of phospholipase A2, or a combination of indomethacin (10 μm), an inhibitor of the cyclo‐oxygenase pathway, and nordihydroguaiaretic acid (10 μm), an inhibitor of the lipoxygenase pathway.
In cells bathed in Ca2+ PSS and dialysed with K+‐based pCa 6.5 pipette solution, voltage‐dependent Ca2+ current (ICa) and K+ current (IK) were recorded simultaneously. AA (3 μm) suppressed IK as well as ICa, whereas CCh (10 μm)) suppressed ICa but not IK.
We conclude from these results that AA or its metabolite is unlikely to be involved in the sustained suppression of voltage‐gated calcium channel current induced by muscarinic receptor stimulation in guinea‐pig ileal smooth muscle cells.
Mediation by neurotensin‐receptors of effects of neurotensin on self‐stimulation of the medial prefrontal cortex
Authors: Fernández R. , Sabater R. , Sáez J.A. , Montes R. , Alba F. , Ferrer J.M.R. 
Published: July 2012

Intracortical microinjections of neurotensin (NT) selectively decreased intracranial self‐stimulation (ICSS) of the medial prefrontal cortex in the rat.
To elucidate whether this effect is mediated by NT receptors or by the formation of NT‐dopamine complexes, we investigated the effects on ICSS of intracortical microinjections of neurotensin (1–11), an NT fragment that forms extracellular complexes with dopamine but does not bind to NT receptors.
We also studied the effects of the peripheral administration of SR 48692, a selective antagonist of NT receptors, on the inhibition of ICSS produced by the intracortical administration of NT.
Unilateral microinjections of neurotensin (1–11) at doses of 10, 20 and 40 nmol into the medial prefrontal cortex did not change the basal ICSS rate of this area.
The intraperitoneal administration of SR 48692 at doses of 0.08 and 0.16 mg kg−1 30 min before microinjection of 10 nmol of NT into the medial prefrontal cortex, antagonized the inhibition of ICSS produced by the neuropeptide.
These results demonstrate that the inhibitory effect of NT on ICSS is mediated by NT receptors.
Increased interleukin‐8 release by β‐adrenoceptor activation in human transformed bronchial epithelial cells
Authors: Lindén Anders 
Published: July 2012

The effect of β‐adrenoceptor activation on release of the neutrophil chemoattractant, interleukin‐8 (IL‐8), was examined in human transformed bronchial epithelial cells (16HBE cells).
The combined β1‐ and β2‐adrenoceptor agonist, isoprenaline, time‐ (100 nM, 2–18 h) and concentration‐ (1–30 nM) dependently increased IL‐8 protein content in the cell culture supernatant as measured by an enzyme immunosorbent assay standardized for DNA by fluoro‐colorimetry.
Isoprenaline (1–100 nM, 15 min) increased cyclic AMP concentration‐dependently.
The effect of isoprenaline (100 nM) was inhibited by the β‐adrenoceptor blocker propranolol (10 μm). The maximum magnitude of IL‐8 increase caused by β‐adrenoceptor activation was 40% of that caused by the pro‐inflammatory cytokine tumor necrosis factor‐alpha (TNF‐α: 100 ng ml−1).
The selective β2‐adrenoceptor agonist salbutamol (1 μm), increased IL‐8 protein similarily to isoprenaline and the cyclic AMP analogue, dibutyryl cyclic AMP (1 mM) produced a corresponding effect.
Pretreatment with isoprenaline (100 nM) followed by TNF‐α (20 ng ml−1) increased IL‐8 additively.
In conclusion, β‐adrenoceptor stimulation increased the release of the neutrophil chemoattractant, IL‐8 in 16HBE cells, via an increase in intracellular cyclic AMP. β‐adrenoceptor stimulation adds to the IL‐8 increase caused by the pro‐inflammatory cytokine TNF‐α. If this mechanism exists in vivo, β‐adrenoceptor activation may increase neutrophil chemotaxis into the airways.
The effects of calcitonin gene‐related peptide on tracheal smooth muscle of guinea‐pigs in vitro
Authors: Ninomiya Hiroki , Uchida Yoshiyuki , Endo Takeo , Ohtsuka Masahito , Nomura Akihiro , Saotome Mikio , Hasegawa Shizuo 
Published: July 2012

The effect of calcitonin gene‐related peptide (CGRP) on airway smooth muscle is controversial. The aim of this study was to determine whether the action of CGRP on tracheal strips of guinea‐pigs is modulated by epithelium and whether this peptide‐induced action involves other mediators including nitric oxide (NO) and endothelin (ET)‐1.
CGRP produced a weak dose‐dependent increase in guinea‐pig tracheal tension in vitro (‐log EC50 = 8.5 ± 0.1, maximum contraction = 8.3 ± 1.2% of 50 mM KCl‐induced contraction, n = 6). In epithelium‐depleted preparations, CGRP (10−7 m)‐induced contraction was significantly potentiated from 9.0 ± 1.9% to 41.1 ± 6.0% (n = 6).
L‐NG‐nitro‐arginine methyl ester (L‐NAME, 10−4 m), which inhibits NO synthesis, enhanced the contractile response to CGRP from 9.0 ± 1.9% to 31.2 ± 1.1% (n = 6). Indomethacin (10−5 m) also enhanced the response to CGRP, although the effect was weak (13.4 ± 3.2%, n = 6).
Anti‐ET‐1 serum changed the CGRP‐induced contraction into a relaxation. After incubation of the trachea with ET‐1 (10−7 m) to attenuate ET‐1‐induced responses, the CGRP‐induced contraction also changed into a relaxation. BQ‐123 (an ETA receptor antagonist) and BQ‐788 (an ETB receptor antagonist) caused the same conversion of the CGRP response, from contraction to relaxation, although the relaxing effect elicited by BQ‐788 was more potent than that by BQ‐123. Maximum inhibitory responses were −31.0 ± 3.3% and −13.0 ± 2.3% of 50 mM KCl‐induced contraction, respectively (n = 6).
In primary culture, guinea‐pig tracheal epithelial cells released ET‐1, and CGRP (10−5 m) significantly increased the release of ET‐1.
These data suggest that the action of CGRP is modulated by airway epithelium and this mechanism involves the release of NO and ET‐1. Especially, the majority of contractile action elicited by CGRP consists of an action of ET‐1 via the predominant ETB receptor.
The P2Y purinoceptor in rat brain microvascular endothelial cells couple to inhibition of adenylate cyclase
Authors: Webb Tania E. , Feolde Erick , Vigne Paul , Neary Joseph T. , Runberg Anna , Frelin Christian , Barnard Eric A. 
Published: July 2012

BIO cells, a clonal line of rat brain capillary endothelial cells, exhibit a single P2 purinoceptor, activation of which leads to increases in free intracellular calcium. In the current study the identity of this P2Y receptor was determined by its binding parameters for a range of purinoceptor ligands and by its complementary DNA (cDNA) sequence. The signal transduction mechanism activated by this receptor was also investigated.
The radioligand [35S]‐dATPαS bound with high affinity (Kd = 9.8nM) to the P2Y purinoceptor expressed on B10 cells, which was found to be extremely abundant (Bmax = 22.5 pmol mg−1 protein). The calculated Ki values of a range of P2 purinoceptor agonists which competitively displaced binding of [35S]‐dATPαS led to the rank order of affinity: dATPαS (Ki 3.4 nM) > 2‐chloroATP (2‐ClATP) (13 nM), ATP (22 nM) > ATPγS (43 nM) > 2‐methylthioATP (2‐MeSATP) (88 nM) > ADP (368 nM) > > UTP, L‐β,γ‐methyleneATP (both > 10,000 nM). The P2 purinoceptor antagonists, Reactive blue 2 and suramin, were also able to displace binding, with Ki values of 833 and 1358 nM respectively. In contrast pyridoxal‐phosphate‐6‐azophenyl‐2′,4′‐disulphonic acid 4‐sodium (PPADS) was able to displace only 20% of [35S]‐dATPαS binding at a concentration of 100 μm
2‐ClATP (EC50 = 0.22 μm), 2‐MeSATP (0.54 μm), ADP (7.9 μm) and ATP (a partial agonist), but not UTP, inhibited the cyclic AMP formation stimulated by cholera toxin, in a manner that was prevented by pertussis toxin. The purinoceptor antagonist, PPADS, was found to be inactive at a concentration of 100 μm
A P2Y receptor cDNA was derived from mRNA from B10 cells and from C6‐2B, a rat glioma cell line known to possess a P2Y receptor that is coupled to the inhibition of adenylate cyclase. Sequence analysis of the entire coding region revealed that both were 100% identical to the rat P2Y1 purinoceptor cDNA. No other P2Y‐type receptor mRNA could be detected in B10 cells. Exactly the same sequence was isolated from rat brain cortical astrocytes, where 2‐MeSATP has been shown to increase phospholipase C activity.
Since the receptor responsible for the transduction shares with the aforementioned binding site significant pharmacological features, including a strong activity of 2‐MeSATP (characteristic of P2Y1 receptors alone among all known P2Y purinoceptors) and an unusual insensitivity to PPADS, and since abundant mRNA is present of the P2Y2 receptor but not of any other type resembling the known P2Y receptors, it is concluded that a P2Y1 receptor on rat brain microvascular endothelial cells can account for all of the observations. This single P2Y1 receptor, therefore, appears to couple in different native cell types to either adenylate cyclase inhibition or to phospholipase C activation.
Lack of beneficial effects of the NO‐donor, molsidomine, in the L‐NAME‐induced pre‐eclamptic syndrome in pregnant rats
Authors: Richer Christine , Boulanger Henri , Es‐Slami Samira , Giudicelli Jean‐François 
Published: July 2012

In pregnant rats, chronic NO‐synthase inhibition induces the development of a pre‐eclamptic syndrome, characterized by an increase in maternal blood pressure, a loss of vascular refractoriness to pressor stimuli, a reduction in litter size and a decrease in pups (and maternal) weight. We investigated whether a NO‐donor, molsidomine, administered during NO synthase inhibition, could restore a normal pregnancy.
Pregnant rats were given daily, starting from day 14 of gestation, saline (controls), or L‐NAME (50 mg kg−1 d−1), or molsidomine (15 or 30 mg kg−1 d−1), or the L‐NAME + molsidomine combinations. Maternal blood pressure and body weight, litter size, pups weight and vascular reactivity to pressor stimuli (angiotensin II, noradrenaline, electrical stimulation of the spinal cord) were investigated.
L‐NAME alone, as compared to controls, increased maternal blood pressure, reduced litter size (−59%), increased foetal reabsorptions (+625%) and decreased foetal weight (−10%). Vascular reactivity to pressor stimuli was enhanced.
Molsidomine alone, as compared to controls, dose‐dependently decreased maternal blood pressure but had no effect on vascular reactivity and, whatever the dose, on foetal outcome.
The L‐NAME‐molsidomine combinations dose (of molsidomine)‐dependently limited the rise in maternal blood pressure induced by L‐NAME alone but unexpectedly, dose‐dependently and significantly worsened pregnancy evolution, e.g., at 30 mg kg−1d−1: litter size (−80%), foetal reabsorptions (+1025%), foetal weight (−24%). Vascular reactivity to pressor stimuli was paradoxically further enhanced.
Thus, in a chronic NO deprivation‐induced model of pre‐eclampsia in rats, molsidomine, possibly because of its hypotensive action, worsens the foetal outcome, which questions the usefulness of NO‐donors in pre‐eclamptic women.
Naphthoquinone colorants from Arnebia nobilis Rech.f
Authors: Arora Anjali , Gupta Deepti , Rastogi Deepali , Gulrajani Mohan 
Published: July 2012

The roots of Arnebia nobilis have traditionally been used as a colorant in food and cosmetic preparations. The deep red colour obtained is attributed to the presence of shikonin and its isomer alkannin and their derivatives. In this study, five colouring components were extracted from the roots of A. nobilis. These were separated and purified chromatographically and characterised using various spectrophotometric techniques. Three of the five components were identified. The major component was found to be alkannin β, β‐dimethylacrylate [5,8‐dihydroxy‐2‐(1′‐β, β‐dimethylacryloxy‐4′‐methylpent‐3′‐enyl)‐1,4‐naphthoquinone], accounting for nearly 25% of the total colouring matter. Alkannin acetate [2‐(1′‐acetoxy‐4′‐methylpent‐3′‐enyl)‐5,8‐dihydroxy‐1,4‐naphthoquinone] made up ca. 8% and shikonin [(5,8‐dihydroxy‐4′‐methylpent‐3′‐enyl)‐1,4‐naphthoquinone] contributed ca. 6% of the colouring matter. Polyester was dyed pink, nylon was dyed blue and all other substrates acquired a purple hue under similar dyeing conditions. The dyed fabrics showed excellent wash, rub and perspiration fastness; however, light fastness was found to be poor.
Implantable Cardioverter Defibrillator Therapy in Patients with Cardiac Sarcoidosis
Authors: SCHULLER JOSEPH L. , ZIPSE MATTHEW , CRAWFORD THOMAS , BOGUN FRANK , BESHAI JOHN , PATEL AMIT R. , SWEISS NADERA J. , NGUYEN DUY T. , ALEONG RYAN G. , VAROSY PAUL D. , WEINBERGER HOWARD D. , SAUER WILLIAM H. 
Published: July 2012

ICD Shocks in Cardiac Sarcoidosis. Background: An implantable cardioverter defibrillator (ICD) is indicated for some patients with cardiac sarcoidosis (CS) for prevention of sudden death. However, there are little data regarding the event rates of ICD therapies in these patients. We sought to identify the incidence and characteristics of ICD therapies in this patient population.Methods: We performed a cohort study of patients with ICDs at 3 institutions. Cases were those patients with CS and an ICD implanted for primary or secondary prevention of sudden death. Additionally, we included a comparison with historical controls of ICD therapy rates reported in clinical trials evaluating the ICD for primary and secondary prevention of sudden death.Results: Of the 112 CS subjects identified, 36 (32.1%) received appropriate therapies for ventricular tachyarrhythmias (VT) over a mean follow‐up period of 29.2 months. VT storm (>3 episodes in 24 hours) occurred in 16 (14.2%) CS subjects. Inappropriate therapies occurred in 13 CS subjects (11.6%). Covariates associated with appropriate ICD therapies included left ventricular ejection fraction (LVEF) <55% (OR 6.52 [95% CI 2.43–17.5]), right ventricular dysfunction (OR 6.73 [95% CI 2.69–16.8]), and symptomatic heart failure (OR 4.33 [95% CI 1.86–10.1]).Conclusions: In our cohort of patients with CS and ICDs, almost one‐third receive appropriate therapies. This may be due to a myocardial inflammatory process leading to increased triggered activity and subsequent scarring leading to reentrant tachyarrhythmias. Adjusted predictors of ICD therapies in this population include left or right ventricular dysfunction. (J Cardiovasc Electrophysiol, Vol. 23, pp. 925‐929, September 2012)
Creating model consumers: Producing ethnicity, race, and class in Asian American advertising
Authors: Shankar Shalini 
Published: July 2012

ABSTRACTHow does Asian American advertising contribute to the construction of race and ethnicity in the contemporary United States? In this article, I consider how executives write advertising copy and create original artwork for Asian American advertisements in ways that index brand identities. I introduce the analytic of “metaproduction,” a process of material and linguistic signification that uses metacultural and metalinguistic values to connect microlevel signification of language and culture with broader social meanings and values. Analysis of ethnographic data from New York City advertising agencies shows how racialization occurs through the transformation of Asian Americans from model minority producers into model minority consumers.
Configuring the authentic value of real food: Farm‐to‐fork, snout‐to‐tail, and local food movements
Authors: Weiss Brad 
Published: July 2012

ABSTRACTThe partibility of pigs and the circulation of their parts—from snout to tail, as the popular culinary phrase puts it—are routinely celebrated in communities committed to eating “local.” In this article, I explore how different kinds of totalities are configured in the practices of such “locavore” actors with respect to pigs and pork. Approaches as varied as Sausseurean structuralism, functionalist sociology, and actor network theory characterize their objects of inquiry as totalities constituted by relationships among component parts. So too the totalities in relationships forged via pigs become (mis)aligned with the totality of pigs as embodied, complex organisms. Such wholes from parts reveal the overdetermination (or fetishization) of the “connections” (between farmers and consumers, chefs and diners, humans and animals) extolled by “local food” actors.
Consumer valuation of safety‐labeled free‐range chicken: results of a field experiment in Hanoi
Authors: Ifft Jennifer , Roland‐Holst David , Zilberman David 
Published: July 2012

AbstractThis article presents results of a field experiment designed to assess willingness to pay for safely produced free‐range chicken in Hanoi, the capital of Vietnam. Improved safety of chicken production and trading is suggested as an important component of avian influenza control strategy, which aims to address the direct costs of avian influenza as well as the global public health externality. However, consumer demand for safely produced free‐range chicken is unknown. Products that have credible food labeling are not common in traditional markets where the majority of free‐range chicken is purchased. Valuing characteristics of products sold in informal markets is a major challenge that our experiment overcomes. As part of the experiment, we provided several vendors from these markets with safety‐labeled free‐range chicken. Consumer valuation of safety labeling was elicited through having experiment participants, who were representative of potential consumers, select between discount coupons for either safety‐labeled chicken or regular chicken. Results indicate that consumers will pay at least $0.50, or a 10–15% premium, per chicken purchase for safety labeling, which emphasizes safe production, processing, and transport conditions. This premium is smaller than the premium currently paid for traditional chicken varieties that are considered to be tastier. Consumers with more education have higher valuation of safety labeling. Hence, safety labeling for high‐quality free‐range chicken can play a role in controlling livestock disease and improving public health.