Effect of human plasma proteins on spontaneous contractile activity of rat mesenteric portal vein

1990 ◽  
Vol 68 (6) ◽  
pp. 737-743 ◽  
Author(s):  
G. Pillai ◽  
M. C. Sutter
Keyword(s):  
Portal Vein ◽  
Spontaneous Activity ◽  
Plasma Proteins ◽  
Mechanical Response ◽  
Contractile Activity ◽  
Physiological Salt Solution ◽  
Portal Veins ◽  
6 Hydroxydopamine ◽  
Dose Dependent Increase ◽  
Dose Dependent

This study examines the effect of various plasma proteins from man on the spontaneous contractile activity of the rat portal vein. Albumin, γ-globulin, α-globulin, β-globulin (the major plasma proteins), and immunoglobulin IgG (the major immunoglobulin present in the γ-globulin fraction) were obtained commercially. Mesenteric portal vein strips were prepared from rats and placed in a physiological salt solution in muscle baths for the measurement of longitudinal mechanical response. Portal veins exposed to albumin or γ-globulin showed a dose-dependent increase in the spontaneous activity, whereas those exposed to α-globulin or α - and β-globulin together showed a dose-dependent inhibition of spontaneous activity. Immunoglobulin IgG produced a dose-dependent increase in the spontaneous activity similar to that of γ-globulin. The increased spontaneous activity produced by albumin was not prevented by ouabain but was inhibited by phentolamine. Spontaneous contractile activity was stimulated by albumin in the chemically (6-hydroxydopamine) denervated portal vein. These findings indicate that albumin acts in a manner similar to noradrenaline. The increased spontaneous activity caused by γ-globulin (IgG) was inhibited by ouabain or verapamil. The effect of IgG was not dependent on α-adrenergic, cholinergic, histaminergic, serotoninergic, or renin angiotensin systems nor was it affected by removal of the endothelium. These observations may have implications in the pathophysiology of essential hypertension.Key words: vasomotion, mesenteric portal vein, plasma proteins, albumin, γ-globulin, inhibitory factor, stimulatory factor, IgG.

Effect of plasma from hypertensive patients on contractile response of vascular smooth muscle from normotensive rat

1989 ◽  
Vol 67 (10) ◽  
pp. 1272-1277 ◽  
Author(s):  
G. Pillai ◽  
M. C. Sutter
Keyword(s):  
Smooth Muscle ◽  
Portal Vein ◽  
Vascular Smooth Muscle ◽  
Spontaneous Activity ◽  
Mechanical Response ◽  
Contractile Response ◽  
Contractile Activity ◽  
Plasma Samples ◽  
Hypertensive Patients ◽  
Plasma Factor

This study examines whether incubation with plasma from essential hypertensive patients increases the contractile activity of vascular smooth muscle from rats in response to noradrenaline (NA) and potassium (K+). Plasma samples were obtained from age- and sex-matched essential hypertensive patients and normotensive people. Vascular strips were prepared from aorta and portal veins of normotensive rats and placed in physiological solution in muscle baths for measurement of mechanical response. Aortic strips exposed to hypertensive plasma showed increased responsiveness to NA compared with normotensive plasma, but K+ caused an opposite effect. Portal vein exposed to normotensive or hypertensive plasma did not produce any response to NA, but the responsiveness produced in the presence of normotensive plasma to K+ was higher than that of hypertensive plasma. Portal vein exposed to normotensive plasma or hypertensive plasma showed a dose-dependent increase in the spontaneous activity up to 50% concentration of the plasma samples, but further increase in the concentration of plasma inhibited the spontaneous activity. Spontaneous activity at any given concentration of hypertensive plasma was significantly higher than that of normotensive plasma. The spontaneous activity in the presence of heated or unheated normotensive plasma or unheated normotensive serum was not significantly different from each other. These results indicate that the plasma factor from hypertensive patients, which alters the reactivity of vascular smooth muscle from normotensive rat, is present in the serum fraction and is not heat sensitive.Key words: hypertension, plasma, contractile response, circulating factor, spontaneous activity.

Functional and molecular identification of ERG channels in murine portal vein myocytes

2002 ◽  
Vol 283 (3) ◽  
pp. C866-C877 ◽  
Author(s):  
Susumu Ohya ◽  
Burton Horowitz ◽  
Iain A. Greenwood
Keyword(s):  
Portal Vein ◽  
Contractile Activity ◽  
Membrane Conductance ◽  
Cell Voltage ◽  
Mean Amplitude ◽  
Isometric Tension ◽  
Real Time Quantitative Pcr ◽  
Inward Currents ◽  
Portal Veins ◽  
Rapid Kinetics

Ion channels encoded by ether-à-go-go-related genes (ERG) have been implicated in repolarization of the cardiac action potential and also as components of the resting membrane conductance in various cells. The aim of the present study was to determine whether ERG channels were expressed in smooth muscle cells isolated from portal vein. RT-PCR demonstrated the expression of murine ERG (mERG), and real-time quantitative PCR showed that the mERG1b isoform predominated over the mERG1a, mERG2, and mERG3 in portal vein. Single myocytes from portal vein displayed membrane staining with an ERG1-specific antibody. Whole cell voltage-clamp experiments were performed to determine whether portal vein myocytes expressed functional ERG channels. Large inward currents with distinctive kinetics were elicited that were inhibited rapidly by E-4031 (mean amplitude of the E-4031-sensitive current at −120 mV was −205 ± 24 pA; n = 14). Deactivation of the E-4031-sensitive current was voltage dependent (mean time constants at −80 and −120 mV were 103 ± 9 and 33 ± 2 ms, respectively; n = 13). Because of the rapid kinetics of mERG currents at more negative potentials, there was a substantial noninactivating “window” current that reached a maximum of −66 ± 10 pA at −70 mV. Complete portal veins exhibited spontaneous contractile activity in isometric tension experiments, and this activity was modified significantly by E-4031. These data show that ERG channels are expressed in murine portal vein myocytes that may contribute to the resting membrane conductance.

Ethanol-induced increase in portal blood flow: role of adenosine

1988 ◽  
Vol 254 (4) ◽  
pp. G495-G501 ◽  
Author(s):  
H. Orrego ◽  
F. J. Carmichael ◽  
V. Saldivia ◽  
H. G. Giles ◽  
S. Sandrin ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Portal Vein ◽  
Portal Blood Flow ◽  
Portal Blood ◽  
Maximal Effect ◽  
Dependent Manner ◽  
Dose Dependent Increase ◽  
Dose Dependent

The mechanism by which ethanol induces an increase in portal vein blood flow was studied in rats using radiolabeled microspheres. Ethanol (2 g/kg) by gavage resulted in an increase of 50-70% in portal vein blood flow. The ethanol-induced increase in portal blood flow was suppressed by the adenosine receptor blocker 8-phenyltheophylline [ethanol, 61.8 +/- 4.1 ml.kg-1.min-1; ethanol + 8-phenyltheophylline (0.2 mg.kg-1.min-1), 44.2 +/- 2.0 ml.kg-1.min-1; P less than 0.05]. By itself, 8-phenyltheophylline (0.2 mg.kg-1.min-1) was without effect on cardiac output or portal blood flow. Adenosine infusion resulted in a dose-dependent increase in portal blood flow with a maximal effect at a dose of 0.17 mg.kg-1.min-1 (control, 41.3 +/- 2.3; adenosine, 81.7 +/- 8.0 ml.kg-1.min-1; P less than 0.05). This adenosine-induced increase in portal blood flow was inhibited by 8-phenyltheophylline in a dose-dependent manner [adenosine, 81.7 +/- 8.0 ml.kg-1.min-1; adenosine + 8-phenyltheophylline (0.2 mg.kg-1.min-1), 49.8 +/- 6.6 ml.kg-1.min; P less than 0.05]. Both alcohol and adenosine significantly reduced preportal vascular resistance by 40% (P less than 0.02) and 60% (P less than 0.01), respectively. These effects were fully suppressed by 8-phenyltheophylline. It is concluded that adenosine is a likely candidate to mediate the ethanol-induced increase in portal vein blood flow. It is suggested that an increase in circulating acetate and liver hypoxia may mediate the effects of alcohol by increasing tissue and interstitial adenosine levels.

Calcium influx and spontaneous phasic contractions of portal veins after treatment with reserpine, 6-hydroxydopamine, and cocaine

1978 ◽  
Vol 56 (2) ◽  
pp. 199-201 ◽  
Author(s):  
M. Kaiman ◽  
S. Shibata
Keyword(s):  
Guinea Pig ◽  
Portal Vein ◽  
Calcium Influx ◽  
Phasic Contraction ◽  
Reserpine Treatment ◽  
Portal Veins ◽  
6 Hydroxydopamine ◽  
Induced Changes

Reserpine treatment increased the amplitude of the spontaneous phasic contraction (SPC) of portal veins obtained from rabbit and guinea pig but did not alter that of rat. The amplitude of the SPC of portal veins from these animals was increased after 6-hydroxydopamine (6-OHDA) but was not changed after cocaine treatment. Reserpine-and 6-OHDA-induced changes in portal vein SPC amplitude were accompanied by an increase in 45Ca influx.These results indicate that the elevation in SPC amplitude is accompanied by an increase in calcium influx.

Source of activator calcium in isolated guinea pig and human gastric muscle cells

1986 ◽  
Vol 250 (3) ◽  
pp. G280-G286 ◽  
Author(s):  
K. N. Bitar ◽  
G. M. Burgess ◽  
J. W. Putney ◽  
G. M. Makhlouf
Keyword(s):  
Guinea Pig ◽  
Channel Blocker ◽  
Contractile Response ◽  
Contractile Activity ◽  
Muscle Cells ◽  
Single Muscle ◽  
Gastric Muscle ◽  
Pig Muscle ◽  
Dose Dependent Increase ◽  
Dose Dependent

The source of Ca2+ responsible for contraction was examined in suspensions of smooth muscle cells and in perfused single muscle cells from guinea pig and human stomach. In both preparations removal of Ca2+ from the medium or addition of the Ca2+ channel blocker methoxyverapamil had no effect on the contractile response to various agonists, including cholecystokinin octapeptide (CCK-8) and acetylcholine, but inhibited the response to high extracellular K+ by 76-82%. Repeated stimulation of guinea pig or human single muscle cells in Ca2+-free medium, or in the presence of methoxyverapamil caused a progressive decrease and eventual abolition of contractile response; response was restored on restitution of Ca2+ to the medium or elimination of methoxyverapamil. Measurement of 45Ca2+ content in guinea pig muscle cells showed that CCK-8 had no effect on the rate of Ca2+ influx but increased the rate of Ca2+ efflux transiently by sixfold. Net peak efflux coincided with the time of peak contraction and was stoichiometrically related to the degree of contraction. Equipotent, maximally effective contractile doses of CCK-8, acetylcholine, and methionine-enkephalin caused equivalent degrees of net Ca2+ efflux. The results indicate that contractile agonists cause release of Ca2+ from a depletable intracellular store in gastric muscle cells. The release is accompanied by a dose-dependent increase in Ca2+ efflux and is capable of sustaining an initial maximal contraction. Repeated contractile activity requires influx of Ca2+ from extracellular sources.

Cerebral arteries can generate 5- and 15-hydroxyeicosatetraenoic acid from arachidonic acid

1990 ◽  
Vol 68 (7) ◽  
pp. 807-813 ◽  
Author(s):  
Richard Schulz ◽  
Sonia Jancar ◽  
David A. Cook
Keyword(s):  
Arachidonic Acid ◽  
Cerebral Artery ◽  
High Performance ◽  
Contractile Activity ◽  
Cerebral Arteries ◽  
Hydroxyeicosatetraenoic Acid ◽  
Lipoxygenase Pathway ◽  
Product Profile ◽  
Dose Dependent Increase ◽  
Dose Dependent

Products of the lipoxygenase pathway have been implicated in the development of the cerebrovascular spasm that arises after subarachnoid hemorrhage. In particular the hydroperoxyeicosatetranenoic acids (HPETEs), which are unstable and break down rapidly to the corresponding 5-hydroxy acids (HETEs), are vasoconstrictor agents that mimic some aspects of cerebrovascular spasm. It is not, however, well established whether segments of cerebral artery can manufacture these products. We have studied the lipoxygenase product profile of cerebral arteries stimulated with arachidonic acid. Rings of bovine cerebral arteries were incubated in Krebs solution containing arachidonic acid. The lipoxygenase products were studied using high performance liquid chromatography. The largest peaks had the retention times of 5- and 15-HETEs, and the identity of these peaks was confirmed using specific radioimmunoassays. Stimulation with arachidonic acid resulted in a time- and dose-dependent increase in the formation of both HETEs, with 15-HETE being most abundant. The release of both HETEs was markedly reduced in the presence of AA-861, an inhibitor of lipoxygenase, but not with the cyclooxygenase inhibitor indomethacin. These data are thus consistent with our previous suggestion that the contractile activity of arachidonic acid in cerebral arteries arises, at least in part, from HPETE formation and with a possible role for these compounds in cerebral vasospasm.Key words: arachidonic acid, cerebral artery, hydroxyeicosatetraenoic acid, lipoxygenase.

Increased Expression of u-PA and u-PAR on Monocytes by LDL and Lp(a) Lipoproteins – Consequences for Plasmin Generation and Monocyte Adhesion

1999 ◽  
Vol 81 (04) ◽  
pp. 594-560 ◽  
Author(s):  
Florence Ganné ◽  
Marc Vasse ◽  
Jean-Louis Beaudeu ◽  
Jacqueline Peynet ◽  
Arnaud François ◽  
...  
Keyword(s):  
Fold Increase ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Atheromatous Plaque ◽  
Monocyte Adhesion ◽  
Blood Monocytes ◽  
Proteolytic Cascade ◽  
Ecm Degradation ◽  
Dose Dependent Increase ◽  
Dose Dependent

SummaryMonocyte-derived foam cells figure prominently in rupture-prone regions of atherosclerotic plaque. As urokinase/urokinase-receptor (u-PA/u-PAR) is the trigger of a proteolytic cascade responsible for ECM degradation, we have examined the effect of atherogenic lipoproteins on monocyte surface expression of u-PAR and u-PA. Peripheral blood monocytes, isolated from 10 healthy volunteers, were incubated with 10 to 200 µg/ml of native or oxidised (ox-) atherogenous lipoproteins for 18 h and cell surface expression of u-PA and u-PAR was analysed by flow cytometry. Both LDL and Lp(a) induced a dose-dependent increase in u-PA (1.6-fold increase with 200 μg/ml of ox-LDL) and u-PAR [1.7-fold increase with 200 μg/ml of ox-Lp(a)]. There is a great variability of the response among the donors, some of them remaining non-responders (absence of increase of u-PA or u-PAR) even at 200 μg/ml of lipoproteins. In positive responders, enhanced u-PA/u-PAR is associated with a significant increase of plasmin generation (1.9-fold increase with 200 μg/ml of ox-LDL), as determined by an amidolytic assay. Furthermore, monocyte adhesion to vitronectin and fibrinogen was significantly enhanced by the lipoproteins [respectively 2-fold and 1.7-fold increase with 200 μg/ml of ox-Lp(a)], due to the increase of u-PAR and ICAM-1, which are receptors for vitronectin and fibrinogen. These data suggest that atherogenous lipoproteins could contribute to the development of atheromatous plaque by increasing monocyte adhesion and trigger plaque weakening by inducing ECM degradation.

LH-RH TEST IN 100 PATIENTS WITH OVARIAN INSUFFICIENCY

1974 ◽  
Vol 75 (3) ◽  
pp. 428-434 ◽  
Author(s):  
P.-J. Czygan ◽  
M. Breckwoldt ◽  
F. Lehmann ◽  
R. Langefeld ◽  
G. Bettendorf
Keyword(s):  
Intravenous Injection ◽  
Functional State ◽  
Clear Correlation ◽  
Normal Range ◽  
Ovarian Insufficiency ◽  
Lh Rh ◽  
Dose Dependent Increase ◽  
Dose Dependent

ABSTRACT The effect of synthetic LH-RH was studied in 100 patients with various types of ovarian insufficiency by following up the FSH- and LH-levels in plasma. LH-RH was administered in doses of 12.5, 25 and 100 μg as a rapid intravenous injection. The patients were classified according to the endocrine state of the pituitary as evidenced by the urinary gonadotrophin levels. A clear correlation between the functional state of the pituitary and its responsiveness to exogenous LH-RH was demonstrated. Most of the patients with undetectable low urinary gonadotrophin levels failed to respond. The majority of patients with gonadotrophin excretion in the normal range and those with elevated levels reacted with a dose dependent increase in circulating LH. The amount of liberated FSH however was related to the injected dose only in patients with high gonadotrophic excretion. The present study indicates that synthetic LH-RH provides a useful tool in the evaluation of the pitutiary function particularly in patients with low and with undetectable gonadotrophin excretion. The data presented in this paper also demonstrate that the functional state of the pituitary is clearly reflected by the urinary gonadotrophin levels.

Evaluation of the Laxative activity of Saponin Enriched Hydroethanolic Pericarp extract of Sapindus emarginatus in Animal models

2020 ◽  
Vol 16 ◽  
Author(s):  
Lalitha Vivekanandan ◽  
Roxanne Gekonge Mandere ◽  
Sivakumar Thangavel
Keyword(s):  
Animal Models ◽  
Gravimetric Analysis ◽  
Triterpene Saponins ◽  
Laxative Effect ◽  
Saponin Content ◽  
The Family ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Efficacious Drug

Background: Constipation is a common, predominant, chronic gastrointestinal functional disorder. The drugs available to treat constipation are limited because of their side effects in long term use. So we need of efficacious drug to treat constipation. Sapindus emarginatus Vahl belongs to the family Sapindaceae, commonly known as soapnut. Traditionally used for the antipruritic, antifertility, constipation, and anti-inflammatory agents. Objective: The present study was undertaken to evaluate the laxative activity of hydroethanolic pericarp extract of Sapindus emarginatus (HESE) in animal models. Methods: The saponin content in extract was measured by gravimetric analysis. The laxative activity of hydroethanolic pericarp extract of Sapindus emarginatus is evaluated by the weight of feces matter, charcoal meal hyperperistalsis test, and loperamide induced constipation model. Results: The saponin content of the soapnut pericarp was 13.48 % and the extract was found to be 11.92 %. The results obtained from these models showed a significant dose-dependent increase in fecal weight, peristalsis index, and moisture content compared to control animals. Conclusion: The present study concluded that the oral administration of HESE showed a significant laxative activity by using different animal models. The presence of triterpene saponins is responsible for this activity. Further studies are needed to confirm their mechanism behind the laxative effect. The administration of extract was found to be a valid candidate in constipation therapy.

scholarly journals Morphological and Behavioral Effects in Zebrafish Embryos after Exposure to Smoke Dyes

Toxics ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 9
Author(s):  
Kimberly T. To ◽  
Lindsey St. Mary ◽  
Allyson H. Wooley ◽  
Mitchell S. Wilbanks ◽  
Anthony J. Bednar ◽  
...  
Keyword(s):  
Dose Dependence ◽  
Behavioral Effects ◽  
Zebrafish Embryos ◽  
Comprehensive Understanding ◽  
Anthraquinone Dyes ◽  
Locomotor Movement ◽  
Different Types ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Significant Mortality

Solvent Violet 47 (SV47) and Disperse Blue 14 (DB14) are two anthraquinone dyes that were previously used in different formulations for the production of violet-colored smoke. Both dyes have shown potential for toxicity; however, there is no comprehensive understanding of their effects. Zebrafish embryos were exposed to SV47 or DB14 from 6 to 120 h post fertilization (hpf) to assess the dyes’ potential adverse effects on developing embryos. The potential ability of both dyes to cross the blood–brain barrier was also assessed. At concentrations between 0.55 and 5.23 mg/L, SV47 showed a dose-dependent increase in mortality, jaw malformation, axis curvature, and edemas. At concentrations between 0.15 and 7.54 mg/L, DB14 did not have this same dose-dependence but had similar morphological outcomes at the highest doses. Nevertheless, while SV47 showed significant mortality from 4.20 mg/L, there was no significant mortality on embryos exposed to DB14. Regardless, decreased locomotor movement was observed at all concentrations of DB14, suggesting an adverse neurodevelopmental effect. Overall, our results showed that at similar concentrations, SV47 and DB14 caused different types of phenotypic effects in zebrafish embryos.

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