Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1832588 (PSS)
 2,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isolated porcine coronary arteries contracted transiently when exposed to 20 mM Na salts of organic acids (acetate, propionate, butyrate and lactate) at constant external pH (pH0 = 7.4). The peak of these phasic contractions, completely inhibited by 1 mM amiloride, amounted to about 10% of that elicited by depolarization with 50 mM K0. The slope of the relaxing branch of the phasic contractions induced by 20 mM acetate in HEPES buffered physiological salt solution decreased from 1.05 +/- 0.12 to 0.49 +/- 0.07 mN/min (S.E.M.; n = 14), when Na0 was reduced from 137 to 20 mM. In Na free HEPES-buffered PSS only sustained contractions were obtained. The EC50 values for the concentration-response curves for contractions induced by K-propionate (2-20 mM) in Tris-PSS were 8.2 +/- 0.5 mM, n = 6. After total isoosmotic replacement of external Na+ by sucrose in bicarbonate-buffered PSS, contractions induced by 20 mM K-propionate had the same height as those induced with 50 mM K0+. Longlasting exposure to 0 Ca0 PSS did not affect significantly contractions induced by 20 mM propionate. During an exposure to procaine (10(-4) M) acetate-induced contractions were transiently and significantly enhanced, when induced in bicarbonate buffered PSS, but not in HEPES buffered PSS. In normally polarized PCA preparations 20 mM NH4+ induced both sustained relaxations and polyphasic responses; in depolarized PCA preparations only polyphasic responses were evoked. The time course of the polyphasic responses to application and removal of weak bases (NH(4+)-pulse technique) or to removal and reintroduction of CO2/HCO3- paralleled exactly the expected pHi perturbations, as they have been described in a great variety of cells and tissues, alkalinization leading however to relaxation, acidification to contraction. In presence of NH4+, a transient relaxation (phase 1) was immediately followed by an overshooting contraction (phase 2); at removal of NH4+ a rebound contraction (phase 3) was observed, reaching a peak and changing thereafter to a relaxation (phase 4), the slope of which was sensitive to variation of the external Na0 concentration. These mechanical effects were abolished by 1 hr exposure to 0 Ca PSS. Phase 2 was enhanced 2-5 fold in presence of TEA, Ba ions, Na3 VO4 or beta-methyldigoxin. Contractile responses of PCA preparations activated by various agonists (acetylcholine, histamine and serotonin) to pHi manipulations were similar and generally amplified when compared to unactivated preparations.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of manipulations of cytoplasmic pH on the mechanical responses of isolated porcine coronary arteries. 769 Dec 15

The vasculature of rat isolated mesentery and small intestine was perfused with a gelatin-containing physiological salt solution (GPSS). When 5-hydroxytryptamine (5HT, 1 x 10(-4) M), or the calcium ionophore A23187 (1 x 10(-4) M), or 12-deoxyphorbol 13-phenylacetate (DOPPA, 1 x 10(-6) M), or 12-deoxyphorbol 13-phenylacetate 20-acetate (DOPPAA, 1 x 10(-6) M) or thymeleatoxin (TMX, 1 x 10(-6) M) was added to the GPSS for 5 min there was a gradual rise in perfusion pressure, whereas resiniferatoxin (RFX, 1 x 10(-6) M) was without effect. Pre-treatment of the tissue with the protein kinase C (PKC) inhibitor Ro 31-8220 (1 x 10(-6) M) significantly reduced the rise in perfusion pressure in response to 5HT, DOPPA, DOPPAA and TMX, but not that to A23187. Platelet-activating factor (PAF, 5 x 10(-6) M) caused an almost immediate but transient rise in perfusion pressure, followed by a more gradual rise, neither response being blocked by Ro 31-8220. When blood vessels of the mesentery alone were perfused with gelatin-free PSS, PAF caused a transient rise in perfusion pressure, but with no subsequent gradual rise over 5 min. After Ca(2+)-depletion this transient response was also absent. In contrast, when blood vessels were perfused with gelatin-free PSS, DOPPA and TMX still caused gradual rises in perfusion pressure, which were totally abolished by Ro 31-8220. TMX had no effect at all when the tissue was depleted of Ca2+, whereas the response to DOPPA was only partially reduced.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasoconstriction in rat isolated mesentery and small intestine in response to various activators of protein kinase C. 774 Oct 37

1. We examined the effects of ethanol on the contractility of strips of porcine coronary artery, with and without endothelium, and following permeabilization with alpha-toxin, and of aortic valvular endothelial cells, in situ. Changes in cytosolic Ca2+ concentration ([Ca2+]i) of the coronary artery smooth muscle cells and of the valvular endothelial cells were monitored using front-surface fluorometry of the calcium indicator dye, fura-2. In permeabilized preparations, [Ca2+]i was clamped using 10 mM ethyleneglycol-bis-(beta-aminoethylether)-N,N,N',N'-tetra ace tic acid (EGTA) and 10 microM A23187 (a calcium ionophore). 2. The strips without endothelium were placed in normal physiological salt solution (normal PSS) in the presence of ethanol (100-1000 mM). There were dose-dependent increases in [Ca2+]i and a rapid sustained rise in tension. In Ca(2+)-free PSS, ethanol increased [Ca2+]i and tension, similar to, but much smaller than, findings with normal PSS. 3. For a given change in [Ca2+]i induced by ethanol, the developed tension was greater than that observed during contractions induced by high [K+]o. Thus, the [Ca2+]-tension curve for ethanol was shifted to the left of that for high [K+]o. The [Ca2+]-tension curve for the contraction induced by ethanol in the absence of extracellular Ca2+ was shifted further to the left from that obtained in the presence of [Ca2+]o. 4. The mechanisms involved in this Ca(2+)-sensitizing effect of ethanol were investigated using alpha-toxin-permeabilized coronary medial strips. Ethanol increased the tension development, in a concentration-dependent manner, at a fixed concentration of Ca2+ (pCa = 6.3) in the presence of guanosine-5'-triphosphate (GTP), an effect antagonized by guanosine-5'-O-(beta-thiodiphosphate) (GDP beta S), a non-hydrolysable GDP analogue. 5. With intact endothelium, the ethanol-induced tension development was markedly reduced, although inhibition in the increase in [Ca2+]i was slight. The [Ca2+]-tension relationship of this contraction overlapped with that obtained with high [K+]o-induced contraction and was shifted to the right from that obtained in the absence of the endothelium. This endothelium-dependent reduction of [Ca2+]i and tension induced by ethanol was inhibited when the strips were exposed to NG-monomethyl-L-arginine (L-NMMA). 6. Ethanol induced a gradual and sustained increase in [Ca2+]i in normal PSS, and a transient, concentration-dependent increase in [Ca2+]i in Ca(2+)-free PSS in porcine aortic valvular endothelial cells in situ.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of GTP-protein and endothelium in contraction induced by ethanol in pig coronary artery. 830 41

To explore possible mechanisms underlying hypoxia-induced pulmonary vasoconstriction, the effect of hypoxia on outward K+ current (Iout) was evaluated in primary cultured rat pulmonary (PA) and mesenteric (MA) arterial smooth muscle cells using the whole cell patch-clamp technique. When the cells were bathed in standard physiological salt solution and the patch pipettes contained Ca(2+)-free media with 10 mM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA), virtually all of the Iout, including both the rapidly inactivating component (Irt) and the steady-state (noninactivating) component (Iss), was mediated by voltage-gated K+ channels. Reduction of O2 tension in the bath solution from 155 Torr to < 74 Torr with sodium dithionite reversibly inhibited both Irt and Iss in PA myocytes, but not in MA myocytes. The hypoxia-sensitive Iss was activated at about -50 mV; thus, some of the channels responsible for this current may be open at the resting membrane potential (-40 +/- 1 mV) of PA cells used in this study. Hypoxia also significantly depolarized PA cells bathed in PSS (1.8 mM Ca2+) from -40.7 +/- 1.3 to -24.0 +/- 2.4 mV, and PA cells bathed in Ca(2+)-free PSS (0.1 mM EGTA) from -38.4 +/- 1.3 to -26.1 +/- 3.9 mV. The hypoxia-induced inhibition of Iout in PA cells was accompanied by an apparent increase in inward Ca2+ current.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypoxia reduces potassium currents in cultured rat pulmonary but not mesenteric arterial myocytes. 844 25

The influence of rubidium-substituted physiological salt solution (Rb-PSS) on the relaxant effects of K+ channel openers was investigated in the human saphenous vein. In tissues precontracted with 20 mM KCl (in K-PSS) levcromakalim and P1060 produced complete, sustained relaxations. However, in Rb-PSS (containing 20 mM RbCl) these effects were inhibited and, although complete relaxations still occurred, were transient. When caffeine was applied at the beginning of this fade of levcromakalim-induced relaxation in Rb-PSS its contractile effect was potentiated. Similarly, the contraction to noradrenaline was potentiated when applied at the beginning of this fade of levcromakalim-induced relaxation, whereas this response was attenuated in control tissues bathed in 20 mM KCl (in K-PSS). Our results show that the relaxant effects of K+ channel openers in human saphenous vein are inhibited in Rb-PSS, in agreement with previous studies in animal tissue, and suggest that an increased Ca2+ uptake into intracellular stores may be contributory to vasorelaxation.
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PMID:Differential vasorelaxant effects of levcromakalim and P1060 in the isolated KCl- and RbCl-precontracted human saphenous vein: possible involvement of intracellular Ca2+ stores. 860 48

1. The clinical success of calcium channel blockers in the management of organ ischaemia is less than theoretically anticipated. Blood gas/pH changes are associated with organ ischaemia; therefore, we studied the possibility that pH changes could alter the pharmacological effects of the calcium channel blocker nifedipine on rat tail artery contracted by either noradrenaline (NA) or potassium. 2. Segments (2-2.5 cm) of the proximal third of the male Sprague-Dawley rat tail ventral artery were initially bathed and perfused with a physiological salt solution (PSS; pH 7.48) for 25-30 min, after which time bathing/perfusion was continued with a nominally calcium-free PSS made acidotic (pH 7.20), alkalotic (pH 7.67) or unaltered (control). After equilibration, the perfusion pressure (PP) responses to increasing concentrations of calcium in the presence of NA (3.0 mumol/L) or potassium (100 mmol/L) with nifedipine or its vehicle were recorded. 3. The calcium sensitivity of potassium- or NA-stimulated rat tail arteries was reduced during acidosis, as was the maximum PP in potassium- but not NA-stimulated tissues. Alkalosis reduced the calcium sensitivity in potassium- but not NA-stimulated contraction and had no effect on maximum PP. 4. The inhibitory effect of nifedipine (0.6 mumol/L) on contraction was enhanced during acidosis in either NA- or potassium-stimulated arteries and also during alkalosis in NA-treated arteries, although it had little effect during normal conditions. 5. The results indicate that changes in pH alter the vascular contractility profile in a manner dependent on the excitation-contraction coupling mode. The calcium antagonistic effect of nifedipine is pH dependent and it is suggested that pH changes associated with ischaemic conditions may alter the therapeutic profile of nifedipine.
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PMID:Effects of acidosis or alkalosis on the actions of nifedipine on excitation-contraction coupling in the rat tail artery. 931 71

1. The main object of the present study was to determine whether ascorbate, an antioxidant which has been shown to protect nitric oxide (NO) from attack by scavenger molecules, might be released from nitrergically-innervated smooth muscle; ascorbate release from the rat anococcygeus was measured by use of h.p.l.c. with electrochemical detection. 2. Incubation of rat anococcygeus muscles in normal physiological salt solution (PSS; 30 min) resulted in release of ascorbate into the bathing medium (7.7 +/- 0.9 nmol g-1 tissue). This release was increased by 96% when muscles were incubated in high K+ (70 mM) PSS. The resting release of ascorbate was unaffected by tetrodotoxin (TTX; 1 microM), omega-conotoxin GVIA (10 nM) or omission of calcium ions from the PSS (with addition of 0.2 mM EGTA), but all three procedures attenuated the increased release observed under depolarizing conditions. Resting release of ascorbate was unaffected by glutamate (100 microM), aspartate (100 microM), gamma-aminobutyric acid (100 microM) or carbachol (50 microM). 3. A second h.p.l.c. peak, which always preceded the ascorbate peak, was identified as urate. Urate release from the anococcygeus, following 30 min incubation in normal PSS, was 64.6 +/- 12.7 nmol g-1 tissue but, unlike ascorbate, urate release was unchanged in high K+ PSS. In functional experiments, urate (100-400 microM) partially protected NO (15 microM)-induced relaxations of the rat anococcygeus from inhibition by 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO; 50 microM), but not from inhibition by hydroquinone or duroquinone (both 100 microM). 4. Muscles chemically sympathectomized with 6-hydroxydopamine (6-OHDA, 500 microM; 2 h) still exhibited release of ascorbate (2.5 +/- 0.4 nmol g-1 tissue) and urate (22.2 +/- 2.9 nmol g-1 tissue); in both cases the release was similar to that observed in time-matched control tissues not exposed to 6-OHDA. High K+ PSS produced a TTX-sensitive increase in release of ascorbate, but not urate, from 6-OHDA-treated muscles. 5. The results demonstrate that significant amounts of ascorbate and urate are released from the rat anococcygeus muscle. Ascorbate, but not urate, release appears to be enhanced by activation of nerves which are resistant to 6-OHDA pretreatment. Since both antioxidants can protect NO from attack by scavenger molecules, their release in nitrergically-innervated tissues may be important for the provision of the correct redox environment to allow NO to fulfill its proposed neurotransmitter role.
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PMID:Release of the antioxidants ascorbate and urate from a nitrergically-innervated smooth muscle. 942 23

The present study was undertaken to investigate the effects of extracellular pH (pHe) and intracellular pH (pHi) on 5-hydroxytryptamine (5-HT)-induced contraction and Ca2+ mobilization in vascular smooth muscles. Strip preparations of the rabbit basilar artery without endothelium were loaded with 40 microM fura-2-AM and 2 microM BCECF-AM and mounted in an organ bath. The isometric tension was recorded by using a force displacement transducer. Administration of 5-HT caused dose-dependent contraction in the rabbit basilar arteries. Acidification of pHe from 7.40 to 6.90 reduced the 5-HT-induced contraction and [Ca2+]i transients. Alkalinization of pHe from 7.40 to 7.90, on the other hand, enhanced the contraction and elevation of [Ca2+]i. In the other series of experiments, pHi (7.12 in normal PSS) was selectively altered by adding either butyric acid or trimethylamine. Intracellular acidification (pHi = 6.89) and alkalinization (pHi = 7.35) without changes in pHe produced qualitatively similar effects to those caused by extracellular acidification and alkalinization, respectively. Ca-sensitivity, which is defined as Deltatension/Delta[Ca2+]i, was not affected by the alteration of pHe nor pHi. In the Ca2+-free solution, the addition of 5-HT produced transient increases in [Ca2+]i and isometric tension that were much smaller than those in the normal physiological salt solution. The 5-HT-induced responses of [Ca2+]i and tension in the Ca2+-free solution were not affected by acidification nor alkalinization. These results suggest that a 5-HT-induced contraction is significantly modulated by pH through changing the [Ca2+]i transients, and that the change of pHi plays, at least in part, a role in the alteration of 5-HT-induced contraction resulting from acidosis or alkalosis in the rabbit basilar artery.
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PMID:Effects of pH on contraction and Ca2+ mobilization in vascular smooth muscles of the rabbit basilar artery. 1021 9

In rings of rabbit facial vein (RFV), depletion of sarcoplasmic reticulum (SR) Ca(2+) by caffeine abolished the subsequent isometric contraction to 25 mM K(+) physiological salt solution (25K-PSS). However, the associated steady-state increase of smooth muscle intracellular free Ca(2+) concentration ([Ca(2+)](i)), measured using fura PE3 and cuvette photometry, was not altered. Treatment with the specific SR Ca(2+) pump inhibitor cyclopiazonic acid (30 microM) after caffeine-induced SR Ca(2+) depletion restored and greatly augmented the 25K-PSS-induced contraction. This suggests that SR Ca(2+) depletion leads to a dissociation of K(+)-induced [Ca(2+)](i) increase from contraction that was dependent on Ca(2+) pump-mediated SR Ca(2+) uptake. Endothelium removal augmented the 25K-PSS-induced [Ca(2+)](i) increase after caffeine-induced SR Ca(2+) depletion. However, this was associated with only a small and transient contraction. Exposure of endothelium-denuded RFV to cyclopiazonic acid after caffeine-induced SR Ca(2+) depletion further amplified the 25K-PSS-induced [Ca(2+)](i) increase, which was associated with a large and sustained contraction. However, the latter [Ca(2+)](i) increase was still higher than in endothelium-intact RFV. This suggests that the endothelium dampens the [Ca(2+)](i) rise associated with K(+)-induced Ca(2+) influx, but independently of Ca(2+) pump-mediated SR Ca(2+) uptake.
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PMID:Sarcoplasmic reticulum and endothelium independently regulate venous smooth muscle [Ca(2+)](i) and contraction. 1044 2

Counterion polarization of sodium and magnesium polystyrenesulfonate (NaPSS and MgPSS), adsorbed in an excess onto ellipsoidal beta-ferric hydrous oxide particles (beta-FeOOH), is studied in both the absence and the presence of added simple electrolytes, NaCl and MgCl(2). The amplitude of the low-frequency (10(2)-10(4) Hz) and the high-frequency (10(4)-10(6) Hz) electro-optical effects of NaPSS is found to decrease with increasing NaCl concentration, while the critical frequency of relaxation of both effects remains unchanged. Addition of MgCl(2) to the suspension containing MgPSS also reduces the amplitude of the low-frequency electro-optical effect, but the amplitude of the high-frequency effect increases. The increased number of mobile (not bound) divalent ions, which produce larger charge fluctuation, could explain the high-frequency effect increase in the presence of a small excess of MgCl(2). Substitution of Na(+) counterions of PSS by Mg(2+) is found to increase the critical frequency of relaxation and to reduce the amplitude of the low-frequency effect, probably due to the strong repulsion between bound divalent counterions. The polyion length remains nearly unchanged during this substitution, as evidenced by the constant relaxation time of the polyelectrolyte-coated particles. The increase of counterion valence is not found to affect the amplitude of the high-frequency electro-optical effect in the absence of added salt. Copyright 1999 Academic Press.
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PMID:Electric Properties of Adsorbed Polystyrenesulfonate. 1055 Feb 48


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