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)

Endothelin-1 (ET-1) is a potent vasoactive peptide that has been reported to cause lung edema. This study tested if the edemagenic effect of ET-1 is due to preferential venoconstriction and, if so, whether the site of resistance is similar with salt solution (PSS) and more physiologic blood perfusate. ET-1 caused concentration-dependent contraction of pulmonary arterial and venous rings, with an EC50 of 1.3 nM in artery and 0.6 nM in vein (p less than 0.05). In PSS-perfused lungs, 5 nM ET-1 caused a 7.0 +/- 0.8 torr pressor response that was associated with a 5.0 +/- 0.3 torr increase in microvascular pressure and a 530 +/- 20 mg increase in lung weight within 10 min. In contrast, KCl-treated lungs had an equivalent pressor response (7.4 +/- 1.1 torr), yet the microvascular pressure increased by only 2.5 +/- 0.4 torr (p less than 0.05 from ET-1) and the lung weight was unchanged. Meclofenamate did not prevent the effect of ET-1 on microvascular pressure or lung weight. In blood-perfused lungs, ET-1 caused a 7.3 +/- 0.1 torr pressor response but only a 2.0 +/- 0.5 torr increase in microvascular pressure and no increase in lung weight. ET-1 had no effect on permeability either of cultured endothelial cell monolayers or in the pulmonary microvasculature in vivo. We conclude that the edemagenic effect of ET-1 in PSS-perfused lungs is mediated through venoconstriction and an increase in microvascular pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endothelin-1 increases the pulmonary microvascular pressure and causes pulmonary edema in salt solution but not blood-perfused rat lungs. 128 Jul 24

1. Using fluorometry of fura-2 and rabbit aortic strips, we studied the effects of glibenclamide (GLB), a sulphonylurea anti-diabetic drug and an inhibitor of opening of K+ channels, on cytosolic calcium concentrations ([Ca2+]i) and on force development. 2. Both high K(+)-depolarization and noradrenaline (NA) increased [Ca2+]i and force, in a concentration-dependent manner, in the presence of extracellular Ca2+ (1.25 mM). However, force development in relation to [Ca2+]i ([Ca2+]i-force relationship) observed with NA was much greater than that observed with K(+)-depolarization. 3. Pretreatment with GLB (10(-6)-10(-4) M) for 10 min partially inhibited, in a concentration-dependent manner, both [Ca2+]i elevation and the force development induced by 118 mM K(+)-depolarization or NA 10(-5) M in the presence of extracellular Ca2+. The [Ca2+]i-force relationship induced by both 118 mM K+ physiological salt solutions and by NA 10(-5) M in the GLB-treated strips overlapped that obtained in the non-treated strips, thereby suggesting that GLB has no effect on the Ca2(+)-sensitivity of the intracellular contractile apparatus. Only high concentrations (10(-4) M) of GLB decreased [Ca2+]i and the force, when applied after the force induced by 118 mM K+ PSS or NA 10(-5) M reached the maximum level. 4. In the absence of extracellular Ca2+, NA induced a transient increase in [Ca2+]i and in the force and these increases were inhibited when the vascular strips were pretreated with GLB for 10 min. The [Ca2+]i-force relationship obtained in the GLB-treated strips overlapped that in the non-treated ones. 5. An ATP-sensitive K+ channel opener, cromakalim (10-5M) reduced the increased [Ca2 + ]i and force induced by 25mm K+-depolarization and NA 10-SM. Subsequent application of GLB concentrationdependently reversed this relaxant effect of cromakalim on the NA-induced contraction (IC50 = 2x 10 7 M). Complete reversal of the effect was observed with 10IsM GLB. 6. We suggest that GLB inhibits both high K+-depolarization- and NA-induced contraction of the rabbit aorta, by decreasing [Ca2+]i and with no effect on the [Ca2+]i-force relationship. However, when NA-induced contractions were inhibited by a K+-channel opener, GLB reversed this inhibitory effect by inhibiting K+-channel opening and increasing [Ca2 +].
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PMID:Effects of glibenclamide on cytosolic calcium concentrations and on contraction of the rabbit aorta. 190 92

The effects of Ryanodine (RY) and Caffeine (CF) on the norepinephrine (NE)-induced contraction were studied in tail artery rings from spontaneously hypertensive rats (SHR) and normotensive, Wistar Kyoto rats (WKY). The NE-sensitive intracellular store of calcium was completely depleted by NE (1 microM) in calcium-free physiological salt solution (Ca = 0-PSS), and accounted for approximately 40% of the total response to NE in regular PSS (Ca = 1.6 mM). However, only 60% of the NE-releasable store was utilized for the full contraction in PSS. Re-exposure to PSS completely replenished the NE-releasable store in 10 minutes. Over twice as much calcium appeared to be taken up by the SHR as by the WKY arteries in these conditions. RY prevented the refilling of the NE-sensitive calcium store in both SHR and WKY, without releasing calcium from the store and without affecting the influx of calcium through membrane pathways. CF also prevented the refilling of the NE-sensitive calcium store, but did release calcium from it. It can be concluded that: 1) Whereas the main action of RY on rat tail artery seems to be the inhibition of calcium uptake by the sarcoplasmic reticulum (SR), CF has several actions: a) inhibition of calcium uptake by the SR, b) release of calcium from the SR, and c) opening of calcium channels in the plasma membrane of the smooth muscle cell. 2) In SHR, but not in WKY, the loss of calcium from the membrane in Ca = 0-PSS renders it more permeable to calcium, permitting an enhanced calcium uptake during subsequent exposure to PSS.
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PMID:[Norepinephrine-sensitive calcium pools in tail arteries of normotensive and spontaneously hypertensive rats: effects of ryanodine and caffeine]. 209 67

The mechanisms that control intracellular pH (pHi) in vascular smooth muscle are not fully understood. These studies were performed to determine the identity and relative importance of the sarcolemmal transport systems that mediate net acid efflux in primary cultured vascular smooth muscle cells from canine femoral artery. In HEPES- or HCO3(-)-buffered physiological salt solution (HEPES-PSS, HCO3(-)-PSS), recovery from an acute acid load was totally dependent on external Na+. 5-[N-ethyl-N-isopropyl]amiloride (EIPA, 50 microM) inhibited pHi recovery 100 and 68% in HEPES-PSS and HCO3(-)-PSS, respectively. EIPA-insensitive pHi recovery in HCO3(-)-PSS was inhibited 48% by 4,4'-diisothyocyanostilbene-2,2'-disulfonic acid (DIDS). An outwardly directed H+ gradient stimulated amiloride-sensitive 22Na+ uptake, and an inwardly directed HCO3- gradient stimulated amiloride-insensitive 22Na+ uptake. The latter was inhibited by DIDS or prior depletion of cell Cl-. In HEPES-PSS, resting pHi was 7.17 +/- 0.03, was not affected by DIDS, but was lowered by EIPA or by removing extracellular Na+. In HCO3(-)-PSS, resting pHi was 7.25 +/- 0.02 (P less than 0.05) and was not affected by EIPA. Removing extracellular Na+ in the presence of EIPA decreased pHi in HCO3(-)-PSS but not in HEPES-PSS. DIDS lowered resting pHi in HCO3(-)-PSS, after which EIPA further lowered pHi. We conclude that acid efflux from these cells is mediated by a Na(+)-H+ exchanger and a Na(+)-dependent Cl(-)-HCO3- exchanger. In HEPES-PSS, acid efflux via the Na(+)-H+ exchanger maintains resting pHi. In HCO3(-)-PSS, additional acid efflux via the Na(+)-dependent Cl(-)-HCO3- exchanger results in a higher pHi. Although the Na(+)-H+ exchanger is primarily responsible for acid efflux after an acute acid load, the Na(+)-dependent Cl(-)-HCO3- exchanger is responsible for acid efflux under physiological conditions.
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PMID:Na(+)-H+ and Na(+)-dependent Cl(-)-HCO3- exchange control pHi in vascular smooth muscle. 216 79

The ability of the Na-Ca exchanger to modify vascular relaxation was studied in rings isolated from tail arteries of stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY). The arteries were contracted with norepinephrine (NE) 1 microM and after stabilization they were transferred to a Ca-free physiological salt solution still in presence of NE. The time to 50% relaxation (T-50) in these conditions was significantly greater in SHRSP (78 +/- 7 s) than in WKY (50 +/- 7 s). When the calcium pump was stopped with vanadate (VAN), the Ca uptake by the sarcoplasmic reticulum with ryanodine (RY) and the Na-Ca exchanger with a Na-free PSS, the relaxation was slowed (T-50 increased to 198 +/- 16 s in SHRSP and to 162 +/- 14 s in WKY). Releasing the Na-Ca exchanger only (i.e. still with VAN and RY but with normal Na in the bath) the T-50 for relaxation in Ca-free PSS was, in WKY, nearly as fast as in control conditions (54 +/- 8 s). However, the Na-Ca exchanger in SHRSP was not so effective, and the T-50 for relaxation was slower than in control conditions (122 +/- 10 s). We conclude that the activity of the Na-Ca exchanger is depressed in tail arteries of SHRSP. This abnormality in resistance vessels, would contribute to the enhanced vascular tone present in hypertension.
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PMID:Decreased activity of the sodium-calcium exchanger in tail artery of stroke-prone spontaneously hypertensive rats. 224 41

The susceptibility of lung tissue to ischemia-reperfusion injury has made distant procurement of heart-lung allografts difficult. The effects of hypothermia, ventilation without perfusion, and various reperfusion solutions (PSS/Ficoll or whole blood) on the development of ischemia-reperfusion lung injury were investigated. Use of an ex vivo rat lung model in which the above variables were individually varied permitted a direct approach for these studies. Normothermic ischemia for 1 hour caused significant damage, documented by increased iodine 125 bovine serum albumin (125I-BSA) in alveolar lavage fluid and lung parenchyma compared with nonischemic controls. Hypothermic (4 degrees C) ischemia for 4 hours in lungs reperfused with salt solution and for as many as 12 hours in lungs reperfused with whole blood caused no significant increase in 125I-BSA in alveolar lavage fluid and lung parenchyma compared with nonischemic controls. Lungs ventilated without perfusion showed no increase in 125I-BSA leakage compared with controls. The ex vivo rat lung model is excellent for studying ischemia-reperfusion injury. It is reproducible, allows for variance of reperfusion solutions, and permits change in temperature and ventilation easily.
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PMID:Hypothermia or continuous ventilation decreases ischemia-reperfusion injury in an ex vivo rat lung model. 265 79

The effects of a synthetic atrial peptide (atriopeptin II; AP II) on the agonist-induced intracellular Ca2+ release was examined in the isolated rabbit aorta. The agonist-induced phasic contraction in a Ca2+-free physiological salt solution containing 2 mM ethyleneglycol-bis(beta-aminoethyl-ether)-N,N'-tetraacetic acid (EGTA-PSS) was used as an indicator of the intracellular Ca2+ release. The addition of AP II (10(-9)-10(-7) M) for 15 min to the tissue during the EGTA-PSS exposure caused a dose-dependent inhibition of norepinephrine (NE; 10(-6) M)-induced phasic contraction. The half-maximal inhibiting concentration of AP II was 3 X 10(-9) M, with 10(-7) M AP II causing 91% inhibition. This was confirmed by studying the inhibitory effect of AP II (10(-7) M) on NE-stimulated 45Ca efflux. Furthermore, the internal Ca2+ release by histamine (10(-5) M) and caffeine (25 mM), both of which share this internal Ca2+ pool with NE, was also inhibited by AP II. Thus AP II appears to be a potent inhibitor of the intracellular Ca2+ release that is utilized by various agonists for the activation of vascular smooth muscle. This may be an important mechanism by which AP II produces relaxation of blood vessels.
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PMID:Synthetic atrial peptide inhibits intracellular calcium release in smooth muscle. 293 90

The vasodilation responses to increased blood flow and acetylcholine require endothelial cells. We noticed that dogs with low hematocrit had reduced endothelial cell dependent responses; infusion of whole blood often restored the responses. Therefore, experiments were designed to test the hypothesis that hemodilution attenuates endothelial cell-dependent dilation. An extracorporeal shunt was created from the femoral artery to the jugular vein in pentobarbital-anesthetized dogs. Femoral artery diameter was measured by sonomicrometry. Blood flow was controlled by a screw clamp placed distally on the shunt tubing, and flow was increased from control (10% maximum) to maximum by opening the clamp for 3 mins. Hemodilution was achieved by withdrawal of whole blood and infusion of either 1) saline, 2) physiologic salt solution (PSS, containing 2.7 mM CaCl2), 3) saline with CaCl2 (2.7 mM), or 4) PSS without CaCl2. Endothelial cell-dependent dilations were evaluated after a 50% decrease in hematocrit. Hemodilution with either PSS or saline with CaCl2 did not decrease dilation responses to increased flow or acetylcholine. However, hemodilution with saline or PSS without CaCl2 markedly attenuated endothelium-dependent dilations. Ionized plasma calcium concentration decreased with saline and PSS without CaCl2 hemodilution, but it was maintained with PSS and saline with CaCl2 hemodilution. These data suggest that a 50% decrease in hematocrit does not influence endothelium-dependent dilation if plasma calcium is maintained. Our data support in vitro results that suggest that extracellular calcium is necessary for the release of endothelium-derived relaxing factor. Furthermore, relatively small changes in ionized calcium, within the physiologic range, have large effects on endothelial cell-mediated dilator responses to flow and acetylcholine. However, relatively large changes in hematocrit have no effect on the endothelium-dependent responses.
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PMID:Effect of hemodilution on endothelium-dependent vasodilation in the in vivo canine femoral artery. 367 33

We examined the diameter responses of isolated and pressurized posterior cerebral artery branches to various static and dynamic pressure alterations. These vessels, dissected from an anatomically identifiable location in the rat brain, developed tone when placed in a normal calcium physiological salt solution (1.6 mM Ca-PSS). Following a series of transmural pressure steps (delta p) of 25 or 50 mm Hg completed in 1-2 s and made every 5 min, they attained additional tone resulting in a mean luminal diameter of 139 micron at 100 mm Hg which was 35% less than their relaxed size measured in 1 mM EGTA-PSS. Continuous measurements of wall thickness and lumen diameter were obtained using a video electronic system in 1-2 mm long arterial segments, and autoregulatory gain factors calculated. Myogenic responses were obtained from each of 6 vessels taken from 6 WKY rats. Diameters following the step pressure changes were usually stable within 2-4 min. The data defined a myogenic regulatory pressure range from 49-145 mm Hg. Gain values averaged about 17% of that necessary for these arteries to maintain perfect flow autoregulation. Our results for myogenicity are comparable with the pressure range for blood flow autoregulation reported by others for the rat. We conclude that myogenic mechanisms, at least in this size artery, are partly responsible for flow autoregulation, and that they are supplemented by metabolic mechanisms operative in the intact rat brain.
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PMID:Influence of transmural pressure of myogenic responses of isolated cerebral arteries of the rat. 403 58

Vascular smooth muscle cells of the rat tail artery were enriched with Na by overnight incubation at 10 degrees C in K-free physiological salt solution (K-free PSS). The cells were then returned to normal PSS in a series of steps so as to define the effect of varying temperature between 3 and 37 degrees C, the effect of ouabain, the effect of readmitting K+ in the continuing presence of ouabain, and, finally, the effect of removing ouabain in the continuing presence of K+. The effects were measured with flow-through Na+ and K+ glass-cannula electrodes as changes in a superfusate moving slowly past the artery. Where possible, confirmatory evidence was obtained by conventional incubations followed by chemical analysis of the tissues. About 10 mmol Na+/kg dry wt is transferred out of the cells when temperature is raised from 3 to 37 degrees C. Exposure of the tissue to ouabain while the tissue is still in the K-free state produces a further loss of about 8 mmol Na+/kg dry wt and 4 mmol k+/kg dry wt. Readmittance of K+ in the continuing presence of ouabain induces a further loss of about 25 mmol Na+/kg dry wt in exchange for an uptake of about 13 mmol K+ measured electrometrically or about 20 mmol K measured chemically. Finally, the removal of ouabain is followed by an extrusion of about 155 mmol Na+/kg dry wt in exchange for an uptake of 133 mmol K%. The ouabain-insensitive exchange of Na+ and K+ is enhanced in spontaneously hypertensive rats as compared with normotensive rats.
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PMID:Ion-selective electrode studies of cell Na components in vascular smooth muscle of WKY and SHR. 708 45


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