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)

In Ca(2+)-free solution containing endothelin-1 (ET-1), depolarization by high KCl increased the force of contraction without any changes in intracellular calcium concentration ([Ca2+]i) in canine coronary artery. The [Ca2+]i-force relationships were examined in the absence or presence of ET-1 in 5 or 90 mM KCl. The relation curve in the presence of ET-1 in 90 mM KCl-PSS was shifted to the left and upward compared with that in 5 mM KCl. These results suggest that KCl-depolarization potentiates the Ca2+ sensitization by ET-1.
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PMID:KCl-depolarization potentiates the Ca2+ sensitization by endothelin-1 in canine coronary artery. 128 78

1. The mechanism of endothelin-1 (ET)-induced contraction of rat aorta in Ca2(+)-free medium was investigated and compared with that of phenylephrine-induced contraction, measuring tension development and inositol 1,4,5-trisphosphate (IP3) formation. 2. After Ca2(+)-deprivation for 10 min, ET (10 nM) induced only a slow sustained contraction, whereas phenylephrine (10 microM) evoked a rapid phasic contraction followed by a small sustained one. Prolonged incubation of the strips in Ca2(+)-free medium (for 100 min) abolished the phasic contraction evoked by phenylephrine, but had no effect on the sustained contraction by either stimulant. 3. ET (100 nM) and phenylephrine (10 microM) stimulated inositol trisphosphate formation and these effects were inhibited by TPA (5 microM). 4. TPA (5 microM) had no effect on ET (10 nM)-induced contraction in Ca2(+)-free medium, but inhibited the contraction by phenylephrine (10 microM). 5. The ET- and phenylephrine-induced contractions in Ca2(+)-free PSS were inhibited by H-7, a protein kinase C inhibitor. 6. The difference and similarity of signal transduction pathways between alpha 1-adrenoceptor and ET receptor systems were discussed.
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PMID:Endothelin-1 induced contraction of rat aorta in Ca2(+)-free medium independent of phosphatidylinositol 4,5-bisphosphate (PIP2) breakdown. 227 89

In all 11 patients with progressive systemic sclerosis (PSS; Barnett type I, 2; type II, 5; type III, 4 cases; male 1; female 10 cases; 45.2 +/- 10.2 years-old), 6 cases of scleroderma spectrum disorders (SSD, male 1; female 5 cases; 51.2 +/- 13.2 years-old) and 7 healthy controls (HC, male 1; female 6 cases; 43.1 +/- 8.4 years-old) were entered to be examined. The plasma endothelin-1 (ET-1) levels of PSS, SSD and HC were 1.98 +/- 0.69, 1.76 +/- 0.39 and 1.15 +/- 0.38 pg/ml, respectively. After the stimulation with the low frequency electrical current, electrical acupuncture, for unilateral side of hand/arm (30 min), the plasma ET-1 levels decreased in 10 cases of PSS treated (1.61 +/- 0.45 pg/ml), but no change of plasma serotonin levels. In 4 of 6 cases of SSD, plasma ET-1 levels increased (2.06 +/- 0.39 pg/ml), however, nitrate levels increased and serotonin decreased in 3 of 5 cases of SSD. In 6 cases of HC treated with the electrical acupuncture, the plasma ET-1 levels increased (1.72 +/- 0.58 pg/ml). Thermographically, 9 of 11 cases of PSS and 5 of 6 cases of SSD showed temporally temperature-elevation of hand/fingers not only in treated sides, but also in non treated sides, although none of 7 HC showed temperature-elevation of hands/fingers. The decrease in plasma ET-1 levels due to the electrical acupuncture was thought to induce the vasodilatation and elevate the surface temperature in patients with PSS. These results will provide an excellent basis to study the efficacy of electrical acupunctural stimulation.
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PMID:The effect of electrical acupuncture-stimulation therapy using thermography and plasma endothelin (ET-1) levels in patients with progressive systemic sclerosis (PSS). 967 97

1 The walls of certain large blood vessels are nourished by the vasa vasorum, a network of microvessels that penetrate the adventitia and media of the vessel wall. The purpose of this study was to characterize endothelin-1 (ET-1)-mediated contraction of vasa and to investigate whether threshold concentrations of ET-1 alters the sensitivity to constrictors. Arterial vasa were dissected from the walls of porcine thoracic aorta and mounted in a tension myograph. 2 ET-1 and ETB-selective agonist, sarafotoxin 6c (S6c), produced concentration-dependent contraction. ETA receptor antagonist, BQ123 (10 microM), caused a biphasic rightward shift of ET-1 response curves. ETB receptor antagonist, BQ788 (1 microM), produced a rightward shift of response curves to ET-1 and S6c of 5- and 80 fold respectively. 3 ET-1 responses were abolished in Ca2+-free PSS but unaffected by selective depletion of intracellular Ca2+ stores. Nifedipine (10 microM), an L-type Ca2+ channel blocker, attenuated ET-1 responses by 44%. Inhibition of receptor-operated Ca2+ channels or non-selective cation entry using SKF 96365 (30 microM) and Ni2+ (1 mM) respectively, attenuated ET-1 contractions by 60%. 4 ET-1 (1-3 nM) enhanced responses to noradrenaline (NA) (4 fold) but not to thromboxane A2-mimetic, whilst K+ (10-20 mM) sensitized vasa to both types of constrictor. 5 Therefore, ET-1-induced contraction of isolated vasa is mediated by ETA and ETB receptors and involves Ca2+ influx through L-type and non-L-type Ca2+ channels. Furthermore elevation of basal tone of vasa vasorum alters the profile of contractile reactivity. These results suggest that ET-1 may be an important regulator of vasa vasorum reactivity.
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PMID:Endothelin alters the reactivity of vasa vasorum: mechanisms and implications for conduit vessel physiology and pathophysiology. 1057 36