Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endothelium-derived relaxing factor (EDRF), believed to be nitric oxide or a compound that releases nitric oxide, has been previously identified in the pulmonary and systemic vasculature of the newborn guinea pig using isolated arterial rings. The aim of our study was to determine if EDRF regulates vasomotor tone at the level of resistance vessels in the neonatal pulmonary circulation. Isolated lungs from guinea pigs (1-3 d old, n = 4-8/protocol) were ventilated with room air and perfused with a Krebs-Henseleit solution containing albumin at a constant flow. Angiotensin II (AII, 6 nM) was added to the perfusate to give a stable elevation in mean pulmonary artery pressure (PAP) from 7.0 +/- 1.1 to 19.7 +/- 1.5 torr, a 182 +/- 32% (mean +/- SEM) increase above baseline. Addition of bradykinin (BK, 10 nM) or L-arginine (2 mM) markedly reduced the AII-induced elevation in PAP. At the steady state response to BK (33% above baseline), addition of Hb (10 microM, binds EDRF), NG-monomethyl-L-arginine (NMA, 100 microM, blocks EDRF production), NMA (200 microM), or NMA + Hb, reversed the effect of BK to the following levels of PAP above baseline: 77 +/- 5, 94 +/- 24, 163 +/- 20, or 246 +/- 25%, respectively (p less than 0.05). Indomethacin had no effect on BK-induced vasodilation. In separate studies, NMA (200 microM) increased baseline PAP by 46 +/- 13% and NMA pretreatment raised the AII-pressor response (AII 6 nM) from 133 +/- 49 to 306 +/- 65% above baseline PAP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endothelium-derived relaxing factor: evidence that it regulates pulmonary vascular resistance in the isolated neonatal guinea pig lung. 186 8

Human adrenocortical tissue obtained, on eight occasions, at the time of nephrectomy for renal carcinoma (outside the adrenal pole) was treated by collagenase to dissociate the cells. These were hen submitted to a short, 2-h, incubation with the N-terminal fragment (16 K) of POMC, its derivative, gamma 3-MSH, beta-lipotropin and beta-endorphin, in parallel with ACTH 1-24 (Synacthen Ciba) and angiotensin II (AII, Hypertensin Ciba). Under the influence of ACTH (10(-10) M), and AII (10(-10) M), basal glucocorticoid output, including more than 80% cortisol, was increased by factors of 3 +/- 0.51 (SEM) and 1.35 +/- 0.12 (SEM), respectively. The corresponding aldosterone responses were 1.60 +/- 0.13 for ACTH and 1.38 +/- 0.09 for AII. With the exception of gamma 3-MSH, the POMC peptides under study had no steroidogenic effect. gamma 3-MSH (10(-9) M) and AII (10(-10) M) stimulated aldosterone production to approximately similar levels of, respectively, 1.23 +/- 0.05 and 1.38 +/- 0.09 times the basal production. In contrast to AII however, gamma 3-MSH showed no apparent effect on glucocorticoid output. Steroidogenic response to ACTH was potentiated by gamma 3-MSH at a concentration of 10(-10) M which, when used alone, proved ineffective. This potentiating effect was pronounced for the aldosterone response, whereas the glucocorticoid production was hardly affected. This action ceased to be visible when the cells reached maximal stimulation by ACTH. These findings suggest that gamma 3-MSH--a portion of the 16 K fragment--may have a possible role in aldosterone secretion.
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PMID:Compared effects of ACTH, angiotensin II and POMC peptides on isolated human adrenal cells. 300 85

Serum HDL cholesterol, apolipoproteins AI and AII and post heparin lipolytic activities (PHLA) have been measured in a group of fourteen hypothyroid women without ovarian oestrogen secretion before and during a 2-month thyroxine treatment. The more rapid and consistent observed event was a decrease in apo AI levels (164 +/- 5 vs. 149 +/- 5 mg dl-1, mean +/- SEM, P less than 0.05) correlated (r = 0.79, P less than 0.05) to a slight increment of PHLA. A slight decrease in apo AII concentration was seen only after 5 days (25 +/- 2 vs. 22 +/- 2 mg dl-1, P less than 0.05) and in HDL cholesterol only after 60 days (1.3 +/- 0.6 vs. 1.1 +/- 0.5 mmol 1-1, P less than 0.05). Apo AI, HDL2 and HDL3 cholesterol were measured in another group of seven hypothyroid postmenopausal women before and after a 2-month thyroxine treatment. We observed a decrease in HDL2 cholesterol (1.69 +/- 0.20 vs. 1.17 +/- 0.09 mmol 1-1, P less than 0.02) with no changes in HDL3 cholesterol (0.88 +/- 0.09 vs. 0.99 +/- 0.06 mmol 1-1, NS). The decrease in HDL2 cholesterol correlated (r = 0.72, P = 0.05) with that for apo AI. The differential influence of thyroxine (T4) administration on the major HDL components might reflect changes in HDL composition due to the multiple effects of thyroid hormones on lipid metabolism. It can be hypothesized that the decrease in apo AI and HDL2 cholesterol concentrations are due, at least in part, to the increase in hepatic lipase activity.
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PMID:Time-course of alterations of high density lipoproteins (HDL) during thyroxine administration to hypothyroid women. 311 68

The purpose of this study was to test the hypothesis that intracarotid infusion of angiotensin via a brachial arterial catheter results in a heightened pressor response in the alert spontaneously hypertensive rat (SHR) as previously observed for intracerebroventricular (ICV) injection of angiotensin. We infused angiotensin II and III since these ligands are equivalently potent with respect to peak pressor effect when delivered ICV. We measured somewhat greater pressor responsiveness to AII than to AIII in the Wistar-Kyoto (WKY) normotensive control strain from a baselevel of 133.1 +/- 5.8 (mean +/- SEM) to 151.3 +/- 6.2 mmHg (+13.7%) at the 100 pmol/kg/min dose of AII, and from 132.5 +/- 5.8 to 146.0 +/- 6.1 mmHg (+10.2%) for AIII. The SHR revealed a heightened pressor sensitivity to AII, from a baselevel of 170.0 +/- 3.8 to 200.6 +/- 5.9 mmHg (+18%) while the response to AIII was less dramatic, from 171.3 +/- 2.1 to 189.8 +/- 2.4 mmHg (+10.8%). These findings suggest that a similar heightened pressor responsiveness occurs to peripheral infusion of angiotensin II in the SHR as previously observed to ICV injection.
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PMID:Heightened blood pressure responsiveness to intracarotid infusion of angiotensins in the spontaneously hypertensive rat. 317 64

Patients with pulmonary dysfunction and CO2 retention have renal hemodynamic abnormalities accompanied by increased plasma renin activity. To determine if hypercapnia impairs renal function, particularly through the renin-angiotensin system, the effects of acute hypercapnic acidosis (HC), using 8.5% CO2, were measured in five unanesthetized dogs during (a) the intact state; (b) renin-angiotensin antagonism using either 1-sarcosine, 8-glycine angiotensin II ( [Sar1, Gly8] AII) or SQ 14,225; and (c) exogenous angiotensin II infusion. As partial arterial carbon dioxide pressure (PaCO2) increased (p less than 0.05) from control (C) of 35 +/- 1 (SEM) to 48 +/- 1 mm Hg during HC, arterial pH fell (p less than 0.05) from 7.36 +/- 0.01 to 7.24 +/- 0.005. Renal function was uncompromised with HC, and glomerular filtration rate (GFR) and urinary sodium excretion increased (p less than 0.05) despite a fourfold rise in plasma renin activity from C of 0.6 +/- 0.3 to 2.2 +/- 0.8 ng AI ml-1 h-1 during HC. Administration of [Sar1, Gly8] AII during HC did not consistently alter systemic or renal hemodynamic responses, and effects of SQ 14,225 during HC were also observed during normocapnia. Although systemic vascular responses to exogenous AII infusion were similar, the renal vasoconstrictor response was antagonized during HC with unchanged GFR and renal blood flow. These findings indicate that despite activation of the renin-angiotensin system, acute hypercapnic acidosis is unassociated with impairment of renal function in unanesthetized dogs. This may be related to diminished renal vascular AII responsiveness during hypercapnia.
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PMID:Renal and cardiovascular responses to acute hypercapnic acidosis in conscious dogs: role of renin--angiotensin. 618 44

The effects of an angiotensin-II analog (saralasin, i.v.) and of a converting enzyme inhibitor (captopril, oral) were compared in 12 sodium-depleted patients with hypertension. The decrease of the mean intraarterial pressure (MAP) with captopril (-21.5 +/- [SEM] 4.3 mm Hg) was more pronounced (P < 0.001) than the change of MAP during saralasin (-10.5 +/- 4.0 mm Hg). The pretreatment arterial plasma renin activity (log PRA) was closely related to the change of MAP during saralasin (r = -0.94; P < 0.001) and also to the captopril-induced change of MAP (r = -0.82; P < 0.001); similar results were obtained for the log plasma angiotensin (PA) I and II levels. The change of MAP was more pronounced, however, with captopril than during saralasin at any level of pretreatment PRA, PAI or PAII. Saralasin did not affect heart rate (P > 0.4), but during captopril the heart rate increased by 5.1 beats/min (P < 0.001). Captopril produced a 70% decrease of PAII, but the change of MAP was poorly related to the changes of PAII (r = -0.57; P < 0.05); PRA and PAI rose threefold to fourfold. PRA, PAI, and PAII all increased during saralasin. These observations may suggest that the antihypertensive action of captopril is not based solely on the inhibition of AII formation, but also the agonistic effect of saralasin has to be considered.
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PMID:Comparative study of an angiotensin-II analog and a converting enzyme inhibitor. 624 56

Local renin and angiotensin-converting enzyme (ACE) activity were recently implicated in development of intimal hyperplasia after vascular injury, but little is known about the local responses of angiotensin I/II (AI/AII) and local ACE activity in vein graft physiology. The activity of the local ACE system of experimental vein grafts was examined in this study. The right carotid artery was divided and bypassed in 21 New Zealand White rabbits, using the right external jugular vein. The left external jugular vein was used as a control. Veins and vein grafts were harvested after 14 days. Rings from both vessels were studied in vitro under isometric tension, and dose-response curves to AI and AII were obtained. AI responses were also measured in the presence of captopril. The tissue concentrations of ACE in both vessels were estimated by spectrophotometry and were localized by immunohistochemistry. The responses of the veins to AI and AII were multiphasic, whereas the responses of vein grafts were sigmoid-shaped. Incubation of vein grafts with captopril significantly decreased the sensitivity to AI (p < 0.0001). Immunohistochemical localization identified ACE in the endothelial layer of the veins and vein grafts, but also at a greater density in the intimal hyperplasia of the vein graft. The concentration of ACE was 1.92 +/- 0.16 U/g (wet weight; mean +/- SEM, n = 9) in vein grafts and 1.39 +/- 0.05 U/g in the veins (38% increase, p < 0.05, n = 9).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased concentrations of angiotensin-converting enzyme in the intimal hyperplasia of experimental vein grafts. 751 9

Capillary barrier function is subject to changes in Starling forces via hemodynamic status (hydrostatic pressure) or protein milieu of fluids bathing the wall (oncotic pressure). Venular function is sensitive to inflammatory mediators leading to white cell sticking, fluid and formed element extravasation, and flow disruption. Thus, we hypothesized that vasoactive hormones and autocrines alter preferentially the venular-capillary (VC) barrier. Hydraulic conductivity (Lp) of frog mesenteric venular- and true-capillaries (TC) was measured by the modified-Landis technique under control (LpC), then during atrial natriuretic peptide (ANP, 10(-7) to 10(-8) M), bradykinin (BKN, 10(-7) M), acetylcholine (ACh, 10(-6) to 10(-5) M), angiotensin II (AII, 10(-7) M), or norepinephrine (NE, 10(-6) M) perfusion. All agents, except AII or NE, elevated Lp: LpANP/LpC = 2.9 +/- 0.3 (mean +/- SEM; (n = 55), LpBKN/LpC = 3.3 +/- 0.8 (n = 16), LpACh/LpC = 1.6 +/- 0.1 (n = 26), LpAII/LpC = 1.1 +/- 0.2 (n = 8), and LpNE/LpC = 1.1 +/- 0.2 (n = 9). Contrary to our hypothesis, VC and TC responded similarly: 3.0 versus 2.9 for ANP, 3.4 versus 3.2 for BKN, and 1.6 versus 1.6 for ACh, respectively. These data are consistent with putative vasodilators lowering capillary barrier resistance independent from changes in Starling forces.
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PMID:Vasoactive hormones and autocrine activation of capillary exchange barrier function. 831 66

This study evaluated the bonding mechanism of Compoglass compomer to dentin in primary teeth. Buccal or labial dentinal surfaces of 20 human extracted, non carious primary teeth stored in 4 degrees C physiological saline solution were obtained by grinding on silicon carbide paper (final grit 600). The specimens were divided into two groups of 10 teeth each: (1) unetched dentin, Compoglass SCA, Compoglass; and (2) dentin etched with 10% phosphoric acid (Etch-AII), Compoglass SCA, Compoglass. The Compoglass SCA and Compoglass compomer were placed according to the instructions of the manufacturer, except Group 2 were the dentin was first etched with 10% phosphoric acid for 30 seconds. Twenty-four hours after placing the compomer over the treated dentinal surface, the specimens were dehydrated with a series of alcohol and freon. Then critically point dried. The specimens were split with a chisel and the compomer/dentin interface evaluation was performed with the SEM. The results showed that when the instructions of the manufacturer were followed (Group 1) the compomer showed a very close relation to the dentin with some tag structures penetrating the dentin. When phosphoric acid etching preceded the compomer placement a hybrid layer with tags penetrating the dentin was noted in most specimens.
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PMID:Bonding mechanism of Compoglass to dentin in primary teeth. 964 Oct 96

This study was to assess the role of different components of the extracellular matrix (ECM) on the mobilization of Cai++ induced by angiotensin II in vascular smooth muscle cells (VSMC) from hypertensive (SHR) and normotensive (WKY) rats. The effect of AII (10-6 M) on Cai++ release was studied in VSMC isolated from the aorta of 5-week-old WKY and SHR using fluorescent imaging microscopy (fura-2). Cai++ mobilization was characterized by amplitude, slope of Cai++ increase and total amount of Cai++. Cells were cultured on glass coverslips (control) or coated with either collagen I, collagen IV, vitronectin, fibronectin and extracellular matrix (ECM) and studied at confluence between passage 3 and 9. A significant increase of Cai++ released by AII has been observed with cells from WKY cultured on collagen I (meam +/- SEM, amplitude: 192 +/- 12% of control values, slope: 194 +/- 13%, total amount Cai++: 173 +/- 12%, n = 270, p < or = 0.0001 for each, unpaired t-test). Conversely, response with SHR was not significatively modified. Cai++ mobilization was not significatively modified after culture of VSMC from SHR and WKY on collagen IV. A significative decrease of the slope (WKY: 66 +/- 6%, p < or = 0.0001; SHR: 83 +/- 5%, p < or = 0.03) and of the amount of Cai++ (WKY: 74 +/- 7%, p < or = 0.01; SHR: 74 +/- 5%, p < or = 0.01) has been observed after culture of VSMC from the 2 strains on vitronectin. A decrease in amplitude (53 +/- 3%, p < or = 0.0001), slope (38 +/- 4%, p < or = 0.0001) and Cai++ release (69 +/- 5%, p < or = 0.004, n = 106) has been observed in VSMC from SHR seeded on fibronectin. Conversely, in VSMC from WKY, Cai++ mobilisation has not been modified compared with control cells. Culture of VSMC from SHR on ECM induced a significative decrease of amplitude (49 +/- 2%), slope (54 +/- 4%) and Cai++ release (53 +/- 3%, p < or = 0.0001 for each, n = 122), while in WKY, ECM induced a significative stimulation of these parameters (amplitude: 157 +/- 11%, slope: 149 +/- 13% and Cai++ release: 130 +/- 9%, p < or = 0.0001 for each, n = 247). These results show that the Cai++ mobilization induced by AII is modified by the adhesion of cells to different ECM components. This suggests a modulation of the A II-associated signalling events via the focal adhesion points. Furthermore, a difference in this modulation is observed between SHR and WKY when cells are seeded on collagen I, fibronectin or ECM. These modulations of Cai++ mobilization could play a role in the regulation of growth and differentiation of cells during the development of hypertension.
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PMID:[Cellular adhesion to elements of the extracellular matrix in the hypertensive rat modulates the effect of angiotensin II]. 1048 64


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