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Angiotensin II decreases neuronal delayed rectifier potassium current: Role of calcium/calmodulin-dependent protein kinase II

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JOURNAL OF NEUROPHYSIOLOGY 1999年第3期82卷 1560-1568页

作者： Zhu, MY Gelband, CH Posner, P Sumners, C Univ Florida Coll Med Dept Physiol Gainesville FL 32610 USA Univ Florida Inst Brain Gainesville FL 32610 USA

Angiotensin II(Ang II) acts at specific receptors located on neurons in the hypothalamus and brain stem to elicit alterations in blood pressure, fluid intake, and hormone secretion. These actions of Ang II. are mediated via Ang II type 1 (AT(1)) receptors and involve modulation of membrane ionic currents and neuronal activity. In previous studies we utilized neurons cultured from the hypothalamus and brain stem of newborn rats to investigate the AT(1) receptor-mediated effects of Ang II on neuronal K+ currents. Our data indicate that Ang II decreases neuronal delayed rectifier (Kv) current, and that this effect is partially due to activation of protein kinase C (PKC),specifically PKC alpha. However, the data also indicated that another Ca2+-dependent mechanism was also involved in addition to PKC. Because Ca2+/calmodulin-dependent protein kinase II (CaM KII) is a known modulator of K+ currents in neurons, we investigated the role of this enzyme in the AT(1) receptor-mediated reduction of neuronal Ky current by Ang II. The reduction of neuronal Ky current by Ang II was attenuated by selective inhibition of either calmodulin or CaM KII and was mimicked by intracellular application of activated (autothiophosphorylated) CaM KII alpha. Concurrent inhibition of CaM KII and PKC completely abolished the reduction of neuronal Ky by Ang II. Consistent with these findings is the demonstration that Ang II increases CaM KII activity in neuronal cultures, as evidenced by increased levels of autophosphorylated CaM KII alpha subunit. Last, single-cell reverse transcriptase (RT)-PCR analysis revealed the presence of AT(1) receptor-, CaM KII alpha-, and PKC alpha subunit mRNAs in neurons that responded to Ang II with a decrease in Ky current. The present data indicate that the AT(1) receptor-mediated reduction of neuronal Ky current by Ang II involves a Ca2+/calmodulin/CaM KII pathway, in addition to the previously documented involvement of PKC.

关键词：血管紧张素ⅱ/药理学血管紧张素Ⅱ/生理学钙-钙调素依赖性蛋白激酶2型钙-钙调素依赖性蛋白激酶类/拮抗剂和抑制剂钙-钙调素依赖性蛋白激酶类/生理学钙调蛋白/拮抗剂和抑制剂延迟整流钾通道导电性酶激活/生理学神经元/代谢钾通道阻滞剂钾通道/药物作用钾通道/生理学钾通道电压门控蛋白激酶C/拮抗剂和抑制剂蛋白激酶C/代谢大鼠 Sprague-Dawley 受体血管紧张素 1型受体血管紧张素 2型受体血管紧张素/生理学动物大鼠

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EFFECTS OF ANGIOTENSIN-II AND NORADRENALINE ON INTRARENAL HEMODYNAMICS IN RAT

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EUROPEAN JOURNAL OF CLINICAL INVESTIGATION 1976年第6期6卷 457-464页

作者： RENTSCH, HP AYER, G VALLOTON, M ZIEGLER, W TRUNIGER, B KANTONSSPITAL MED KLIN CH-6000 LUCERNE SWITZERLAND

The hemodynamic effects of angiotensin II [A-II] and noradrenaline [norepinephrine] were studied in the rat kidney. These pressors were given by i.v. infusion in stepwise increasing doses. Intrarenal hemodynamics were analyzed by the 133Xe washout technique, 85Kr autoradiography and silastic casting of the renal vascular tree. A-II induced significant changes in intrarenal hemodynamics before any changes in systemic blood pressure were detected. The decrease in mean renal blood flow (2.91 ml/min per g in controls, 1.76 ml/min per g in rats given 50 .mu.g of A-II/kg per h) reflected a reduction in component I blood flow rate (from 3.9-2.9 ml/min-1 per g-1) and a decrease in the fraction of total renal blood flow supplied to component I of the washout curve (from 84-62%). With noradrenaline an increase in total renal resistance occurred simultaneously with the elevation of mean arterial blood pressure. The resulting reduction in mean renal blood flow (from 2.76 ml/min per g in controls to 1.55 ml/min per g in rats given 1000 .mu.g of noradrenaline kg/h) reflected a decrease in component I blood flow rate with lower infusion rates and a drop in component I flow fraction (from 82-52%) with higher doses. In contrast to canine kidneys, no evidence for a patchy cortical vasoconstriction was found in the rat. Using autoradiography it was possible to attribute component I to the renal cortex and subcortical area of the kidney.

关键词：血管紧张素ⅱ/药理学血压/药物作用剂量效应关系药物肾/生理学肾皮质/生理学去甲肾上腺素/药理学局部血流/药物作用种特异性血管阻力/药物作用动物狗人类男(雄)性大鼠

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The relationship between activation of phosphoinositide-specific phospholipase C and growth stimulation by Ca²⁺-mobilizing hormones in hepatocytes

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PHARMACOLOGY & TOXICOLOGY 1999年第5期84卷 234-240页

作者： Sandnes, D Dajani, O Bjorneby, A Christoffersen, T Univ Oslo Dept Pharmacol Fac Med N-0316 Oslo Norway

Previous studies have shown that while vasopressin and angiotensin II are markedly more effective than norepinephrine and prostaglandin F-2 alpha in eliciting an acute elevation of inositol 1,4,5-trisphosphate (IP3), norepinephrine and prostaglandin F-2 alpha produce larger enhancement of DNA synthesis. This suggests that the initial activation of phosphoinositide-specific phospholipase C is not a common factor for the growth response to these agonists, but does not exclude a role of the integral of phospholipase C activity over a prolonged part of the prereplicative period, during which agonist-specific changes in responsiveness might occur. We show that vasopressin and angiotensin II also cause a prolonged elevation of cellular Ig levels, which remain elevated for at least 60 min., while norepinephrine and prostaglandin F-2a elevate IP3 levers slightly and transiently For vasopressin the dose-effect curves for IP3 accumulation and stimulation of DNA synthesis were closely parallel, while this was not the case for angiotensin II, norepinephrine, or prostaglandin F-2 alpha After cultivation of the hepatocytes, hormone-stimulated IP3 accumulation rapidly declined, particularly in response to norepinephrine and prostaglandin F-2 alpha. When the IP3 response to norepinephrine and prostaglandin F-2 alpha was completely down-regulated, these agonists still enhanced the DNA synthesis. These results suggest that other mechanisms in addition to IP3 accumulation and Ca2+ release are likely to be involved in the growth stimulatory effects of the Ca2+-mobilizing: agonists studied here, ia particular For angiotensin II, norepinephrine, and prostaglandin F-2a.

关键词：血管紧张素ⅱ/药理学钙信号/药物作用细胞分裂/药物作用细胞培养的 DNA/生物合成 DNA/药物作用地诺前列素/药理学减量调节酶激活肌醇1 4 5-三磷酸/代谢肝/细胞学肝/药物作用肝/代谢去甲肾上腺素/药理学磷脂酰肌醇类/代谢大鼠 Wistar 时间因素血管升压素类/药理学动物男(雄)性大鼠

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COMPARISON OF PULMONARY VASCULAR-RESPONSE TO PROSTAGLANDIN-A1, PROSTAGLANDIN-F2ALPHA AND ANGIOTENSINII - METABOLISM OF PGA1 IN LUNG

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LIFE SCIENCES 1976年第11期19卷 1653-1661页

作者： GROSS, KB GILLIS, CN YALE UNIV SCH MEDDEPT ANESTHESIOLNEW HAVENCT 06510 YALE UNIV SCH MEDDEPT PHARMACOLNEW HAVENCT 06510

A rabbit lung preparation, perfused in vitro , was used to examine pulmonary metabolism of prostaglandin A1 (PGA1 ) and to compare the vasoconstrictor actions of PGA1 , prostaglandin F2α (PGF2α ) and angiotensin II. PGF2α caused significantly more, and angiotensin II significantly less, vasoconstriction than did an equimolar concentration of PGA1 . Of three likely PGA1 metabolites only 15-keto-PGA1 had any significant vasoconstrictor action. Furosemide and aminophylline (10−3 M) reduced PGA1 , PGF2α or angiotensin II-induced vasoconstruction. Diphloretin phosphate potentiated the vascular effect of angiotensin II. Furosemide (10−3 M) and DPP (9.5 × 10−6 M) significantly reduced pulmonary metabolism of PGA1 while aminophylline (10−3 M) had no effect on this process. Perfusion of the lungs with a hypoxic medium had no effect on PGA1 metabolism.

关键词：氨茶碱/药理学血管紧张素ⅱ/药理学缺氧/代谢呋塞米/药理学肺/代谢多根皮素磷酸盐/药理学前列腺素拮抗药/药理学前列腺素A类/代谢前列腺素A类/药理学前列腺素E类/药理学肺循环/药物作用温度血管舒缩系统/药物作用动物兔

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Role for early growth response-1 protein in α₁-adrenergic stimulation of fibroblast growth factor-2 promoter activity in cardiac myocytes

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MOLECULAR PHARMACOLOGY 2000年第5期57卷 984-990页

作者： Jin, Y Sheikh, F Detillieux, KA Cattini, PA Univ Manitoba Dept Physiol Winnipeg MB R3E 3J7 Canada Univ Manitoba Dept Pharmacol & Therapeut Winnipeg MB R3E 3J7 Canada

Fibroblast growth factor-2 (FGF-2), a mitogenic, angiogenic, and cardioprotective agent, is released from the postnatal heart by a mechanism of transient remodelling of the sarcolemma during contraction. Both release of FGF-2 and its synthesis can be increased with adrenergic stimulation. We reported previously that FGF-2 synthesis can be regulated at the transcriptional level by alpha-adrenergic stimulation of cultured neonatal rat cardiac myocytes as well as in the adult mouse heart. Examination of the proximal promoter region of both human and rat FGF-2 gene sequences revealed binding sites for the early growth response-1 (Egr-1) protein. Using gel mobility shift assays, we observed a transient increase in a complex between nuclear extracts from neonatal rat cardiac myocytes treated with inducers of Egr-1, including the alpha-adrenergic agonist phenylephrine, angiotensin II, and phorbol ester, and a consensus Egr-1 DNA element. A similar complex was seen with the FGF-2 promoter region -7/+42 as the DNA probe, but not when the Egr-1 element at nucleotides +3/+31 was disrupted. Participation of Egr-1 protein in the complex was confirmed by competition with Egr-1 DNA elements and antibodies. With deletion analysis and transfection of neonatal rat cardiac myocytes, the alpha-adrenergic response was localized to nucleotides -110/+42 of the FGF-2 gene in the context of a hybrid FGF-2/luciferase reporter gene, -***. Overexpression of Egr-1 increased -*** gene expression, whereas mutation of its Egr-1 element at nucleotides +3/+31 abolished alpha-adrenergic responsiveness. These data indicate that Egr-1 is involved in the alpha-adrenergic stimulation of the FGF-2 promoter region in neonatal cardiac myocytes.

关键词：血管紧张素ⅱ/药理学细胞培养的 DNA/代谢 DNA结合蛋白质类/生物合成 DNA结合蛋白质类/代谢 DNA结合蛋白质类/生理学早期生长反应蛋白质1 成纤维细胞生长因子2/遗传学成纤维细胞生长因子2/代谢基因表达调控心脏/药物作用心脏/生理学即早蛋白质类心肌/代谢核蛋白质类/代谢苯福林/药理学启动区(遗传学) 受体肾上腺素能α1/生理学十四酰佛波乙酯/药理学转录因子/生物合成转录因子/代谢转录因子/生理学转染动物人类小鼠大鼠

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Angiotensin II (AT₁) receptor blockade reduces vascular tissue factor in angiotensin II-induced cardiac vasculopathy

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AMERICAN JOURNAL OF PATHOLOGY 2000年第1期157卷 111-122页

作者： Müller, DN Mervaala, EMA Dechend, R Fiebeler, A Park, JK Schmidt, F Theuer, J Breu, V Mackman, N Luther, T Schneider, W Gulba, D Ganten, D Haller, H Luft, FC Humboldt Univ Fac Med Charite Franz Volhard Clin D-13125 Berlin Germany Univ Helsinki Inst Biomed Helsinki Finland Max Delbruck Ctr Mol Med Berlin Germany Hannover Med Sch D-3000 Hannover Germany F Hoffmann La Roche Basel Switzerland Tech Univ Dresden Inst Pathol D-8027 Dresden Germany Scripps Res Inst Dept Immunol La Jolla CA 92037 USA

Tissue factor (TF), a main initiator of clotting, is upregulated in vasculopathy, We tested the hypothesis that chronic in vivo angiotensin (ANG) II receptor AT, receptor blockade inhibits TF expression in a model of ANG II-induced cardiac vasculopathy. Furthermore, we explored the mechanisms by examining transcription factor activation and analyzing the TF promoter. Untreated transgenic rats overexpressing the human renin and angiotensinogen genes (dTGR) feature hypertension and severe left ventricular hypertrophy with focal areas of necrosis, and die at age 7 weeks. Plasma and cardiac ANG IT was three- to fivefold increased compared to Sprague-Dawley rats. Chronic treatment with valsartan normalized blood pressure and coronary resistance completely, and ameliorated cardiac hypertrophpy (p < 0.001). Valsartan prevented monocyte/macrophage infiltration, nuclear factor-KB (NF-kappa B) and activator protein-1 CAP-I) activation, and c-fos expression in dTGR hearts. NF-kappa B subunit p65 and TF expression was Increased in the endothelium and media of cardiac vessels and markedly reduced by valsartan treatment. To analyze the mechanism of TF transcription, we then transfected human coronary artery smooth muscle cells and Chinese hamster ovary cells overexpressing the AT, receptor with plasmids containing the human TF promoter and the luciferase reporter gene. ANG II induced the full-length TF promoter in both transfected cell Lines. TF transcription was abolished by AT, receptor blockade. Deletion of both AP-1 and NF-kappa B sites reduced ANG II-induced TF gene transcription completely, whereas the deletion of AP-1 sites reduced transcription. Thus, the present study clearly shows atl aberrant TF expression in the endothelium and media in rats with ANG II-induced vasculopathy. The beneficial effects of BT, receptor blockade in this model are mediated via the inhibition of NF-kappa B and AP-1 activation, thereby preventing TF expression, cardiac vasculopathy, and microin

关键词：血管紧张素ⅱ/药理学动物基因修饰抗高血压药/药理学血液凝固因子/代谢血压/药物作用 CHO细胞细胞系冠心病/化学诱导冠心病/代谢冠心病/死亡率冠状血管/药物作用冠状血管/生理学仓鼠亚科细胞外基质蛋白质类/药物作用细胞外基质蛋白质类/代谢心室/药物作用心室/代谢炎症/病理生理学整合素α4β1 整合素类/药物作用整合素类/代谢 NF-κB/代谢原癌基因蛋白质c-fos/遗传学 RNA 信使/遗传学 RNA 信使/代谢大鼠 Sprague-Dawley 受体血管紧张素 1型受体血管紧张素 2型受体淋巴细胞归巢/药物作用受体淋巴细胞归巢/代谢四唑类/药理学凝血致活酶/药物作用凝血致活酶/遗传学凝血致活酶/代谢转录因子AP-1/代谢缬氨酸/类似物和衍生物缬氨酸/药理学血管阻力/药物作用动物人类大鼠

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STIMULATION OF PROSTAGLANDIN-E SYNTHESIS IN CULTURED HUMAN UMBILICAL VEIN SMOOTH-MUSCLE CELLS

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 1976年第5期73卷 1617-1620页

作者： ALEXANDER, RW GIMBRONE, MA NHLI HYPERTENSION ENDOCRINE BRANCH BETHESDA MD 20014 USA NCI PATHOPHYSIOL LAB BETHESDA MD 20014 USA PETER BENT BRIGHAM HOSP DEPT PATHOL BOSTON MA 02115 USA

Cultured human umbilical vein smooth muscle cells secreted 1.26 .+-. 0.20 .mu.g of immunoreactive prostaglandin E (iPGE) per mg of cell protein per 24 h (mean .+-. SE of the mean). Indomethacin, an inhibitor of PG synthesis, abolished greater than 95% of this basal iPGE production (median inhibitory dose [ID50] = 1.8 nM). The vasoactive mediators bradykinin, angiotensin II and histamine stimulated iPGE production in a dose-dependent manner (maximal levels 10-, 3.5-, and 2.3-times basal, respectively) during 2 h incubations in serum-free medium. Serotonin (5-hydroxytryptamine) elicited small (less than 50%) increases, whereas norepinephrine was inconsistent in stimulating iPGE production. Exogenous PG are extremely potent vasoactive substances, which can increase or decrease the tone of resistance and capacitance vessels. Endogenous PG production in vascular smooth muscle cells may represent an intrinsic control mechanism affecting basal tone and modulating the response of blood vessels to vasoactive mediators. Cell culture techniques may prove to be useful generally in the study of the biochemical events involved in agonist-vascular smooth muscle receptor interaction.

关键词：血管紧张素ⅱ/药理学缓激肽/药理学细胞培养的组胺/药理学吲哚美辛/药理学肌平滑/药物作用肌平滑/代谢去甲肾上腺素/药理学前列腺素E类/生物合成血清素/药理学脐静脉

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Adrenocortical function in a new world primate, the marmoset monkey, Callithrix jacchus

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GENERAL AND COMPARATIVE ENDOCRINOLOGY 2000年第1期120卷 2-7页

作者： Whitehouse, BJ Abayasekara, DRE Kings Coll London GKT Sch Biomed Sci Endocrinol & Reprod Res Grp London SE1 1UL England Univ London Royal Vet Coll Dept Vet Basic Sci London NW1 0TU England

The function of the adrenal cortex of the marmoset monkey Callithrix jacchus has been investigated. In common with other New World primates, these animals seem to be glucocorticoid resistant. Blood and adrenal glands were obtained from male and female animals under terminal pentobarbitone anesthesia. Dispersed adrenal cell preparations were obtained by treatment with collagenase and incubated with ACTH(1-24), (0.1-1000 nM) angiotensin II (0.1-1000 nM), dibutyryl cyclic AMP (dbcAMP;30-1000 muM), and forskolin (FSK;1-30 muM). Plasma cortisol levels (2113 +/- 449 ng/ml male;3858 +/- 429 ng/ml female) were found to be 10- to 20-fold higher than those quoted for Old World primates and man. The cell preparations showed no significant response to any dose of ACTH tested (0.1-1000 nM), although addition of exogenous precursor (22R-hydroxycholesterol, 2.5 muM) resulted:in an increased yield of cortisol and aldosterone. Cyclic AMP production was increased in response to forskolin (1-30 muM) but not ACTH(1-24) (1-1000 nM). In addition, dose-related responses to angiotensin II (maximal stimulation of 316 +/- 49% basal aldosterone at 100 nM angiotensin II), dbcAMP (maximal stimulation of 449 +/- 24% basal cortisol at 300 muM dbcAMP), and forskolin (maximal stimulation of 394 +/- 31% basal cortisol at 10 muM FSK) were obtained. The lack of a response in vitro to ACTH in C. jacchus cannot, therefore, be attributed either to general failure of the cells or to defects in postreceptor signaling mechanisms. The results suggest that there is a reduction in adrenal ACTH receptor number or affinity, with a high basal production rate in vivo maintaining the elevated plasma cortisol levels. (C) 2000 Academic Press.

关键词：肾上腺皮质/解剖学和组织学肾上腺皮质/药物作用肾上腺皮质/生理学促肾上腺皮质激素/投药和剂量促肾上腺皮质激素/药理学醛固酮/血液血管紧张素Ⅱ/投药和剂量血管紧张素ⅱ/药理学布拉地新/药理学狨猴属/生理学环AMP/生物合成剂量效应关系药物福司柯林/投药和剂量福司柯林/药理学氢化可的松/血液动物女(雌)性男(雄)性

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The effects of angiotensin II on blood perfusion in the rat renal papilla

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JOURNAL OF PHYSIOLOGY-LONDON 1999年第1期519卷 273-278页

作者： Walker, LL Rajaratne, AAJ Blair-West, JR Harris, PJ Univ Melbourne Dept Physiol Parkville Vic 3052 Australia

1. Systemic infusion of angiotensin II (ATI) increased papillary blood perfusion (PBP) measured by laser-Doppler flowmetry in rats, aged about 5 weeks. The mechanisms involved in this response were determined by infusion of AII in the presence of systemic doses of losartan (a type 1 AII receptor antagonist), HOE-140 (a bradykinin B-2 receptor antagonist), and an inhibitor of NO production - N-omega-nitro-L-arginine (NOLA). 3. Mean arterial blood pressure (MAP) and PBP increased in a dose-dependent manner in response to intravenous infusions of AII. Infusion of losartan abolished these responses to AII but HOE-140 was without effect. Infusion of NOLA abolished the increase in PBP but did not affect the presser response to AII. Systemic infusion of sodium nitroprusside restored the response to AII in experiments with NOLA infusion. 4. The results indicate that the increase in PBP caused by AII is mediated via angiotensin AT, receptors and does not involve bradykinin B-2 receptors. The AII-induced increase in PBP is dependent upon the presence of NO, thus providing a mechanism for maintenance of papillary perfusion in the face of generalized renal vasoconstriction due to AII.

关键词：血管紧张素ⅱ/药理学血压/药物作用缓激肽/类似物和衍生物缓激肽/药理学肾髓质/血液供给肾髓质/超声检查激光多普勒流量测定洛沙坦/药理学硝基精氨酸/药理学硝普钠/药理学大鼠 Sprague-Dawley 受体缓激肽B2 受体缓激肽/拮抗剂和抑制剂局部血流/药物作用肾循环/药物作用动物大鼠

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Acute infusion of nicotine potentiates norepinephrine-induced vasoconstriction in the hamster cheek pouch

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JOURNAL OF LABORATORY AND CLINICAL MEDICINE 1999年第1期133卷 48-54页

作者： Mayhan, WG Univ Nebraska Med Ctr Dept Physiol & Biophys 600 S 42nd St Omaha NE 68198 USA

Although cigarette smoking and the components of cigarette smoke appear to alter nitric oxide synthase-dependent dilation of blood vessels, the effect of these substances on constrictor responses of resistance arterioles has not been examined. Thus the goal of this study was to examine the effect of a major component of cigarette smoke-that is, nicotine-on constrictor responses of cheek pouch arterioles. The diameter of cheek pouch arterioles (similar to 50 mu m in diameter) was measured by using intravital microscopy. We examined the responses of arterioles to angiotensin II, arginine vasopressin, norepinephrine, and the thromboxane analog U-46619 before and after treatment with vehicle (saline solution), N-G-monomethyl-L-arginine (L-NMMA;1.0 mu mol/L), or nicotine (2.0 mu g/kg/min IV for 30 minutes followed by a maintenance dose of 0.35 mu g/kg/min for 30 minutes). Topical application of angiotensin II (0.01 and 0.1 nmol/L), arginine vasopressin (1.0 and 10 pmol/L), norepinephrine (1.0 and 10 nmol/L), and U-46619 (0.01 and 0.1 nmol/L) produced marked reproducible constriction of cheek pouch arterioles in hamsters treated with vehicle. Topical application of L-NMMA potentiated constrictor responses of arterioles to the high dose of arginine vasopressin (28% +/- 4% versus 36% +/- 4%;P < .05) and to both doses of norepinephrine (14% +/- 1% and 24% +/- 2% versus 19% +/- 1% and 31% +/- 3%;P < .05). The infusion of nicotine did not alter responses to angiotensin II, arginine vasopressin, or U-46619 but modestly potentiated vasoconstriction in response to norepinephrine (12% +/- 2% and 22% +/- 2% versus 14% +/- 2% and 26% +/- 2%;P < .05). These findings suggest that the synthesis/release of nitric oxide may modulate constrictor responses of cheek pouch resistance arterioles to selected agonists, In addition, nicotine, at levels observed in smokers, may potentiate norepinephrine-induced vasoconstriction. We suggest that preservation/potentiation of vasoconstrictor respons

关键词：血管紧张素ⅱ/药理学精氨酸加压素/药理学小动脉/药物作用小动脉/生理学颊仓鼠亚科剂量效应关系药物药物协同作用输注静脉内口腔黏膜/血液供给口腔黏膜/药物作用尼古丁/投药和剂量烟碱激动剂/投药和剂量去甲肾上腺素/药理学血管收缩/药物作用血管收缩/生理学 ωN-甲基精氨酸/药理学动物男(雄)性

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