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Sensory channel specific modulation in the nucleus of the solitary tract

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JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM 2000年第3期80卷 117-129页

作者： Paton, JFR Kasparov, S Univ Bristol Sch Med Sci Dept Physiol Bristol BS8 1TD Avon England

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Sodium-induced cardiac aldosterone synthesis causes cardiac hypertrophy

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ENDOCRINOLOGY 2000年第5期141卷 1901-1904页

作者： Takeda, Y Yoneda, T Demura, M Miyamori, I Mabuchi, H Kanazawa Univ Sch Med Dept Internal Med 2 Kanazawa Ishikawa 920 Japan Kanazawa Univ Sch Med Dept Hlth Sci Kanazawa Ishikawa 920 Japan Fukui Med Sch Dept Internal Med 3 Fukui 91011 Japan

High sodium intake causes cardiac hypertrophy independently of increases in blood pressure. Aldosterone is synthesized in extraadrenal tissues such as blood vessels, brain, and heart. Effects of 8 weeks of high sodium intake on cardiac aldosterone synthesis, as well as cardiac structure, mass, and aldosterone production, levels of mRNA coding for aldosterone synthase (CYP11B2) and the angiotensin TI AT 1 receptor, were studied in normotensive Wistar-Kyoto (WKY) rats. Isolated rat hearts were perfused for 2 hr, and the perfusate was analyzed by high-performance liquid chromatography and mass spectrometry. Aldosterone synthase activity was estimated from the conversion of [C-14]deoxycorticosterone to [C-14]aldosterone. Levels of mRNA for CYP11BZ and AT 1 receptor were determined by competitive polymerase chain reactions. A high sodium intake for 8 weeks produced left ventricular hypertrophy without elevation of blood pressure. Plasma aldosterone concentrations and plasma renin concentrations were decreased by high sodium intake. Aldosterone production, activity of aldosterone synthase, and expression of mRNA for CYP11B2 and AT 1 receptor were increased in hearts of rats with high sodium intake. These results suggest that high sodium intake increases cardiac aldosterone synthesis, which may contribute to cardiac hypertrophy independently of the circulating renin-angiotensin-aldosterone system.

关键词：醛固酮/生物合成醛固酮合酶/遗传学醛固酮合酶/代谢血管紧张素ⅱ/代谢心脏扩大心脏/药物作用心肌/代谢 RNA 信使/代谢大鼠近交WKY 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/生物合成钠/药理学动物男(雄)性大鼠

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Na⁺/H⁺ exchange hyperactivity and myocardial hypertrophy:: Are they linked phenomena?

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CARDIOVASCULAR RESEARCH 1999年第3期44卷 462-467页

作者： Cingolani, HE Ctr Invest Cardiovasc RA-1900 La Plata Argentina

Time for primary review 22 days. 1 The Na+/H+ exchanger Intracellular pH (pHi) in the majority of living cells is about 6.8–7.2, considerably more alkaline than that predicted for passive distribution of H+ across the cell membrane. For the average membrane potential and for an extracellular pH of 7.4, a pHi value of 6.4 should be expected if H+ were in electrochemical equilibrium. At such a pHi, metabolism and a variety of other cellular functions would be impaired. The existence of mechanisms extruding H+ (or acid equivalents) can explain the maintenance of pHi well above the equilibrium. The Na+/H+ exchanger (NHE) is one of these mechanisms and plays a central role in the regulation of pHi as well as in the control of cell volume and of intracellular Na+ concentration ([Na+]i). In addition, the exchanger appears to facilitate the induction of cellular growth and proliferation in response to numerous growth factors. The NHE has been found in virtually all living cells and may be phylogenetically one of the most primitive transport systems. The system catalyses the electroneutral exchange of Na+ for H+, with a coupled 1:1 stoichiometry. Under physiological conditions, the inwardly directed Na+ gradient, which is maintained by the activity of the Na+–K+-ATPase and the Na+/Ca2+ exchanger, provides a constant driving force for H+ extrusion. According to the electrochemical transmembrane gradients, the NHE should extrude intracellular H+ in exchange for extracellular Na+ until a pHi far beyond physiological values (8.2–8.5) is obtained. However, at a pHi of around 7.1–7.2 the antiporter extrudes only the protons generated by the intermediate metabolism and those leaking into the cell, so that pHi reaches a steady state value. This pHi at which the NHE is almost quiescent (preventing the rise to non-physiological values) is called “set-point”, and can be shifted to more alkaline pHi values by various stimuli. A prominent feature of this exchanger is that growth factors

关键词：血管紧张素ⅱ/代谢血管紧张素转换酶抑制药/药理学抗高血压药/药理学反向转运物/代谢心脏扩大/代谢红细胞/代谢氢离子浓度高血压/代谢心肌/代谢信号传导/药物作用钠氢反向转运物/代谢动物人类

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Tyrosine kinase inhibition affects type 1 angiotensin II receptor internalization

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JOURNAL OF RECEPTOR AND SIGNAL TRANSDUCTION RESEARCH 1999年第6期19卷 975-993页

作者： Becker, BN Kondo, S Chen, JK Harris, RC Vanderbilt Univ Med Ctr Sch Med Dept Med Nashville TN 37232 USA Dept Vet Affairs Med Ctr Nashville TN 37232 USA

Growth factor receptors activate tyrosine kinases and undergo endocytosis. Recent data suggest that tyrosine kinase inhibition can affect growth factor receptor internalization. The type 1 angiotensin II receptor (AT(1)R) which is a G-protein-coupled receptor, also activates tyrosine kinases and undergoes endocytosis. Thus, we examined whether tyrosine kinase inhibition affected AT(1)R internalization. To verify protein tyrosine phosphorylation, both LLCPKCl4 cells expressing rabbit AT(1)R (LLCPKAT1R) and cultured rat mesangial cells (MSC) were treated with angiotensin II (Ang II) [1-100 nM] then solubilized and immunoprecipitated with antiphosphotyrosine antisera. Immunoblots of these samples demonstrated that Ang II stimulated protein tyrosine phosphorylation in both cell types. Losartan [1 mu M], an AT(1)R antagonist, inhibited Ang II-stimulated protein tyrosine phosphorylation, LLCPKAT1R cells displayed specific I-125-Ang 11 binding at apical (AP) and basolateral (BL) membranes, and both AP and BL AT(1)R activated tyrosine phosphorylation. LLCPKAT1R cells, incubated with genistein (Gen) [200 mu M] or tyrphostin B-48 (TB-48) [50 mu M], were assayed for acid-resistant specific I-125-Ang II binding, a measure of Ang TI internalization. Both Gen (n=7) and TB-48 (n=3) inhibited AP I-125-Ang II internalization (80 +/- 7% inhibition;p < 0.025 vs. control). Neither compound affected BL internalization. TB-1, a non-tyrosine kinase-inhibiting tyrphostin, did not affect AP I-125-Ang 11 endocytosis (n=3), suggesting that the TB-48 effect was specific for tyrosine kinase inhibition. Incubating MSC with Gen (n=5) or herbimycin A [150 ng/ml] (n=4) also inhibited MSC I-125-Ang II internalization (82 +/- 11% inhibition;p<0.005 vs. control). Thus, tyrosine kinase inhibition prevented Ang IT internalization in MSC and selectively decreased AP Ang II internalization in LLCPKAT1R cells suggesting that AP AT(1)R in LLCPKATIR cells and MSC AT(1)R have similar endocytic phenotypes, and

关键词：血管紧张素ⅱ/代谢酶抑制剂/药理学染料木黄酮/药理学肾小球膜/代谢蛋白酪氨酸激酶类/拮抗剂和抑制剂受体血管紧张素/代谢信号传导/药物作用酪氨酸磷酸化抑制剂/药理学动物兔大鼠

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No expression of angiotensin II receptors and angiotensin-converting enzyme in myxomatous canine mitral valve leaflets. An autoradiographic study

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JOURNAL OF VETERINARY MEDICINE SERIES A-PHYSIOLOGY PATHOLOGY CLINICAL MEDICINE 1999年第8期46卷 465-472页

作者： Mow, T Pedersen, HD Royal Vet & Agr Univ Dept Anat & Physiol DK-1870 Frederiksberg C Denmark Royal Vet & Agr Univ Small Anim Hosp Dept Clin Sci Frederiksberg Denmark

The renin-angiotensin system, including angiotensin (Ang) II and angiotensin-converting enzyme (ACE), plays an important role in cardiac fibrous tissue formation. Since changes in valvular collagen are a central part of myxomatous mitral valve disease in the dog, we speculated that Ang II and ACE might pla! a role in the pathogenesis of this disease. In 10 mitral valves, five with and five without clear myxomatous changes, thr presence and distribution of Ang II receptors and ACE was examined autoradiographically, using I-125-Ang II and I-125-lisinopril, respectively. At postmortem examination, diseased valves were taken from old dogs, control valves from young adult dogs. No significant level of Ang II and lisinopril binding was found in normal as well as diseased valve leaflets. Equally low, insignificant levels of I-125-Ang II binding were found in the myocardium of dogs with and without valvular disease. No significant level of myocardial I-125-lisinopril binding was found. The lack of autoradiographic evidence of Ang II receptors and ACF, in normal and diseased canine mitral valve leaflets suggests that the renin-angiotensin system does not play a major role in the pathogenesis of the valvular changes.

关键词：血管紧张素ⅱ/代谢放射自显影术狗疾病/代谢心脏肿瘤/代谢心脏肿瘤/兽医学碘放射性同位素二尖瓣/代谢心肌/代谢黏液瘤/代谢黏液瘤/兽医学肽基二肽酶A/分析受体血管紧张素/分析参考值动物狗

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Effects of BAY 10-6734 (Embusartan), a new angiotensin II type I receptor antagonist, on vascular smooth muscle cell growth

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第1期289卷 181-187页

作者： Iouzalen, L Stepien, O Marche, P Univ Paris 05 Fac Med Necker Necker Med Sch Dept PharmacolCNRSURA 1482 F-75015 Paris France

Angiotensin II (AII), an important hypertrophic factor in the cardiovascular system, exerts most of its known effects in vivo through the AII receptor type 1 (AT(1)) subclass of AII receptors. These receptors are also responsible for the growth-related effects of AII in cultured vascular smooth muscle cells (VSMCs). We presently investigated the effects of BAY 10-6734 (Embusartan), a new orally active AT(1) antagonist, on VSMC growth and proliferation of cultured VSMCs isolated from the aortae of Wistar Kyoto rats and spontaneously hypertensive rats. BAY 10-6734 and losartan (considered as AT(1) receptor antagonist of reference), as well as their respective active metabolites, were studied for their inhibition of: 1) [I-125]AII binding to its receptors, 2) AII-induced DNA and protein synthesis (by measuring the incorporation of 5-bromo-2'-deoxyuridine and [H-3]L-leucine, respectively), and 3) AII-induced variations in intracellular Ca2+ concentration, using cells labeled with Fura-2. All of the tested compounds inhibited the aforementioned parameters in a concentration-dependent manner. Half-maximal inhibitory concentration values indicated that BAY 10-6734 was significantly more potent than losartan and that spontaneously hypertensive rat-derived VSMCs were more sensitive than Wistar Kyoto rat-derived ones. Neither BAY 10-6734 nor losartan affected the intracellular Ca2+ concentration of unstimulated VSMCs but both compounds inhibited both AII-induced Ca2+ mobilization from internal stores and Ca2+ influx. Neither compound affected arginine-vasopressin-, basic fibroblast growth factor-, or serum-induced DNA and protein synthesis. BAY 10-6734 appears therefore as a potent and specific new inhibitor of AII-induced growth-related events in VSMCs.

关键词：血管紧张素ⅱ/代谢钙/代谢细胞分裂/药物作用细胞培养的胞质溶胶/药物作用胞质溶胶/代谢 DNA/生物合成二氢吡啶类/药理学咪唑类/药理学洛沙坦/药理学肌平滑血管/细胞学肌平滑血管/药物作用蛋白质生物合成放射配体测定大鼠近交SHR 大鼠近交WKY 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/拮抗剂和抑制剂种特异性四唑类/药理学动物男(雄)性大鼠

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Myocardial insulin resistance in cardiac hypertrophy

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CARDIOVASCULAR RESEARCH 1999年第1期42卷 12-14页

作者： Verma, S Dumont, AS McNeill, JH Univ British Columbia Fac Pharmaceut Sci Vancouver BC V6T 1Z3 Canada Univ Calgary Fac Med Calgary AB Canada

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Transport of [³H]losartan across isolated perfused rabbit proximal tubule

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第1期290卷 38-42页

作者： Edwards, RM Stack, EJ Trizna, W SmithKline Beecham Pharmaceut Dept Renal Pharmacol King Of Prussia PA 19406 USA

The transport of the angiotensin II receptor antagonist rosarian and its interaction with organic anion transport were examined in the isolated perfused rabbit proximal tubule. Losartan reversibly inhibited the secretion of para-aminohippurate (PAH) in a concentration-dependent manner (IC50 = 15 +/- 0.5 mu M). Other angiotensin II receptor antagonists also inhibited PAH secretion with similar potencies: eprosartan, 11 +/- 2.3 mu M;irbesartan, 17 +/- 2.2 mu M, and valsartan 3 +/- 0.6 mu M. [H-3]Losartan was secreted by the proximal tubule by a saturable and probenecid-sensitive mechanism. The affinity of losartan for the organic anion transporter (K-m = 12.3 +/- 1.8 mu M) was significantly greater than that of PAH (K-m = 88.5 +/- 10.7 mu M) [H-3]losartan secretion was stimulated in the presence of cu-ketoglutarate, suggesting that losartan, like PAH, enters the cell in exchange for a dicarboxylate. These results demonstrate that losartan and probably other nonpeptide angiotensin II receptor antagonists are secreted by an organic anion transporter that is similar to, if not identical with, the classic PAH transporter.

关键词：血管紧张素ⅱ/代谢酮戊二酸类/药理学肾小管近端/代谢洛沙坦/代谢灌流丙磺舒/药理学受体血管紧张素/拮抗剂和抑制剂肾脏用药/药理学 p-氨基马尿酸/代谢 p-氨基马尿酸/药理学动物男(雄)性兔

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Pathological expression of renin and angiotensin II in the renal tubule after subtotal nephrectomy - Implications for the pathogenesis of tubulointerstitial fibrosis

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AMERICAN JOURNAL OF PATHOLOGY 1999年第2期155卷 429-440页

作者： Gilbert, RE Wu, LL Kelly, DJ Cox, A Wilkinson-Berka, JL Johnston, CI Cooper, ME Univ Melbourne Dept Med Heidelberg Vic 3081 Australia Univ Melbourne Austin & Repatriat Med Ctr Heidelberg Vic 3081 Australia Univ Melbourne Dept Physiol Heidelberg Vic 3081 Australia

The finding that the systemic renin-angiotensin system (RAS) is not activated in most types of chronic renal disease has led to the suggestion that a local, intrarenal RAS may be an important determinant in the relentless progression of renal disease. Therefore, cell specific changes in various components of the RAS in response to renal mass reduction and angiotensin converting enzyme (ACE) inhibition were examined. Thirty Sprague-Dawley rats mere randomly assigned to sham surgery, subtotal nephrectomy (STNx) alone or STNx treated with the ACE inhibitor, perindopril, and sacrificed after 12 weeks, In sham rats, renin mRNA and protein were only present in the juxtaglomerular apparatus, In contrast, in STNx kidneys, renin and angiotensin II expression mere noted predominantly in renal tubular epithelial cells in association with overexpression of the prosclerotic cytokine, transforming growth factor-beta 1 (TGF-beta 1), In perindopril-treated STNx rats expression of renin and TGF-beta 1 were similar to control animals. These finding indicate that following renal mass reduction there is pathological tubular expression of various components of the RAS, Furthermore, in contrast to the juxtaglomerular apparatus, tubular renin expression was reduced with. ACE inhibition. These changes within the intrarenal RAS may be pathogenetically Linked to the development of tubulointerstitial injury.

关键词：血管紧张素Ⅱ/分析血管紧张素ⅱ/代谢胶原/分析胶原/代谢免疫组织化学原位杂交肾/解剖学和组织学肾/病理学肾/外科学肾小管/解剖学和组织学肾小管/代谢肾小管/外科学肾切除术肾炎间质性/代谢肽基二肽酶A/分析肽基二肽酶A/代谢大鼠 Sprague-Dawley 肾素/分析肾素/代谢转化生长因子α/分析转化生长因子α/代谢转化生长因子β/分析转化生长因子β/代谢动物男(雄)性大鼠

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Interaction between neutral endopeptidase and angiotensin converting enzyme inhibition in rats with myocardial infarction: Effects on cardiac hypertrophy and angiotensin and bradykinin peptide levels

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第1期289卷 295-303页

作者： Duncan, AM James, GM Anastasopoulos, F Kladis, A Briscoe, TA Campbell, DJ St Vincents Inst Med Res Fitzroy Vic 3065 Australia

Combined inhibition of neutral endopeptidase 24.11 (NEP) and angiotensin converting enzyme (ACE) is a candidate therapy for hypertension and cardiac failure. Given that NEP and ACE metabolize angiotensin (Ang) and bradykinin (BK) peptides, we investigated the effects of NEP inhibition and combined NEP and ACE inhibition on Ang and BK levels in rats with myocardial infarction. We administered the NEP inhibitor ecadotril (0, 0.1, 1, 10, and 100 mg/kg/day), either alone or together with the ACE inhibitor perindopril (0.2 mg/kg/day) by 12-hourly gavage from day 2 to 28 after infarction. Ecadotril increased urine cyclic GMP and BK-(1-9) excretion. Perindopril potentiated the effect of ecadotril on urine cyclic GMP excretion. Neither perindopril nor ecadotril reduced cardiac hypertrophy when administered separately, whereas the combination of perindopril and 10 or 100 mg/kg/day ecadotril reduced heart weight/body weight ratio by 10%. Administration of ecadotril to perindopril-treated rats decreased plasma Ang-(1-7) levels, increased cardiac BK(1-9) levels, and increased Ang II levels in plasma, kidney, aorta, and lung. These data demonstrate interactions between the effects of NEP and ACE inhibition on remodeling of the infarcted heart and on Ang and BK peptide levels. Whereas increased cardiac BK-(1-9) levels may contribute to the reduction of cardiac hypertrophy, the reduction in plasma Ang-(1-7) levels and increase in Ang II levels in plasma and tissues may compromise the therapeutic effects of combined NEP/ACE inhibition.

关键词：血管紧张素ⅱ/代谢血管紧张素转换酶抑制药/药理学体重/药物作用缓激肽/代谢心脏扩大/并发症心脏扩大/病理学环GMP/尿药物协同作用吲哚类/药理学心肌梗死/并发症心肌梗死/代谢心肌梗死/病理学心肌梗死/病理生理学脑啡肽酶/拮抗剂和抑制剂肽基二肽酶A/血液培哚普利钾/尿蛋白酶抑制药/药理学放射免疫测定大鼠 Sprague-Dawley 肾素/血液钠/尿硫甲基氧代苯丙甘氨酸/类似物和衍生物硫甲基氧代苯丙甘氨酸/药理学动物男(雄)性大鼠

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