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Resistance artery smooth muscle function in pregnancy and preeclampsia (vol 186, pg 148, 2002)

AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY 2002年第4期186卷 722-722页

作者： Van Wijk, MJ Boer, K van der Meulen, FT Bleker, OP Spaan, JAF VanBavel, E DepartmentofObstetricsandGynecology AcademicMedicalCenterAmsterdamTheNetherlands.M.J.vanWijk@amc.uva.nl

Objective: The purpose of this study was to investigate whether the altered vascular resistance in pregnancy and preeclampsia results from alterations in intrinsic vascular smooth muscle properties or from external influences on vascular smooth muscle function. Study Design: We studied subcutaneous resistance arteries from women with preeclampsia, from normal pregnant women, and from nonpregnant women, that were obtained during cesarean delivery or gynecologic surgical procedures, in a pressure myograph. Arteries were denervated, and smooth muscle cells were loaded with calcium indicator fura-2. Contractile properties were tested in physiologic saline solution and during potassium- and norepinephrine-induced constriction at various pressures. In addition, endothelial function was assessed. Intracellular calcium and tone were measured continuously. Results: No significant differences in basal tone, constrictor, and myogenic responses were found between groups. Contractile element calcium sensitivity was significantly increased in women with preeclampsia. Norepinephrine caused an increase in calcium sensitivity in all groups. Conclusion: Vascular smooth muscle calcium sensitivity is increased in preeclampsia. (Am J Obstet Gynecol 2002;186:148-54.)

关键词：动脉/药物作用动脉/病理生理学钙/生理学肌平滑血管/病理生理学去甲肾上腺素/药理学先兆子痫/病理生理学妊娠/生理学参考值血管阻力血管收缩/生理学血管收缩药/药理学血管舒缩系统/病理生理学成年人女(雌)性人类

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Endothelium-independent coronary microvascular function: All vessels are not created equally

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AMERICAN HEART JOURNAL 2003年第4期145卷 567-568页

作者： Hasdai, D Rabin Med Ctr Dept Cardiol IL-49100 Petah Tiqwa Israel

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Effects of chronic pulmonary overcirculation on pulmonary vasomotor tone

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ANNALS OF THORACIC SURGERY 1999年第2期67卷 522-527页

作者： Parviz, M Bousamra, M Chammas, JH Birks, EK Presberg, KW Jacobs, ER Nelin, LD Med Coll Wisconsin Cardiovasc Res Ctr Dept Gen Surg Dept PhysiolDiv Cardiothorac Surg Milwaukee WI 53226 USA Med Coll Wisconsin Dept Med Milwaukee WI 53226 USA Med Coll Wisconsin Dept Pediat Milwaukee WI 53226 USA

Background. A model of shunt-induced pulmonary hypertension was used to study the effects of pulmonary overcirculation on endothelial nitric oxide synthase (eNOS) and cytochrome P450-4A (cP450-4A) vasodilatory mechanisms and related hemodynamic responses. Methods. An aortopulmonary shunt was constructed in 6-week-old piglets (n = 7, sham-operated controls n = 8). Hemodynamic measurements were made 4 weeks later under serial experimental conditions: baseline (fractional concentration of oxygen, 0.4);inhaled nitric oxide, 25 ppm (INO);hypoxia (fractional concentration of oxygen, 0.14);hypoxia + INO;N-omega-nitro-L-arginine methylester (L-NAME 30 mg/kg intravenously, competitive NOS inhibitor);and L-NAME + INO. Lung protein levels of eNOS and cP450-4A and NOS activity were compared between groups. Results, Shunted animals had a higher baseline pulmonary artery pressure (p < 0.05). L-NAME resulted in a greater increase in pulmonary vascular resistance in shunted animals (150% +/- 26% shunt versus 69% +/- 14% control;p = 0.01). The INO administered during baseline conditions decreased pulmonary vascular resistance only in control animals (p < 0.05). Protein levels of eNOS and NOS activity were similar in both groups;however, cP450-4A protein levels were decreased in the shunted group (p = 0.02). Conclusions. The NO production was preserved in shunted animals but they demonstrated greater vasodilatory dependence on NO, evidenced by an exaggerated increase in pulmonary vascular resistance after NOS inhibition. Loss of the cP450-4A vasodilatory system may be the driving force for NO dependency in the shunted pulmonary circulation. (C) 1999 by The Society of Thoracic Surgeons.

关键词：烷烃1-单氧酶细胞色素P450酶系统/血液内皮血管/病理学内皮血管/病理生理学高血压肺性/病理学高血压肺性/病理生理学混合功能氧化酶类/血液一氧化氮合酶/血液肺动脉/病理学肺动脉/病理生理学肺楔压/生理学猪血管阻力/生理学血管舒缩系统/病理学血管舒缩系统/病理生理学动物

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Contribution of bradykinin receptor dysfunction to abnormal coronary vasomotion in humans

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JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 2000年第5期36卷 1467-1473页

作者： Prasad, A Husain, S Schenke, W Mincemoyer, R Epstein, N Quyyumi, AA NHLBI NIH Cardiol Branch Bethesda MD 20892 USA

OBJECTIVES The aim of our study was to investigate coronary vascular kinin receptor function in patients with atherosclerosis or its risk factors. BACKGROUND Although acetylcholine (ACH) is used as a probe for testing vascular function in vivo, endogenous bradykinin (BK) regulates resting and flow-mediated epicardial tone. METHODS In 53 patients with mild atherosclerosis or its risk factors and 9 control subjects, endothelium-dependent vasomotion was tested with intracoronary ACH (30 mug/min) and BK (62.5 ng/min and 4 mug/min), and endothelium independent function with sodium nitroprusside. Metabolic vasodilation was assessed during cardiac pacing (n = 19). Correlation with serum angiotensin-converting enzyme (ACE) levels and the ACE insertion/deletion genotype was performed. RESULTS There was progressive impairment in AGH-mediated microvascular dilation with increasing numbers of risk factors (p = 0.025, analysis of variance). By contrast, BK- and sodium nitroprusside-mediated microvascular dilation was similar in all groups. Similarly, there was no correlation between epicardial coronary responses to ACH and BK;segments that constricted or dilated with ACH had similar dilator responses with BK. Bradykinin, but not ACH-mediated vasomotion, was depressed in epicardial segments that constricted with pacing. Finally, epicardial BK responses were depressed in patients with high ACE levels and in those with the ACE DD genotype. CONCLUSIONS Endothelial dysfunction in atherosclerosis appears to be receptor-specific, involving the muscarinic receptor with relative sparing of the kinin receptor pathways. Abnormal reactivity of epicardial coronary arteries during physiologic stress is better represented by BK and not by ACH responses. Bradykinin activity and, hence, physiologic coronary vasomotion appears to be influenced by serum ACE levels and the ACE insertion/deletion genotype. (C) 2000 by the American College of Cardiology.

关键词：乙酰胆碱/药理学腺苷/药理学动脉硬化/病理生理学缓激肽/药理学冠状血管/药物作用冠状血管/病理生理学血流动力学一氧化氮/生理学硝普钠/药理学肽基二肽酶A/血液肽基二肽酶A/遗传学多态现象遗传受体缓激肽/药物作用受体缓激肽/生理学危险因素血管舒缩系统/药物作用血管舒缩系统/病理生理学 ωN-甲基精氨酸/药理学女(雌)性人类男(雄)性中年人

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NEURAL FACTORS IN ATHEROGENESIS - EXPERIMENTAL STUDIES

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ANNALS OF THE NEW YORK ACADEMY OF SCIENCES 1976年第AUG27期275卷 117-130页

作者： GUTSTEIN, WH PARL, F BJORNSON, LK NEW YORK MED COLL DEPT PATHOLVALHALLANY 10595 LONG ISLAND COLL HOSP SPECIAL CHEM LABBROOKLYNNY 11201

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Current management of patients with pulmonary hypertension and right ventricular insufficiency

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Current Cardiology Reports 2000年第3期2卷 244-251页

作者： Hankins, Shelley R. Horn, Evelyn M. Albert Einstein College of Medicine Bronx NY 10461 1300 Morris Park Avenue United States Heart Failure Research Center New York Presbyterian Hospital Columbia-Presbyterian Campus New York NY 10032 177 Fort Washington Avenue United States

Pulmonary hypertension is a pathologic condition characterized by elevated pulmonary artery pressures and an associated vasculopathy. Primary pulmonary hypertension (PPH) is a rare condition with a sporadic occurrence and a familial form of the disorder. Abnormal vasomotor tone in the pulmonary vasculature results from an imbalance of the action of various vasoconstrictors/vascular proliferative agents (endothelin and thromboxane) versus vasodilators /anti-proliferative agents (prostacyclin and nitric oxide). The mainstay of outpatient therapy has been the use of digitalis, diuretics, oxygen, and coumadin and the judicious use of vasodilator therapy. Calcium channel blockers in a select group and intravenous prostacyclin have dramatically improved survival for those with primary pulmonary hypertension. Use of prostaglandin I2 (PGI2) in other forms of chronic pulmonary arterial hypertension is not as clear, although evidence of initial beneficial response is promising. Importantly, over the next few years both pharmacologic and nonpharmacologic treatment modalities for pulmonary hypertension may rapidly change as we focus more on the abnormal pulmonary vascular biology and concomitant hemodynamic and neurohormonal milieu. Copyright © 2000 by Current Science Inc.

关键词：抗高血压药/治疗应用强心药/治疗应用内皮血管/病理生理学依前列醇/治疗应用高血压肺性/药物疗法高血压肺性/病理生理学血管舒张药/治疗应用血管舒缩系统/病理生理学心室功能障碍右/药物疗法心室功能障碍右/病理生理学人类

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The possible role of prolactin in pre-eclampsia

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Medical Hypotheses 1975年第4期1卷 159-164页

作者： Horrobin, D.F. Clinical Research Institute Montreal 110 Pine Avenue West Canada

The primary feature of pre-eclampsia is the pregnancy-associated rise in arterial pressure. Oedema and proteinuria also frequently occur. There is increased responsiveness to pressor agents. Prolactin is present in elevated amounts in human pregnancy and is found in very large quantities in amniotic fluid. Prolactin can cause renal retention of fluid and electrolytes, can elevate arterial pressure and can potentiate responses to pressor agents. It is suggested that either elevated prolactin levels or an increased responsiveness to normal prolactin levels may play a key role in the pathogenesis of preeclampsia. © 1975.

关键词：肾/病理生理学先兆子痫/病因学先兆子痫/代谢先兆子痫/治疗孕酮/药理学催乳素/代谢血管舒缩系统/病理生理学女(雌)性人类妊娠

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Changes in protein kinase C isoforms in association with vascular hyporeactivity in cirrhotic rat aortas

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GASTROENTEROLOGY 2000年第1期119卷 201-210页

作者： Tazi, KA Moreau, R Heller, J Poirel, O Lebrec, D Hop Beaujon INSERM U481 Lab Hemodynam Splanchn & Biol Vasc F-92118 Clichy France

Background & Aims: Although protein kinase C (PKC) alterations may play a role in the abnormal reactivity of cirrhotic rat aortas, its isoforms and cellular distribution are unknown. We therefore studied the protein expression and cellular distribution of PKC isoforms and their activation in cirrhotic rat aortas. Methods: Endothelium-denuded aortas from control and cirrhotic rats were examined. immunoblots were performed with PKC isoform-specific antibodies. Aortic reactivity was determined for phorbol myristate acetate and phenylephrine after PKC down-regulation. Results: PKC-alpha expression was reduced in both the cytosolic and membrane fractions in cirrhotic aortas. Trace amounts of PKC-beta were detected in cirrhotic aortas. PKC-delta was detected in the cytosolic fraction of control and cirrhotic aortas. PKC-zeta was detected in the membrane fraction in control aortas and in the cytosolic fraction in cirrhotic aortas. Phorbol myristate acetate and phenylephrine triggered translocation of PKC-alpha and PKC-delta isoforms from the cytosol to the membrane in control aortas;in cirrhotic aortas, only PKC-alpha was translocated. Aortic reactivities were reduced after PKC downregulation. PKC-alpha and -delta activities were reduced in cirrhotic aortas. Conclusions: These results suggest that a change in PKC isoforms may be responsible in part for the abnormal reactivity and intracellular transduction through the PKC pathway in cirrhotic rat aortas.

关键词：主动脉/病理生理学生物转运/药物作用减量调节细胞内膜/酶学同工酶类/代谢肝硬化实验性/病理生理学苯福林/药理学蛋白激酶C/代谢大鼠 Sprague-Dawley 参考值十四酰佛波乙酯/药理学时间因素组织分布血管收缩/生理学血管收缩药/药理学血管舒缩系统/病理生理学动物男(雄)性大鼠

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Influence of ageing on vasomotor responses of human epicardial coronary arteries

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PHARMACOLOGY & TOXICOLOGY 2000年第4期86卷 183-191页

作者： Opgaard, OS Ytterberg, HT Saxena, PR Edvinsson, L Erasmus Univ Dept Pharmacol NL-3000 DR Rotterdam Netherlands Univ Hosp Dept Internal Med Lund Sweden

Vasomotor responses to various agonists were studied on isolated circular segments of human epicardial coronary arteries from three different age groups;23-38 pars, 44-58 years and 63-86 years. Noradrenaline had no or only weak contractile effect on coronary arteries from younger patients but induced contraction of all artery segments from older patients. The E-max value was significantly (P<0.0001) higher in arteries from the oldest group compared to each of the two younger age groups, whereas the potency was similar in all three groups. Linear regression analysis of noradrenaline-induced contraction in individual patients revealed a significantly positive age-correlation (correlation coefficient 0.67, P<0.0001). Contraction induced by endothelin-1 and relaxation induced by substance P, calcitonin gene-related peptide and vasoactive intestinal peptide on arteries precontracted with U46619 showed no significant differences in maximum responses and potencies between the three age groups, and no significant linear age-correlation. These data demonstrate a large variability in contractile responses to noradrenaline with contractions seen mostly in coronary arteries from older patients. It thus seems that sympathetic activation could contribute to coronary ischaemia in some patients.

关键词： 15-羟基-11α 9α-(环氧亚甲基)前列腺-5 13-二烯酸/药理学衰老降钙素基因相关肽/药理学心肌疾病/病理生理学冠状血管/药物作用冠状血管/生理学冠状血管/病理生理学剂量效应关系药物内皮缩血管肽类/药理学去甲肾上腺素/药理学 P物质/药理学血管活性肠肽/药理学血管收缩/药物作用血管收缩药/药理学血管舒张/药物作用血管舒缩系统/药物作用血管舒缩系统/生理学血管舒缩系统/病理生理学成年人老年人老年人 80以上人类中年人

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A PHARMACOLOGICAL AND HISTOLOGICAL INVESTIGATION OF THE INVOLVEMENT OF MAST CELLS IN CUTANEOUS AXON REFLEX VASODILATATION

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Quarterly Journal of Experimental Physiology and Cognate Medical Sciences 1975年第2期60卷 123-130页

作者： Kiernan, J.A. Department of Anatomy Health Sciences Centre The University of Western Ontario London Ontario Canada

Arteriolar vasodilatation following injury to the pinna of the left ear was measured thermometrically in 43 rats. Quantitative histological assessments were made of the intact and degranulating dermal mast cells in the left and right ears of the animals. Vasodilatation, with associated increased proportions of degranulating mast cells, was found only in animals in which the sensory innervation of the left ear was intact, allowing the occurrence of axon reflexes. In rats depleted of mast cells by treatment for 5 days with compound 48/80, axon reflex vasodilatation was suppressed, indicating that mast cells are essential for the development of the flare in the triple response. Vasodilatation was also suppressed in animals injected with aspirin 20—30 min prior to injury. In these latter rats, there was no increase in the proportion of degranulating dermal mast cells It is suggested that aspirin protects the mast cells from the degranulating effect of axon reflexes. These results indicate that the arteriolar flare around the site of a cutaneous injury is mediated by the action of axon reflexes upon dermal mast cells. This conclusion is discussed in relation to other observations on vasodilatation in injured and diseased skin. © 1975 The Physiological Society

关键词：阿司匹林/药理学轴突/生理学血管/药物作用血管/病理生理学去神经支配肥大细胞/细胞学肥大细胞/药物作用肥大细胞/生理学局部血流皮肤/血液供给皮肤/损伤皮肤温度血管舒缩系统/病理生理学 p-甲氧基-N-苯丙胺/药理学动物男(雄)性大鼠

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