Wyniki wyszukiwania

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Mechanisms of vasodilatatory effect of perivascular tissue of human internal thoracic artery

100%

Malinowski M., Deja M. A., Janusiewicz P., Golba K. S., Roleder T., Wos S.

Journal of Physiology and Pharmacology

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2013

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tom 64

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nr 3

2

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Isoprostanes in atherosclerosis

100%

Oguogho A., Sinzinger H.

Journal of Physiology and Pharmacology

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2000

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tom 51

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nr 4,1

3

The role of the adenosine triphosphate-sensitive potassium channels in pinacidil-induced vasodilatation of the human saphenous vein in patients with and without type 2 diabetes mellitus

84%

Rajkovic J., Peric M., Stanisic J., Novakovic R., Djokic V., Rakocevic J., Tepavcevic S., Lubudovic-Borovic M., Gostimirovic M., Heinle H., Gojkovic-Bukarica L.

Journal of Physiology and Pharmacology

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2020

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tom 71

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nr 1

4

Effects of meconium on airway reactivity to histamine and acetylcholine in vitro

84%

Mokry J., Mokra D., Nosalova G.

Journal of Physiology and Pharmacology. Supplement

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2007

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tom 58

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nr 5

5

Selective inhibition of guanylate cyclase prevents impairment of hypoxic pulmonary vasoconstriction in endotoxemic mice

84%

Spohr F., Busch C. J., Teschendorf P., Weimann J.

Journal of Physiology and Pharmacology

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2009

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tom 60

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nr 2

107-112

Nitric oxide (NO) may cause sepsis-induced impairment of hypoxic pulmonary vasoconstriction (HPV). Although NO exerts many of its actions by activating soluble guanylate cyclase (sGC), there are several cGC-independent mechanisms that may lead to NO-induced vasodilation during endotoxemia. We investigated the role of sGC for the regulation of HPV during lipopolysaccharide (LPS) induced endotoxemia using 1H-(1,2,4)oxadiazole(4,3-)quinoxaline-1-one (ODQ), a specific inhibitor of sGC, in isolated, perfused, and ventilated mouse lungs. Without ODQ, lungs from LPS-challenged mice constricted significantly less in response to hypoxia as compared to lungs from mice not treated with LPS (26 ± 27% vs. 134 ± 37%, respectively, p < 0.05). 20 mg/kg ODQ, but not 2 mg/kg or 10 mg/kg, restored the blunted HPV response in LPS-challenged mice as compared to mice not challenged with LPS (80±14 % vs. 98±21 %). ODQ had no effect on baseline perfusion pressures under normoxic conditions. Analysis of pulmonary vascular P-Q relationships suggested that the restoration of pulmonary vascular response to hypoxia by ODQ is associated with a restoration of pulmonary vascular properties during normoxia. Our data show in a murine model that specific inhibition of sGC may be a new approach to restore HPV during endotoxemia.

6

The effect of vasoconstrictors on oxygen consumption in resting and contracting skeletal muscle of the autologous pump-perfused rat hindlimb

84%

Hoy A. J., Peoples G. E., McLennan P. L.

Journal of Physiology and Pharmacology

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2009

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tom 60

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nr 3

155-160

This study used a novel in vivo model to test the hypothesis that nutritive and non-nutritive blood flow distribution can still be observed under conditions of high vascular tone and oxygen delivery at rest and in metabolically active (twitch contracting) skeletal muscle. Experiments were performed in a constant flow autologous pump-perfused hindlimb in anaesthetised male Wistar rats. Agonists were tested at rest with a flow rate of 1ml•min-1, and during hindlimb muscle twitch contractions (sciatic nerve stimulation: 6V, 1Hz, 0.05ms, 3min) at a flow rate of 2ml•min-1. Oxygen consumption was determined from hindlimb venous and arterial blood samples. Resting perfusion pressure at 1ml•min-1 was 92±3 mmHg (N=15) and oxygen consumption was 0.41±0.05 µmol•min-1•g-1. Serotonin increased perfusion pressure and significantly decreased basal hindlimb oxygen consumption at rest. During acute muscle contraction this effect on oxygen consumption was diminished. Noradrenaline significantly increased perfusion pressure but had no significant effect on basal hindlimb oxygen consumption. Vasoconstriction that impacts upon muscle metabolism occurs in vivo, which potentially could be due to selective redistribution of blood flow. However, during muscle contraction local release of vasodilatory regulation can overcome exogenously-induced vasoconstriction. These results support the hypothesis that dual vascular pathways may explain differential vasoconstriction and how it impacts upon muscle metabolism.

7

Mechanisms of vascular dysfunction after subarachnoid hemorrhage

84%

Kozniewska E., Michalik R., Rafalowska J., Gadamski R., Walski M., Frontczak-Baniewicz M., Piotrowski P., Czernicki Z.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 11

145-160

The main consequence of subarachnoid hemorrhage, for those who survive bleeding, is delayed, persistent vasospasm of intracranial conduit arteries which occurs between the third and seventh day after the insult and results in symptomatic brain ischemia in about 40% of cases. This vasospasm is considered to be a major cause of disability of post-SAH patients. Despite extensive experimental and clinical research, mechanisms of vasospasm are not fully understood. Dysfunction of the endothelium resulting in enhanced production of vasoconstrictors, phenotypic changes of the receptors in endothelium and smooth muscle cells, increased sensitivity of vascular smooth muscle cells to vasoconstrictors, release of spasmogens from lysed blood clot and inflammatory response of the vascular wall have been demonstrated and discussed as pathological mechanisms participating in the development of spasm. In recent years more attention is paid to the functional and structural changes in microcirculation and a concept of microvascular spasm is evolving. Our experimental studies in rat model of SAH strongly suggest that microcirculatory dysfunction and delayed vasospasm are related to the severity of acute, transient ischemia caused by critical decrease of perfusion pressure and active vasoconstriction immediately after the bleeding.

8

Mechanisms of hydrogen peroxide-induced vasoconstriction in the isolated perfused rat kidney

84%

Moreno J. M., Rodriguez Gomez I., Wangensteen R., Perez-Abud R., Duarte J., Osuna A., Vargas F.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 3

325-332

The vasoconstrictor effect of hydrogen peroxide (H2O2) on isolated perfused rat kidney was investigated. H2O2 induced vasoconstriction in the isolated rat kidney in a concentration-dependent manner. The vasoconstrictor effects of H2O2 were completely inhibited by 1200 U/ml catalase. Endothelium-removal potentiated the renal response to H2O2. The H2O2 dose-response curve was not significantly modified by administration of the NO inhibitor L-NAME (10-4 mol/l), whereas it was increased by the non-specific inhibitor of K+-channels, tetraethylammonium (3·10-3 mol/l). Separately, removal of extracellular Ca2+, administration of a mixture of calcium desensitizing agents (nitroprusside, papaverine, and diazoxide), and administration of a protein kinase C (PKC) inhibitor (chelerythrine, 10-5 mol/l) each significantly attenuated the vasoconstrictor response to H2O2, which was virtually suppressed when they were performed together. The pressor response to H2O2 was not affected by: dimethyl sulfoxide (7·10-3 mol/l) plus mannitol (3·10-3 mol/l); intracellular Ca2+ chelation using BAPTA (10-5 mol/l); calcium store depletion after repeated doses of phenylephrine (10-5 g/g kidney); or the presence of indomethacin (10-5 mol/l), ODYA (2·10-6 mol/l) or genistein (10-5 mol/l). We conclude that the vasoconstrictor response to H2O2 in the rat renal vasculature comprises the following components: 1) extracellular calcium influx, 2) activation of PKC, and 3) stimulation of pathways leading to sensitization of contractile elements to calcium. Moreover, a reduced pressor responsiveness to H2O2 in female kidneys was observed.

9

CGP 42112A abolishes facilitation of recognition caused by angiotensin II and angiotensin II[3-7] in rats

84%

Braszko J. J., Kulakowska A., Winnicka M. M., Karwowska-Polecka W.

Acta Neurobiologiae Experimentalis

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1997

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tom 57

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nr 3

10

Positive and negative outcomes of L-arginine therapy in cardiovascular diseases

67%

Herbaczynska-Cedro K.

Journal of Physiology and Pharmacology

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1999

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tom 50

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nr 4

Ograniczanie wyników

Mechanisms of vasodilatatory effect of perivascular tissue of human internal thoracic artery

Isoprostanes in atherosclerosis

The role of the adenosine triphosphate-sensitive potassium channels in pinacidil-induced vasodilatation of the human saphenous vein in patients with and without type 2 diabetes mellitus

Effects of meconium on airway reactivity to histamine and acetylcholine in vitro

Selective inhibition of guanylate cyclase prevents impairment of hypoxic pulmonary vasoconstriction in endotoxemic mice

The effect of vasoconstrictors on oxygen consumption in resting and contracting skeletal muscle of the autologous pump-perfused rat hindlimb

Mechanisms of vascular dysfunction after subarachnoid hemorrhage

Mechanisms of hydrogen peroxide-induced vasoconstriction in the isolated perfused rat kidney

CGP 42112A abolishes facilitation of recognition caused by angiotensin II and angiotensin II[3-7] in rats

Positive and negative outcomes of L-arginine therapy in cardiovascular diseases