1,720,976 research outputs found
Studies of the cardiovascular effects of nociceptin and related peptides
No full textNociceptin, a novel opioid peptide, and its ORL1 receptor share structural similarities with other opioid ligands and receptors. Although
NC exerts evident cardiovascular effects at a central and peripheral level, its role in homeostatic mechanisms and disease states are just
beginning to be understood, as only recently selective receptor antagonists became available. In this review, some of the new observations
regarding the cardiovascular actions of NC, related peptides and newly synthesized receptor antagonists are discussed
Ramipril improves hemodynamic recovery but not microvascular response to ischemia in spontaneously hypertensive rats
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Enhanced blood pressure sensitivity to deoxycorticosterone in mice with disruption of bradykinin B2 receptor gene.
No full textAngiotensin II type 1 receptor blockade prevents cardiac remodeling in bradykinin B(2) receptor knockout mice
No full textRole of the bradykinin B2 receptor in the maturation of blood pressure phenotype: lesson from transgenic and knockout mice
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Transplantation of low dose CD34+KDR+ cells promotes vascular and muscular regeneration in ischemic limbs
No full textHematopoietic progenitor cell transplantation can contribute to revascularization of ischemic tissues. Yet, the optimal cell population to be transplanted has yet to be determined. We have compared the therapeutic potential of two subsets of human cord blood CD34+ progenitors, either expressing the VEGF-A receptor 2 (KDR) or not. In serum-free starvation culture, CD34+KDR+ cells reportedly showed greater resistance to apoptosis and ability to release VEGF-A, as compared with CD34+KDR- cells. When injected into the hind muscles in immunodeficient SCIDbg mice subjected to unilateral ischemia, a low number (10(3)) of CD34+KDR+ cells improved limb salvage and hemodynamic recovery better than a larger dosage (10(4)) of CD34+KDR- cells. The neovascularization induced by KDR+ cells was significantly superior to that promoted by KDR- cells. Similarly, endothelial cell apoptosis and interstitial fibrosis were significantly attenuated by KDR+ cells, which differentiated into mature human endothelial cells and also apparently skeletal muscle cells. This study demonstrates that a low number of CD34+KDR+ cells favors reparative neovascularization and possibly myogenesis in limb ischemia, suggesting the potential use of this cell population in regenerative medicine
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Cardiovascular effects of nociceptin in unanesthetized mice
No full textWe evaluated the systemic hemodynamic effects induced by nociceptin (NC) and NC-related peptides,
including the NC receptor antagonist [Phe1c(CH2-NH)Gly2]NC(1–13)NH2 ([F/G]NC(1–13)NH2) in unanesthetized
normotensive Swiss Morini mice. Bolus intravenous injection of NC decreased mean blood pressure and heart rate. The
hypotensive response to 10 nmol/kg NC lasted ,10 minutes, whereas a more prolonged hypotension was evoked by 100
nmol/kg (from 11463 to 9762 mm Hg at 10 minutes, P,0.01). The latter dose reduced heart rate from 542643 to
479631 beats/min (P,0.05) and increased aortic blood flow by 4165% (P,0.05). Hypotension and bradycardia were
also evoked by NC(1–17)NH2 and NC(1–13)NH2 fragments, whereas NC(1–13)OH and NC(1–9)NH2 were ineffective.
Thiorphan, an inhibitor of neutral endopeptidase 24.11, enhanced the hypotension induced by NC(1–13)NH2 and
revealed the ability of NC(1–13)OH to decrease mean blood pressure. [F/G]NC(1–13)NH2, a recently synthesized
antagonist of the NC receptor, did not alter basal mean blood pressure or heart rate, but it prevented the hypotension,
bradycardia, and increase in aortic blood flow evoked by NC. In contrast, [F/G]NC(1–13)NH2 did not alter the
hypotension induced by bradykinin or endomorphin-1 (a m-receptor agonist), and the bradycardia induced by
leu-enkephalin (a d-receptor agonist) or U504885 (a synthetic k-receptor agonist). In conclusion, NC and some of its
fragments cause hypotension and bradycardia and increase aortic blood flow in mice, with the NC(1–13) sequence being
critical for these biological effects. Our results also demonstrate that the compound [F/G]NC(1–13)NH2 is a potent and
selective antagonist of the NC receptor in vivo
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