"Spont\u00E1nn\u00ED i soln\u00E1 hypertenze jsou charakterizov\u00E1ny sympatickou hyperaktivitou a relativn\u00ED nedostate\u010Dnost\u00ED NO syst\u00E9mu, co\u017E m\u00E1 za n\u00E1sledek nerovnov\u00E1hu vazoaktivn\u00EDch syst\u00E9m\u016F. P\u0159evaha vazokonstrik\u010Dn\u00EDch nad vazodilata\u010Dn\u00EDmi mechanismy je u hypertenzn\u00EDch potkan\u016F spojena se zv\u011Bt\u0161enou nifedipin-senzitivn\u00ED slo\u017Ekou krevn\u00EDho tlaku. \u00DAkolem tohoto projektu je p\u0159isp\u011Bt ke studiu \u00FAlohy norepinefrinu (NE) a oxidu dusnat\u00E9ho (NO) v regulaci v\u00E1pn\u00EDkov\u00E9ho influxu skrze nifedipin-senzitivn\u00ED nap\u011B\u0165ov\u011B \u0159\u00EDzen\u00E9 v\u00E1pn\u00EDkov\u00E9 kan\u00E1ly (VDCC) v c\u00E9v\u00E1ch normotenzn\u00EDch a hypertenzn\u00EDch potkan\u016F. Na\u0161e paraleln\u00ED in vivo a in vitro experimenty s antagonisty v\u00E1pn\u00EDkov\u00FDch kan\u00E1l\u016F by m\u011Bly uk\u00E1zat 1) zda za hlavn\u00ED \u010D\u00E1st sympatick\u00E9 vazokonstrikce odpov\u00EDd\u00E1 otev\u0159en\u00ED VDCC, a 2) zda NO-dependentn\u00ED vazodilatace je zprost\u0159edkov\u00E1na zejm\u00E9na uzav\u0159en\u00EDm VDCC. Zvl\u00E1\u0161tn\u00ED pozornost bude zam\u011B\u0159ena na cesty (G(alfa)i proteiny, Ca+-dependentn\u00ED K+ kan\u00E1ly), jejich\u017E prost\u0159ednictv\u00EDm mohou NE a NO ovliv\u0148ovat otev\u0159en\u00ED VDCC." . "2011-03-18+01:00"^^ . . " vasoconstriction" . " calcium influx" . "0"^^ . . " nitric oxide" . . "1"^^ . "voltage-dependent calcium channels" . "2013-06-28+02:00"^^ . . "Both spontaneous and salt hypertension are characterized by sympathetic hyperactivity and relative NO deficiency resulting in the imbalance of pressor and depressor systems. The dominance of vasoconstrictor over vasodilator mechanisms in hypertensive rats is associated with enhanced nifedipine-sensitive blood pressure (BP) component. The aim of this project is to determine the involvement of norepinephrine (NE) and nitric oxide (NO) in the control of calcium influx through nifedipine-sensitive voltage-dependent calcium channels (VDCC) in blood vessels of normotensive and hypertensive rats. Our parallel in vivo and in vitro experiments with calcium channel antagonists should demonstrate 1) if a major part of sympathetic vasoconstriction is due to the opening od VDCC, and 2) if NO-dependent vasodilation is mediated mainly by closing of VDCC. Special attention will be paid to the pathways (G(alpha)i proteins, Ca2+-dependent K+ channels) by which NE and NO can influence the state of VDCC."@en . "0"^^ . . . . . "Neurohumoral control of calcium influx: nifedipine-sensitive component of blood pressure in experimental hypertension"@en . . "15"^^ . "15"^^ . . " norepinephrine" . . "2011-12-31+01:00"^^ . . "Neurohumor\u00E1ln\u00ED kontrola v\u00E1pn\u00EDkov\u00E9ho influxu: nifedipin-senzitivn\u00ED slo\u017Eka krevn\u00EDho tlaku u experiment\u00E1ln\u00ED hypertenze" . "2009-01-01+01:00"^^ . . . . "voltage-dependent calcium channels; calcium influx; norepinephrine; nitric oxide; vasoconstriction; genetic hypertension; salt hypertension"@en . . "U genetick\u00E9 hypertenze byla prok\u00E1z\u00E1na 1) \u00FAloha zv\u00FD\u0161en\u00E9ho vstupu v\u00E1pn\u00EDku v d\u016Fsledku nadm\u011Brn\u00E9 sympatick\u00E9 aktivity i nedostate\u010Dn\u00E9ho dilata\u010Dn\u00EDho p\u016Fsoben\u00ED NO, 2) v\u00FDznam inhibi\u010Dn\u00EDch G protein\u016F pro sympatickou vasokonstrikci a 3) kompenza\u010Dn\u00ED aktivace K+ kan\u00E1l\u016F"@cs . "The importance of increased Ca2+ entry due to high sympathetic activity or low dilatory action of NO, the role of inhibitory G proteins for sympathetic vasoconstriction and compensatory activation of K+ channels was demonstrated in genetic hypertension"@en . . " genetic hypertension" . . "http://www.isvav.cz/projectDetail.do?rowId=IAA500110902"^^ . . "IAA500110902" .