|1.||Zhao, Qing: 2 articles (12/2007 - 04/2006)|
|2.||Jinnah, H A: 2 articles (11/2003 - 05/2000)|
|3.||Lagler, Michael: 1 article (09/2013)|
|4.||Rubi, Lena: 1 article (09/2013)|
|5.||Schandl, Ulla: 1 article (09/2013)|
|6.||Geier, Petra: 1 article (09/2013)|
|7.||Gupta, Kuheli Das: 1 article (09/2013)|
|8.||Boehm, Stefan: 1 article (09/2013)|
|9.||Spies, Daniel: 1 article (09/2013)|
|10.||Kubista, Helmut: 1 article (09/2013)|
09/01/2013 - "However, long-lasting seizure-like activity induced by various pharmacological means was affected by Bay K8644 in a bimodal manner, with increases in one group of neurons and decreases in another group. "
01/01/1995 - "The highest dose of BAY K 8644 also induced fatal convulsions in 3 animals. "
11/01/1992 - "5. These results show that Bay k 8644 seizures are relatively resistant to some anticonvulsant compounds. "
11/01/1992 - "2. Seizures were induced by intracerebroventricular injection of Bay k 8644. "
07/01/1990 - "BAY K 8644 increased the number of mice dying from tonic-extension convulsions to PTZ. "
12/01/1995 - "Therefore, the potency of relaxin was determined against spasms reliant predominantly upon either extracellular Ca2+ or intracellular Ca2+. Uterine spasms dependent upon extracellular Ca2+ were elicited by (i) oxytocin (0.2 nM) (ii) Bay K 8644 (1 microM) in 10 mM K(+)-rich PSS and (iii) KCl (80 mM). "
09/01/1985 - "In trachea bathed by Krebs solution containing indomethacin 0.8 mumol l-1, Bay K 8644 (0.01-1 mumol l-1) evoked mild spasm. "
12/01/1995 - "6. Relaxin was much less potent against the spasm dependent upon intracellular Ca2+ (that induced by oxytocin (20 nM) + nifedipine (500 nM)) than against the spasms dependent upon extracellular Ca2+, those induced by oxytocin (0.2 nM) and Bay K 8644 (1 microM). "
12/01/1995 - "3. Relaxin and nifedipine were slightly less potent against the spasm induced by Bay K 8644 (1 microM) than against spasm induced by oxytocin (0.2 nM) (15 fold and 13 fold respectively). "
05/01/2000 - "In a porcine model of coronary spasm with balloon injury, both receptor-mediated stimulation of L-type Ca2+ channels by serotonin and direct stimulation of the channels by Bay K 8644 (a dihydropyridine Ca2+ channel agonist) repeatedly induced coronary spasm in vivo, which was abolished by pretreatment with nifedipine, a dihydropyridine Ca2+ channel antagonist. "
10/01/2010 - "Appropriate BayK8644 preconditioning can induce transient Ca²+ influx, and elicit strong protection against the lung ischemia-reperfusion injury, which can simulate the endogenous protective effect of ischemic preconditioning."
10/01/2010 - "To explore the protective effect of calcium channel agonist BayK8644 preconditioning on the lungs against ischemia-reperfusion injury (I/R) and its mechanism in rabbits. "
10/01/2010 - "[Protective effect of calcium channel agonist BayK8644 on lungs against ischemia-reperfusion injury in rabbits]."
12/01/1998 - "The aim of the present study was to measure the effects of the L-type Ca2+ channel activator, Bay K 8644, on the haemodynamics of rats with cirrhosis. "
12/01/1998 - "In conclusion, in rats with cirrhosis, Bay K 8644 administration reduced vasodilation in splanchnic and systemic arteries and did not affect hepatocollateral vascular resistance. "
02/01/1995 - "Pressor responses to Bay K 8644 did not differ between normal rats and rats with cirrhosis (8.8 +/- 0.9 vs. 10.5 +/- 2.1 micrograms/kg). "
12/01/1998 - "In vitro and in vivo vascular responses to the L-type calcium channel activator, Bay K 8644, in rats with cirrhosis."
02/01/1995 - "Lack of vascular hyporesponsiveness to the L-type calcium channel activator, Bay K 8644, in rats with cirrhosis."
|5.||Hypertension (High Blood Pressure)
06/01/2012 - "The sensitivity of LTCCs increased during hypertension, as in vivo there was a greater increase in mean arterial pressure (MAP) to BAYK8644 [10 µg kg(-1), WKY: 59.5 (9.3)%; SHR: 97.7 (6.3)%, P<0.05] with exaggerated constriction of arterioles [10 µg kg(-1), WKY: 9.1 (2.5)%; SHR: 19.1 (2.6)%, P<0.05]. "
03/01/1997 - "Several observations using various experimental approaches support this hypothesis: 1) the contractile activity in response to depolarizing stimuli is increased in arteries from hypertensive animals demonstrating increased voltage-dependent Ca2+ channel activity in hypertension; 2) Ca2+ channel agonists such as Bay K 8644 produce contractions in isolated arterial segments from hypertensive rats and minimal contraction in those from normotensive rats; 3) intracellular Ca2+ concentration is abnormally increased in vascular myocytes from hypertensive animals following treatment with Ca2+ channel agonists and depolarizing interventions, and 4) using the voltage-clamp technique, the inward Ca2+ current in arterial myocytes from hypertensive rats is nearly twice as large as that from myocytes of normotensive rats. "
02/03/1994 - "Hypertension is associated with a hypersensitive response to the Ca2+ channel activator, Bay K 8644. "
05/01/1993 - "Contractile responses to Bay K 8644 in rats with coarctation-induced hypertension."
01/01/1990 - "Increased vascular reactivity to Bay K 8644 in genetic hypertension."
|9.||Calcium Channels (Calcium Channel)
|10.||Calcium Channel Agonists
|3.||Sodium-Restricted Diet (Diet, Sodium Restricted)