Blockade of voltage-sensitive Ca2+-channels markedly diminishes nitric oxide- but not L-S-nitrosocysteine- or endothelium-dependent vasodilation in vivo

European Journal of Pharmacology

Volumn 408, Issue 3, 2000, Pages 289-298

  Travis, Mark D ^a   Hoque, Azizul ^b   Bates, James N ^a   Lewis, Stephen J ^c  

^a UNIVERSITY OF IOWA   (United States)

^b UNIVERSITY OF LOUISVILLE   (United States)

^c UNIVERSITY OF GEORGIA   (United States)

Author keywords

Ca2+ channel, voltage sensitive; EDRF (endothelium derived relaxing factor); Nitric oxide (NO); S Nitrosothiol; Vasodilation

Indexed keywords

ACETYLCHOLINE; CALCIUM; CALCIUM CHANNEL; ENDOTHELIUM DERIVED RELAXING FACTOR; INDOMETACIN; NIFEDIPINE; NITRIC OXIDE; NITROPRUSSIDE SODIUM; S NITROSOCYSTEINE; VASODILATOR AGENT;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CONTROLLED STUDY; HEMODYNAMICS; MALE; MEAN ARTERIAL PRESSURE; NONHUMAN; PRIORITY JOURNAL; RAT; VASCULAR RESISTANCE; VASCULAR SMOOTH MUSCLE; VASODILATATION;

ACETYLCHOLINE; ANIMALS; CALCIUM CHANNEL BLOCKERS; CALCIUM CHANNELS; CYSTEINE; ENDOTHELIUM, VASCULAR; HEMODYNAMIC PROCESSES; HYDRAZINES; INDOMETHACIN; MALE; NIFEDIPINE; NITRIC OXIDE; NITROPRUSSIDE; NITROSO COMPOUNDS; RATS; RATS, SPRAGUE-DAWLEY; S-NITROSOTHIOLS; SODIUM CHLORIDE; VASODILATION; VASODILATOR AGENTS;

EID: 0034711577     PISSN: 00142999     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0014-2999(00)00792-5     Document Type: Article

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