Synchronization in the Heart Rate and the Vasomotion in Rat Aorta: Effect of Arsenic Trioxide

Abstract

Arsenic trioxide (As2O3) is used clinically in the management of acute promyelocytic leukemia, and the use of electrocardiogram (ECG) in this management is important as arsenic use may cause distortion of the electrical properties with its attendant sequel. We studied the effect of As2O3 on vasomotion in rat aortic rings using isometric tension recordings and ECG in anesthetized rats. The results showed that As2O3 (10(-5) M) significantly (p < 0.01) reduced the frequency of acetylcholine (10(-5) M ACh)- and KCl (10 mM)-induced vasomotion, and it also increased the relaxation time (R t) of vasomotion. This effect was restored by 10(-8) M sodium nitroprusside (nitric oxide donor). ACh-induced NO release in the aorta was blunted in the presence of As2O3. The corrected QT interval (QTc) of the ECG, and time dilation (T d) of the pulse wave in the tail artery of the anesthetized rat were significantly (p < 0.05) increased in the arsenic-treated group (50 ppb As) versus control. In conclusion, data suggest that arsenic-induced reduction in vasomotion frequency of the isolated aortic rings is associated with a decreased bioavailability of NO, an increase in QTc and a decrease in the frequency of the pulse wave generated by the cardiac cycle in anesthetized rats.

8-Oxo-9-Dihydromakomakine Isolated from Aristotelia chilensis Induces Vasodilation in Rat Aorta: Role of the Extracellular Calcium Influx

“…The KCl-induced contraction was caused by an increase of extracellular potassium, leading to membrane depolarization, which increases calcium influx from extracellular sources, involving voltage-dependent calcium channels [ 9 ]. BaCl 2 and TEA block inward rectifying potassium channels [ 10 ], or potassium channels activated by calcium [ 11 ], respectively, thus depolarizing the plasma membrane and vasoconstriction. Similar results were obtained with the inhibition of Na,K-ATPase, which causes depolarization of plasma membrane and induced vasoconstriction [ 12 ].…”

“…After the equilibration period for 30 min, the aortic rings were stabilized by three successive near-maximum contractions with KCl (6 × 10 −2 M) for 10 min. The passive tension on aorta was 1.0 g, which was determined to be the resting tension for obtaining maximum active tension induced by 6 × 10 −2 M KCl [ 10 ].…”

Modulatory Effect of Guinep (Melicoccus bijugatus Jacq) Fruit Pulp Extract on Isoproterenol-Induced Myocardial Damage in Rats. Identification of Major Metabolites Using High Resolution UHPLC Q-Orbitrap Mass Spectrometry

“…The RR interval was taken as the time elapsed between two consecutive maxima of the R-waves. The corrected QT interval (QTc) was calculated in accordance with the formula [40,41]: QTc = QT/(RR) 1/2 …”

Modulatory Effect of 2-(4-Hydroxyphenyl)amino-1,4-naphthoquinone on Endothelial Vasodilation in Rat Aorta

“…This might affect critically NO levels in the rat aorta. Q7 increased the formation of L-citrulline in HUVEC, compatible with increased NO generation and eNOS activity [ 41 ]. This paradoxical result can be explained in part because the ROS produced by redox-cycling of Q7 react rapidly with generated NO, leading to a reduction of its level [ 38 ].…”

“…In the presence of Q7 , the addition of KCl (10 −2 M) was unable to provoke a total vasodilation in rat aorta preconstricted with BaCl 2 (10 −3 M), an effect which was however obtained at 100% by adding SNP (10 −8 M). The increase of KCl over 2 × 10 −2 M caused repolarization and vasodilation, because the membrane potential moves towards the new K + equilibrium potential, and voltage-dependent Ca 2+ -sensitive K + channels are again opened [ 29 , 41 , 51 ]. These findings may be explained by previous studies, showing that juglone (5-hydroxy-1,4-naphthoquinone) partially blocks voltage-dependent potassium channels, causing depolarization of the membrane [ 52 ].…”