RESUMEN
In the present study, lidocaine relaxed, in a concentration-dependent manner, the contractions induced by either phenylephrine or a high concentration of KCl (60 mM) in endothelium-intact rat aortic rings. Mechanical removal of endothelium did not significantly modify lidocaine-induced vasorelaxation. In endothelium-denuded aortic rings depolarized by 60 mM KCl, lidocaine inhibited Ca2+-induced contraction. Lidocaine also reduced the transient contraction elicited by phenylephrine in Ca2+-free medium. Pretreatment of endothelium-denuded aorta nonspecific K+ with tetraethylammonium, a channel blocker, had no effect on the relaxant effect of lidocaine. These results indicate that lidocaine induces an endothelium-independent relaxation in rat aortic rings. The main mechanisms may include suppression in Ca2+ through the voltage-sensitive Ca2+ influx intracellular Ca2+ channels and inhibition of release in the vascular smooth muscle cells.
RESUMEN
To investigate the vasorelaxant effect of puerarin, tension was recorded from rat thoracic aortic rings. Puerarin completely relaxed the contractions induced by phenylephrine (PE) in a concentration-dependent manner in endothelium-intact and endothelium-denuded rat aorta, while had no effect on those preconstricted by a high concentration of potassium chloride (60 mM). Also, puerarin had no effects on the transient contraction elicited by PE or caffeine in Ca2+- free medium. The relaxant effect of puerarin was significantly inhibited by pretreatment of endothelium-denuded aorta with potassium channel antagonists tetraethylammonium and 4-aminopyridine, but not glibenclamide. These results indicate that puerarin induces an endothelium-independent relaxation in rat aortic rings. The mechanisms may involve the reduction in Ca2+ influx through the non-voltage-sensitive calcium channels and the activation of the potassium channels (voltage-activated K+ channels and large conductance Ca2+ -activated K+ channels, but not ATP-sensitive K+ channels).
RESUMEN
The present study investigated the role of the dorsal column (DC) in the mechanism of the hypotensive effect induced by simulating acupuncture on rat hindlimb. The femoral arterial pressure and electrocardiogram (ECG) of rats were recorded when the hypothalamic paraventricular nucleus (PVN) was electrically stimulated with or without DC lesion. Stimulation of the deep peroneal nerve (DPN) decreased the pressor response elicited by electrical stimulation of the PVN. Thirty minutes after micro-dissection of the right DC, the inhibitory effect of stimulating the right or left DPN on the pressor response induced by stimulation of the contralateral PVN was not altered. Of 6 rats tested, the inhibitory effect of stimulating the right or left DPN could still be observed five days after the right DC was destroyed. The pain responses of both hindlimbs of the rats with the right DC destroyed showed no obvious difference when compared with the sham control rats. These data suggest that the DC is not involved in the inhibitory effect of stimulating the DPN on the pressor response induced by the PVN activation.
RESUMEN
An integrated laboratory course of physiological sciences has been put into use at Zhejiang University School of Medicine since 1993. This course guides students in taking a scientific approach to understanding the contemporary issues in physiology, pathophysioiogy and pharmacology. Students learn to use a variety of basic experimental methods to laboratory work. More importantly, research-oriented experiments are integrated in this course, offering students an opportunity to hone their skills in critical thinking and problem solving. Research presentation skills, both written and oral, are also emphasized. This integrated laboratory course is highly appreciated by students and medical educators. We recommend this innovative teaching format as a more integrated approach to medical education.
RESUMEN
We have investigated the effects of bradykinin (BK) and ATP on Ca2+ transient induced by electrical-field stimulation in freshly isolated rabbit ventricular myocytes, in the presence or absence of rabbit aortic endothelial cells. BK and ATP induced an increase in intracellular Ca2+ concentration ([Ca2+]i) in the endothelial cells, but had no significant effect on Ca2+ transient in electrical-field stimulated ventricular myocytes. In the presence of cultured endothelial cells, the amplitude of Ca2+ transient induced by electrical stimulation in ventricular myocytes was decreased. BK and ATP further reduced the amplitude of Ca2+ transient induced by electrical stimulation in ventricular myocytes. These data show that BK and ATP have endothelium-dependent depressing effects on ventricular myocytes and indicate that substances released from endothelial cells in response to BK and ATP stimulation can modulate ventricular myocytes excitation-contraction coupling. However, identification of the cardioactive mediators produced by the endothelial cells requires further study.