Effects of Breviscapine on the contraction of rabbit aorta strips induced by noradrenaline and high potassium / 中国药理学通报

Aim To observe the effects of Breviscapine (Bre) on the contractions induced by noradrenaline (NA) and high potassium in rabbit aorta strips and to investigate the relationships of these effects to the changes of intracellular free calcium( i). Methods The effects of Bre on the concentration-response curves for NA and high potassium, and on the transient contractions induced by NA and caffeine in Ca 2+-free medium and the sustained contraction by NA after replenishing Ca 2+ were surveyed using rabbit aorta strips; the changes of i increased by NA and high potassium in the presence of Bre were determined using fura-2/AM loaded cultured smooth muscle cells of rabbit aorta. Results Bre shifted the concentration-response curve for NA to right in a dose-dependent manner , but shifted that for high potassium to left; it inhibited the transient contraction induced by NA and caffeine in the Ca 2+-free medium and the sustained contraction induced by NA after replenishing Ca 2+; Bre inhibited the i increased by NA, but enhanced that increased by high potassium in the smooth muscle cells of rabbit aorta. Conclusion Bre inhibits the contraction induced by NA through its inhibition effects on Ca 2+-influx and Ca 2+-release ; it enhances the Ca 2+-influx induced by high potassium, but the mechanism by which Bre enhances the high potassium inducing Ca 2+ -influx is not known.

The Effect of Saponin on the Vascular Contractility of the Rabbit Aortic Ring

PURPOSE: There have been conflicting reports on vascular response to Panax ginseng. The conflicting reports may be due to difference of ingredient of Panax ginseng. The aim of the present study was to investigate the effect of saponin, the main ingredient of Panax ginseng, on the vascular contractility. METHODS: The rabbit aortic rings were cut and mounted on the force transducer to record an isometric tension on polygraph. To elucidate the mechanism of saponin effect on vascular smooth muscle, the contractility of the vascular smooth muscle were measured under varying experimental condition. RESULTS: 1) When the aortic rings were precontracted with norepinephrine, saponin caused biphasic(initial relaxation-sustained contraction) dose-response in the endothelium dependent manner. But saponin had no effect on the resting tension. 2) When EDRF inhibitors such as methylene blue(10(-5)M), hemoglobin(10(-5)M), N-omega-nitro-L-arginine(100microM) were added to precontracted ring with norepinephrine, the initial relaxation caused by 2mg% saponin was inhibited. 3) When Ca(2+)-channel blocker, nifedipine(5x10(-7)M), was added to precontracted rings with norepinephrine, the sustsined contraction by saponin was inhibited. 4) When hemoglobin(10(-5)M) was added to precontracted rings with norepinephrine, the contractility by norepinephrine was increased and this effect was further augmented by 2mg% saponin. CONCLUSIONS: From the above results, it may be concluded that saponin stimulated the release of both an endothelium-dependent relaxing factor and endothelium-dependent contracting factor.

Effects of mastoparan on a vascular contractility in rabbit aorta

Mastoparan is an amphiphilic tetradecapeptide derived from wasp venom which activates G-proteins. Several secondary effects have been attributed to this peptide, including activation of phospholipase and phosphatidylinositol kinase. The aim of the present study was to investigate the effects of mastoparan on vascular contractility. Rabbit aortic rings were cut and mounted on a force transducer to record isometric tension on a polygraph. The effects of mastoparan were then investigated on the contractile responses in the isolated rabbit aorta with or without endothelium. The results were summarized as follows; 1. Mastoparan caused biphasic response, a transient relaxation followed by a further contraction, in norepinephrine (NE)-precontracted ring with endothelium. These effects were not observed in the aorta in the absence of endothelium. 2. Mastoparan-induced transient relaxation was significantly inhibited by treatment with a N-omega-nitro-L-arginine or methylene blue. 3. When an inhibitor of phospholipase C, neomycin was added to the precontracted aortic ring with NE, the transient relaxation induced by mastoparan was inhibited, but sustained contraction was not inhibited. 4. When an inhibitor of phospholipase A2, quinacrine and inhibitor of the cyclooxygenase pathway, indomethacin, were added to a precontracted ring with NE, the transient relaxation induced by mastoparan was not inhibited, but sustained contraction was inhibited. 5. Mastoparan induced a contraction of the aorta either with or without endothelium. Indomethacin and nifedipine inhibited mastoparan-induced contraction. From the above results, we concluded that mastoparan acts on the endothelium and modifies the release of endothelium-derived relaxing factors such as nitric oxide and also endothelium-derived contracting factors such as metabolites of arachidonic acid.

STUDIES ON EFFECTS OF ANISODAMINE TO INTRA-AND EXTRACELLULAR Ca~(2+) IN ISOLATED RABBIT AORTA AND GUINEA PIG ATRIA / 中国药理学通报

In the isolated rabbit aorta, like verapamil ( Ver ) anisodamine ( Ani ) might inhibit the contraction induced by phenylephrine ( PE ) and high K+ with IC50 value of 120 and 86 ? mol/L, respectively. PE/K+ ratio of IC50 was 1.4 which was less than that of Ver. It showed that although PDC may be more sensitive to Ani than ROC, the difference in sensitivity of Ani on 2 calcium chan- nel are less marked than that of some calcium antagonists. Ani had inhibitory effects on 2 contractile components of serotonin (5-HT ) . Ani and Ver could obviously inhibit post-resting potentiatipn and staircase phenomenon in guinea pig atria. Ani also might inhibit the contraction induced by calcium and shift concentration-response nonparallelly to right on both tissues above.The results suggest that Ani possesses nonspecific calcium antagonistic effect and reduces the tension by affecting PDC and ROC to decrease extracellular calcium influx and inhibiting intracellular calcium release.

Mechanism of inhibitory effects of atropine and anisodamine on contractions of rabbit thoracic aorta / 西安交通大学学报(医学版)

0.05, respectively), but those to noradrenaline (NA: 0.01?mol/L), histamine (His: 3?mol/L), and 5-hydroxytryptamine (5-HT: 0.1?mol/L), significantly reduced (P0.05, respectively). Under atropine or Ani pretreatment, the NA-, His- and 5-HT-elicited contractions in endothelium-denuded aorta were similar to those in endothelium-intact aorta. Conclusion Atropine and Ani can inhibit receptors-mediated constrictions of rabbit aortic vascular smooth muscle cells; the actions are endothelia independent.