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1.
Chinese Pharmacological Bulletin ; (12): 74-83, 2017.
Article in Chinese | WPRIM | ID: wpr-509258

ABSTRACT

Aim To explore the effects of hypertension on the contractibility of rat basilar artery and its inter-actions with the sodium pump activity.Methods The basilar artery was respectively isolated from Wistar and SHR rats,and the isometric tension of arterial rings was measured by Multi Myograph System-610M.The cont-ractibilities of arterial rings induced by KCl or 5-HT were compared between the basilar arteries of the two groups of rats to analyze the effect of hypertension on the cerebral vascular tension and the activity of sodium pump.Results In SHR rats,the concentration-re-sponse curves of the contraction of isolated basilar ar-tery rings induced by KCl and 5-HT were significantly shifted to right,and the relaxation of vascular tone in-duced by K+which was reintroduced from the external was attenuated compared with those in the WR.These results suggested that hypertension could significantly decrease the activity of the sodium pump and the con-tractile responses of KCl and 5-HT.OUA could con-tract the basilar artery in a concentration-dependent manner,and its concentration-response curve was opti-mally fitted by a two-site binding model:Kd was 1.7 ×10 -8 and 1.6 ×10 -5 mol·L-1,respectively.The results indicated that the two different function sodium pumps existed in the rat basilar artery:one with the high OUA affinity and the other with the low OUA af-finity.If the high and low affinity sodium pumps were inhibited by 5 ×10 -7 and 10 -4 mol · L-1 OUA,re-spectively,the concentration-response curves of KCl and 5-HT would shift to left in SHR rats but not in WR rats.It suggested that OUA could enhance the contrac-tion induced by KCl and 5-HT significantly,and a concentration-dependent effect was observed in the SHR vascular contraction induced by 5-HT (r =0.9393 ,P<0.05 ).When the two concentrations of OUA were applied,there was no significant difference in the shift left of the concentration-response curves in-duced by KCl in the SHR cerebral vessels.However, the marked difference was shown in the shift left in-duced by 5-HT.The results implied that only the high affinity sodium pump was involved in the contractile re-sponse of SHR cerebral vascular to KCl,whereas,the contractile response of SHR cerebral vascular to 5-HT was induced by both high and low affinity sodium pumps.Conclusion Hypertension could lower the contractile response of the basilar artery to vasocon-strictors,and the mechanism might relate to the de-creased sensitivity of the sodium pump induced by hy-pertension or the increased sensibility of the sodium pump to OUA.

2.
Chinese Journal of Pathophysiology ; (12): 819-822,832, 2010.
Article in Chinese | WPRIM | ID: wpr-594462

ABSTRACT

Pulmonary artery hypertension is a serious disease in respiratory system and a key tache in the mechanism of pulmonary-heart disease. The pathological changes include the contraction and remodeling of the pulmonary vessels. There are more and more studies on the pulmonary artery hypertension because of its refractory character and the following increasing mortality. This article summarizes the updating research of the factors and mechanism studied on pulmonary artery hypertension recently, to provide a new view for the clinical and basic medical investigation.

3.
Chinese Pharmacological Bulletin ; (12)2003.
Article in Chinese | WPRIM | ID: wpr-564539

ABSTRACT

Aim Series of compounds,which were considered to be the antagonists of ET-1 receptor,were synthesized by Beijing Institute of Pharmacology and Toxicology.The biological activity of these compounds was screened and some active compounds were selected for further pharmacological characterization on pulmonary hypertension.Methods Radioligand binding assay was performed to study the binding affinity of compounds for ETA and ETB receptors.The biological activity of compounds was evaluated in isolated rat aortic ring and in systemic arterial pressure(SAP)of anesthetized rat experiments.In addition,hypotensive effect of compounds was investigated on monocrotaline induced pulmonary hypertension in rats.Results Compounds bind to ETA receptor had over 10 000 fold higher affinity than to ETB receptor.Contraction induced by ET-1 in isolated rat aortic ring was inhibited by compounds,and 1 ?mol?L-1 ETP-508 shifted the cumulative concentration-contraction response curve to ET-1 to right with no change in the maximal response.In vivo,the increase in SAP induced by ET-1 〔3.7 ?g?(0.5 ml)-1?kg-1〕 was inhibited by 2 mg?kg-1 compounds by intravenous infusion.Furthermore,BQ-485 and ETP-508 by intravenous infusion(0.4 mg?h-1)significantly inhibited 80 mg?kg-1(sc)monocrotaline induced pulmonary hypertension in rats.Conclusions These results indicate that ETP-508 and BQ-485 are highly selective ETA receptor antagonists and significantly inhibite monocrotaline induced pulmonary hypertension in rats.

4.
Korean Journal of Nephrology ; : 381-392, 2001.
Article in Korean | WPRIM | ID: wpr-98004

ABSTRACT

It is well known that the endothelium plays an important role in the circulation by modulating contractile responses of vascular smooth muscle. This study was designed to investigate the alterations and the mechanisms of endothelial modulation in chronic 2-kidney, 1 clip(2K1C) hypertensive rats. 2K1C hypertension was made by clipping the left renal artery and age-matched control rats received a sham treatment. Aortic rings were mounted in tissue baths for measurement of isometric tension. In rings with endothelium, norepinephrine evoked concentration-dependent contraction. Endothelium removal markedly enhanced the contraction, and the responses were less pronounced in 2K1C rats than control rats. Similar fashion of the contractions by endothelium removal was observed with norepinephrine and the alpha1 drenoceptor agonist phenylephrine in control rats, while phenylephrine did not alter the contraction by endothelium removal in 2K1C rats. The alpha2 drenoceptor agonist clonidine also greatly enhanced the contraction after endothelium removal, however the endothelial inhibition was still shown in 2K1C rats. In contrast to norepinephrine-induced contractions, the enhancement of serotonin-or prostaglandin F2alpha - induced contractions after endothelium removal was small and similar in 2K1C and control rats. NG-nitro-L-arginine methyl ester enhanced the contraction induced by agonists in aortic rings with endothelium, which was similar to the response in rings without endothelium. The relaxation response to acetylcholine was attenuated in 2K1C rats, while the response to sodium nitroprusside remained unaltered. These results indicate the endothelium plays an inhibitory role against contractions in rat aorta by releasing nitric oxide, but the characteristics of the endothelial inhibition are not identical against various agonists. The negative endothelial modulation is more pronounced during alpha1 and alpha2 renoceptor- mediated contractions than during contractions mediated by other receptors. In addition, the inhibitory role of the endothelium against alpha1 drenoceptor agonist-induced contraction is impaired in 2K1C renal hypertension.


Subject(s)
Animals , Rats , Acetylcholine , Aorta , Baths , Clonidine , Dinoprost , Endothelium , Hypertension , Hypertension, Renal , Muscle, Smooth, Vascular , NG-Nitroarginine Methyl Ester , Nitric Oxide , Nitroprusside , Norepinephrine , Phenylephrine , Placebos , Relaxation , Renal Artery , Vasoconstriction
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