{"title":"PO-101抑制有氧运动对高血压患者PKC/CaV1.2通路的影响,增强血管平滑肌功能","authors":"Yu Chen, Lijun Shi","doi":"10.14428/EBR.V1I4.8723","DOIUrl":null,"url":null,"abstract":"Objective The purpose of this study was to investigate the effects of aerobic exercise on PKC/CaV1.2 pathway in mesenteric arterial smooth muscle from spontaneously hypertensive rats (SHRs) \nMethods Twelve-week-old male normotensive Wistar–Kyoto (WKY) rats and SHRs were randomly assigned to sedentary groups (SHR-SED, WKY-SED) and exercise training groups (SHR-EX, WKY-EX). Exercise groups were performed an 8-week moderate-intensity treadmill running. After 8 weeks, vascular contractility of mesenteric arteries was measured. Vascular smooth muscle cells (VSMCs) were obtained with an enzymatic isolation method. CaV1.2 channel currents were examined by using whole-cell patch clamp recording technique. \nResults 1) Body weight and systolic blood pressure (SBP) in both WKY-EX and SHR-EX were significantly lower than those of their sedentary counterparts (both P<0.05). Body weight in SHR-SED was remarkably lower than WKY-SED (P<0.05), while SBP was much higher than WKY-SED (P<0.05). 2) PDBu (PKC activator) elicited a tension increase, and Gö6976 (PKC inhibitor) induced vasodilation. Both the responses of PDBu and Gö6976 in SHR-SED were notably increased compared with WKY-SED (both P<0.05), however, exercise training significantly suppressed these increases (both P<0.05). 3) Nifedipine (CaV1.2 inhibitor) induced vasodilation. Response to nifedipine in SHR-SED was more sensitive than both SHR-EX and WKY-SED (both P<0.05). 4). The current density of SHR-SED and WKY-EX exhibited an increase compared to the WKY-SED (both P<0.05), and the current density of the SHR-EX decreased obviously in contrast with SHR-SED (P<0.05). Besides, PDBu enlarged current density of all the groups, while Gö6976 decreased current density. The increase or decrease amplitude in SHR-SED was significantly higher than WKY-SED (both P<0.05), whereas exercise training markedly inhibited those responses (both P<0.05). \nConclusions Aerobic exercise efficiently prevents the upregulation of PKC/CaV1.2 pathway in hypertension, and enhances the function of vascular smooth muscle.","PeriodicalId":12276,"journal":{"name":"Exercise Biochemistry Review","volume":"44 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2018-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"PO-101 Inhibition of Aerobic Exercise on PKC/CaV1.2 pathway enhanced the function of vascular smooth muscle in hypertension\",\"authors\":\"Yu Chen, Lijun Shi\",\"doi\":\"10.14428/EBR.V1I4.8723\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Objective The purpose of this study was to investigate the effects of aerobic exercise on PKC/CaV1.2 pathway in mesenteric arterial smooth muscle from spontaneously hypertensive rats (SHRs) \\nMethods Twelve-week-old male normotensive Wistar–Kyoto (WKY) rats and SHRs were randomly assigned to sedentary groups (SHR-SED, WKY-SED) and exercise training groups (SHR-EX, WKY-EX). Exercise groups were performed an 8-week moderate-intensity treadmill running. After 8 weeks, vascular contractility of mesenteric arteries was measured. Vascular smooth muscle cells (VSMCs) were obtained with an enzymatic isolation method. CaV1.2 channel currents were examined by using whole-cell patch clamp recording technique. \\nResults 1) Body weight and systolic blood pressure (SBP) in both WKY-EX and SHR-EX were significantly lower than those of their sedentary counterparts (both P<0.05). Body weight in SHR-SED was remarkably lower than WKY-SED (P<0.05), while SBP was much higher than WKY-SED (P<0.05). 2) PDBu (PKC activator) elicited a tension increase, and Gö6976 (PKC inhibitor) induced vasodilation. Both the responses of PDBu and Gö6976 in SHR-SED were notably increased compared with WKY-SED (both P<0.05), however, exercise training significantly suppressed these increases (both P<0.05). 3) Nifedipine (CaV1.2 inhibitor) induced vasodilation. Response to nifedipine in SHR-SED was more sensitive than both SHR-EX and WKY-SED (both P<0.05). 4). The current density of SHR-SED and WKY-EX exhibited an increase compared to the WKY-SED (both P<0.05), and the current density of the SHR-EX decreased obviously in contrast with SHR-SED (P<0.05). Besides, PDBu enlarged current density of all the groups, while Gö6976 decreased current density. The increase or decrease amplitude in SHR-SED was significantly higher than WKY-SED (both P<0.05), whereas exercise training markedly inhibited those responses (both P<0.05). \\nConclusions Aerobic exercise efficiently prevents the upregulation of PKC/CaV1.2 pathway in hypertension, and enhances the function of vascular smooth muscle.\",\"PeriodicalId\":12276,\"journal\":{\"name\":\"Exercise Biochemistry Review\",\"volume\":\"44 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2018-10-22\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Exercise Biochemistry Review\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.14428/EBR.V1I4.8723\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Exercise Biochemistry Review","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.14428/EBR.V1I4.8723","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
PO-101 Inhibition of Aerobic Exercise on PKC/CaV1.2 pathway enhanced the function of vascular smooth muscle in hypertension
Objective The purpose of this study was to investigate the effects of aerobic exercise on PKC/CaV1.2 pathway in mesenteric arterial smooth muscle from spontaneously hypertensive rats (SHRs)
Methods Twelve-week-old male normotensive Wistar–Kyoto (WKY) rats and SHRs were randomly assigned to sedentary groups (SHR-SED, WKY-SED) and exercise training groups (SHR-EX, WKY-EX). Exercise groups were performed an 8-week moderate-intensity treadmill running. After 8 weeks, vascular contractility of mesenteric arteries was measured. Vascular smooth muscle cells (VSMCs) were obtained with an enzymatic isolation method. CaV1.2 channel currents were examined by using whole-cell patch clamp recording technique.
Results 1) Body weight and systolic blood pressure (SBP) in both WKY-EX and SHR-EX were significantly lower than those of their sedentary counterparts (both P<0.05). Body weight in SHR-SED was remarkably lower than WKY-SED (P<0.05), while SBP was much higher than WKY-SED (P<0.05). 2) PDBu (PKC activator) elicited a tension increase, and Gö6976 (PKC inhibitor) induced vasodilation. Both the responses of PDBu and Gö6976 in SHR-SED were notably increased compared with WKY-SED (both P<0.05), however, exercise training significantly suppressed these increases (both P<0.05). 3) Nifedipine (CaV1.2 inhibitor) induced vasodilation. Response to nifedipine in SHR-SED was more sensitive than both SHR-EX and WKY-SED (both P<0.05). 4). The current density of SHR-SED and WKY-EX exhibited an increase compared to the WKY-SED (both P<0.05), and the current density of the SHR-EX decreased obviously in contrast with SHR-SED (P<0.05). Besides, PDBu enlarged current density of all the groups, while Gö6976 decreased current density. The increase or decrease amplitude in SHR-SED was significantly higher than WKY-SED (both P<0.05), whereas exercise training markedly inhibited those responses (both P<0.05).
Conclusions Aerobic exercise efficiently prevents the upregulation of PKC/CaV1.2 pathway in hypertension, and enhances the function of vascular smooth muscle.