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)
 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.

Highlights

  • Inhibition of Aerobic Exercise on PKC/CaV1.2 pathway enhanced the function of vascular smooth muscle in hypertension

  • 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)

  • Response to nifedipine in SHRSED was more sensitive than both SHR-EX and WKY-SED

Read more

Summary

Introduction

Inhibition of Aerobic Exercise on PKC/CaV1.2 pathway enhanced the function of vascular smooth muscle in hypertension Yu Chen,Lijun Shi Department of Exercise Physiology, Beijing Sport University 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).

Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call