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Abstract Details

Abstract Title

Exercise Prevents Increased Functional Coupling of BKCa Channels to Ryanodine Receptors in Cerebral Arterial Smooth Muscle Cells from Spontaneously Hypertensive Rats

Abstract Theme

Physical activity and health

Type Presentation

Oral presentation

Abstract Authors

Presenter Lijun Shi - Beijing Sport University (Department of Exercise Physiology) - CN

Presentation Details

Room: Marte        Date: 1 September        Time: 14:20:00        Presenter: Lijun Shi

Abstract Resume

Background: Regular exercise is an effective non-pharmacological therapy for prevention and control of hypertension. However, the underlying molecular mechanisms remain unresolved. We
tested the hypothesis that hypertension would increase the functional coupling of large-conductance Ca2+-activated K+ (BKCa) channels with ryanodine receptors (RyRs) in spontaneously hypertensive rats
(SHR) as a compensatory response to an increase in intracellular Ca2+ concentration in cerebral arterial smooth muscle cells (CASMCs). We also hypothesized that exercise training would prevent this
increase in functional coupling.


Methods: Male SHRs and Wistar-Kyoto rats (WKYs), 12 weeks age, were separated into sedentary groups (SHR-SED and WKY-SED) and exercise groups (SHR-EX and WKY-EX) at random. Rats in
exercise group were subjected to a treadmill training protocol: 18~20 m/min (about 55-65% of maximal aerobic velocity), 0% grade, 60 min/d, 5 d/wk for 8 weeks.


Results: Cerebral myocytes displayed spontaneous transient outward currents (STOCs) at membrane potentials more positive than -40 mV. STOC amplitude in SHR-SED was higher than that in
WKY-SED at the same holding potential. The amplitude of the spontaneous Ca2+ sparks in isolated CASMCs was significantly enhanced in SHRs. Moreover, hypertension displayed increased whole-cell BKCa,
Cav1.2 but decreased KV currents in CASMCs. The single BKCa channel activity was markedly enhanced, and protein expression of BKCa (β1, but not α-subunit) was significantly increased but KV1.2 was
decreased in SHRs. Exercise training ameliorated all of these functional and molecular alterations in hypertensive rats.


Conclusions: These data indicate that hypertension leads to an enhanced functional coupling of RyRs-BKCa to buffer pressure-induced constriction of cerebral arteries, which attributes
not only to an upregulation of BKCa β1-subunit function but also to an increase of Ca2+ release from RyRs. However, regular aerobic exercise can efficiently prevent the augmented coupling to alleviate
the pathological compensation to restore the cerebral arterial function.


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