Expressions of Nitric Oxide Synthases and Akt in the Tibialis Anterior Muscle of the Spontaneously Hypertensive Rat after Ischemic Preconditioning / 체질인류학회지

ABSTRACT

Nitric oxide (NO) generated during ischemic-reperfusion phase is known to activate various transcriptional factors. NO is generated by 3 nitric oxide synthase (NOS) isoforms, nNOS, iNOS, eNOS. Akt plays a important role of the cell survival. Ischemic preconditioning (IP) reduces ischemic injury by changing of the expression of the NOSs and Akt. The alterations of the NOSs is related to the development of hypertension, and hypertension has been known to induce the skeletal muscle changes including decreased fatigue resistance and contractile force. The purpose of this study was to observe the effect of IP on the expressions of the NOSs and Akt in the skeletal muscle of the spontaneously hypertensive rat (SHR). Nine weeks old male normotensive rat (Wistar-Kyoto rat, WKY) and SHR were divided into control and IP groups. The IP group was further divided into 3 or 10 cycles of IP. For IP, left common iliac artery was occluded 3 or 10 cycles of 5 min of ischemia/5 min of reperfusion using rodent vascular clamp. The animals were sacrificed at 0, 0.5, 1, 3 and 24 hours after reperfusion and the tibialis anterior muscles were removed. The expressions of nNOS, iNOS, eNOS, and Akt were examined with immunohistochemical methods and Western blot analysis. In the SHR, the expression of nNOS was decreased, iNOS was increased and the expressions of eNOS and AKT were decreased, compare to WKY. The expression of iNOS was increased, and nNOS, eNOS and Akt were decreased in SHR by 10IP. In summary, IP increased the expression of iNOS, and decreased the expression of eNOS and Akt in the SHR. It is suggested that hypertension may aggravate injury of the tibialis anterior muscle induced by repetitive ischemic conditioning.