{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:49:52Z","timestamp":1787017792058,"version":"build-2736575974"},"reference-count":57,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[2009,6]]},"abstract":"<jats:p>\n                    Low-amplitude pulses to the vasculature increase pulsatile shear stress to the endothelium. This activates endothelial nitric oxide (NO) synthase (eNOS) to promote NO release and endothelial-dependent vasodilatation. Descent of the dicrotic notch on the arterial pulse waveform and a-to- b ratio ( a\/ b; where a is the height of the pulse amplitude and b is the height of the dicrotic notch above the end-diastolic level) reflects vasodilator (increased a\/ b) and vasoconstrictor effects (decreased a\/ b) due to NO level change. Periodic acceleration (pG\n                    <jats:sub>z<\/jats:sub>\n                    ) (motion of the supine body head to foot on a platform) provides systemic additional pulsatile shear stress. The purpose of this study was to determine whether or not pG\n                    <jats:sub>z<\/jats:sub>\n                    applied to rats produced endothelial-dependent vasodilatation and increased NO production, and whether the latter was regulated by the Akt\/phosphatidylinositol 3-kinase (PI3K) pathway. Male rats were anesthetized and instrumented, and pG\n                    <jats:sub>z<\/jats:sub>\n                    was applied. Sodium nitroprusside, N\n                    <jats:sup>G<\/jats:sup>\n                    -nitro-l-arginine methyl ester (l-NAME), and wortmannin (WM; to block Akt\/PI3K pathway) were administered to compare changes in a\/ b and mean aortic pressure. Descent of the dicrotic notch occurred within 2 s of initiating pG\n                    <jats:sub>z<\/jats:sub>\n                    . Dose-dependent increase of a\/ b and decrease of mean aortic pressure took place with SNP. l-NAME produced a dose-dependent rise in mean aortic pressure and decrease of a\/ b, which was blunted with pG\n                    <jats:sub>z<\/jats:sub>\n                    . In the presence of WM, pG\n                    <jats:sub>z<\/jats:sub>\n                    did not decrease aortic pressure or increase a\/ b. WM also abolished the pG\n                    <jats:sub>z<\/jats:sub>\n                    blunting effect on blood pressure and a\/ b of l-NAME-treated animals. eNOS expression was increased in aortic tissue after pG\n                    <jats:sub>z<\/jats:sub>\n                    . This study indicates that addition of low-amplitude pulses to circulation through pG\n                    <jats:sub>z<\/jats:sub>\n                    produces endothelial-dependent vasodilatation due to increased NO in rats, which is mediated via activation of eNOS, in part, by the Akt\/PI3K pathway.\n                  <\/jats:p>","DOI":"10.1152\/japplphysiol.91612.2008","type":"journal-article","created":{"date-parts":[[2009,3,26]],"date-time":"2009-03-26T21:10:37Z","timestamp":1238101837000},"page":"1840-1847","source":"Crossref","is-referenced-by-count":35,"title":["Low-amplitude pulses to the circulation through periodic acceleration induces endothelial-dependent 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