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This Article Full Text Full Text (PDF) All Versions of this Article: 106/6/1840    most recent 91612.2008v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Uryash, A. Articles by Adams, J. A. PubMed PubMed Citation Articles by Uryash, A. Articles by Adams, J. A.

Low-amplitude pulses to the circulation through periodic acceleration induces endothelial-dependent vasodilatation

¹Division of Neonatology and Department of Research, and ²Division of Pulmonary Disease, Mount Sinai Medical Center, and ³Florida Heart Research Institute, Miami, Florida

Submitted 18 December 2008 ; accepted in final form 24 March 2009

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_z) (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_z 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_z was applied. Sodium nitroprusside, N^G-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_z. 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_z. In the presence of WM, pG_z did not decrease aortic pressure or increase a/b. WM also abolished the pG_z blunting effect on blood pressure and a/b of L-NAME-treated animals. eNOS expression was increased in aortic tissue after pG_z. This study indicates that addition of low-amplitude pulses to circulation through pG_z produces endothelial-dependent vasodilatation due to increased NO in rats, which is mediated via activation of eNOS, in part, by the Akt/PI3K pathway.

vascular resistance; N^G-nitro-L-arginine methyl ester, wortmannin; nitric oxide