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1 Department of Health and Kinesiology, Texas A&M University, College Station, Texas, USA
2 Department of Anesthesiology, Baylor College of Medicine, Houston, Texas, USA
3 Department of Physiology, Texas A&M University Health Science Center, College Station, Texas, USA
4 Department of Health and Kinesiology, Texas A&M University, College Station, Texas, USA; Department of Physiology, Texas A&M University Health Science Center, College Station, Texas, USA
* To whom correspondence should be addressed. E-mail: mdd{at}hlkn.tamu.edu.
Elevations in arterial pressure associated with hypertension, microgravity and prolonged bedrest alter cerebrovascular autoregulation in humans. Using the head-down tail-suspended (HDT) rat to induce cephalic fluid shifts and elevate arterial pressure, the purpose of this study was to test the hypothesis that 2 wk HDT enhances cerebral artery vasoconstriction through an endothelial nitric oxide (NO) mechanism, and that an enhanced vasoconstriction described in vitro will have corollary in vivo alterations in regional cerebral blood flow (CBF) and vascular resistance (CVR) during standing and head-up tilt. To test this hypothesis, basal tone and vasoconstrictor responses to increases in transmural pressure, shear stress and K+ were determined in vitro in middle cerebral arteries (MCAs) from HDT and control rats. All in vitro measurements were done in the presence and absence of the nitric oxide synthase (NOS) inhibitor L-NAME (10-5 M), the inducible NOS (iNOS) inhibitor aminoguanidine (AG, 10-4 mol/L), the neuronal NOS (nNOS) inhibitor trifluoromethylphenylimidazole (TRIM, 10-4 mol/L), and with endothelium removal. Endothelial NOS (eNOS) mRNA and protein expression levels were measured by RT-PCR and immunoblot, respectively. Regional CBF and CVR were determined using a radiolabeled tracer technique and quantitative autoradiography. Basal tone and transmural pressure, shear stress and K+-induced vasoconstrictor responses were greater in MCAs from HDT rats. L-NAME and endothelium removal abolished these differences between groups, and HDT was associated with lower levels of MCA eNOS protein; iNOS and nNOS inhibition had no effect on MCA vasoconstrictor responses. CBF in select regions was lower and CVR higher during standing and head-up tilt in HDT rats. These results indicate that chronic cephalic fluid shifts enhanced basal tone and vasoconstriction through alterations in the endothelial NOS signaling mechanism. The functional consequence of these vascular alterations with HDT is regional elevations in CVR and corresponding reductions in cerebral perfusion.
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