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1 Department of Cell Biology & Physiology, University of New Mexico Health Sciences Center, Albuquerque, NM, USA
* To whom correspondence should be addressed. E-mail: searley{at}salud.unm.edu.
Attenuated vasoconstrictor reactivity following chronic hypoxia (CH) is associated with endothelium-dependent vascular smooth muscle (VSM) cell hyperpolarization and diminished intracellular [Ca2+]. We tested the hypothesis that increased production of nitric oxide (NO) following CH contributes to blunted vasoconstrictor responsiveness. We found that basal NO production of mesenteric arteries from CH rats (PB = 380 torr; 48 hours) was greater than that of controls (PB = 630 torr). In addition, studies employing pressurized mesenteric arteries (i.d. 100-200 µm) abluminally loaded with the Ca2+ indicator fura-2AM demonstrated that although NO synthase (NOS) inhibition normalized agonist-induced vasoconstrictor responses between groups, VSM cell [Ca2+] in vessels from CH rats remained diminished compared to controls. To determine if elevated NO production following CH results from increased NOS protein levels, we performed Western blots for NOS isoforms using mesenteric arteries from control and CH rats. Endothelial NOS (eNOS) levels did not differ between groups and other NOS isoforms were not detected in these samples. Selective endothelial loading of fura-2AM was employed to test the hypothesis that elevated endothelial cell [Ca2+] following CH accounts for enhanced NOS activity. These experiments demonstrated greater endothelial cell [Ca2+] in mesenteric arteries isolated from CH rats compared to controls. We conclude that enhanced production of NO resulting from elevated endothelial cell [Ca2+] contributes to attenuated reactivity following CH by decreasing VSM cell Ca2+ sensitivity.
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