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Vascular Biology Center and Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia 30912
In borderline hypertensive rats (BHR),
behavioral stress produces hypertension, which has been attributed to
increases in sympathetic nervous system activity and peripheral changes
in vascular structure. However, the mechanisms mediating development of
stress-induced hypertension have not been well defined. Experiments were designed to determine hemodynamic effects and changes in small
mesenteric artery (
300 µm) vascular reactivity in response to 10 days of air-jet stress (2 h/day) in BHR and in Wistar-Kyoto (WKY) rats.
The acute stress-induced increase in mean arterial pressure (AP) was
impaired in WKY rats compared with BHR on
day 1, and habituation developed to the
increase in AP in BHR, but not WKY rats. Conversely, WKY rats adapted
to the stress-induced tachycardia to a larger extent than BHR. The
mechanisms mediating endothelium-dependent relaxation to acetylcholine
(ACh) were altered in small mesenteric arteries isolated from WKY rats
and BHR after 10 days of air-jet stress. Inhibition of nitric oxide
synthase activity had a significantly larger inhibitory effect on
ACh-induced relaxation in vessels from stressed compared with control
BHR. Also, cyclooxygenase products contributed to ACh-induced
relaxation of small mesenteric arteries from stressed WKY rats, but not
control WKY rats. Endothelium-independent relaxation to nitroprusside was impaired in vessels from stressed WKY rats, but not stressed BHR.
Finally, contraction to phenylephrine was impaired in vessels from
stressed BHR, but not WKY rats. In conclusion, changes in vascular
reactivity induced by air-jet stress appear to correlate with, and may
contribute to, the differential hemodynamic adaptations to stress
observed in WKY rats and BHR.
mesenteric artery; vascular reactivity
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