Key result
Acute increases in intravascular pressure to 80 and 120 mmHg progressively and significantly attenuated both endothelium-dependent and -independent dilation responses in rat small mesenteric arteries.
Why the study?
Does high intravascular pressure attenuate vascular dilation responses in isolated small mesenteric arteries of rats?
Does high intravascular pressure attenuate vascular dilation responses in isolated small mesenteric arteries of rats?
Acute increases in intravascular pressure progressively attenuate both endothelium-dependent and -independent dilation responses in small mesenteric arteries of normotensive rats.
Answers are grounded in this paper and cite their sources.
Requires accounting for acute pressure effects in ex vivo artery studies; leaves open relevance to human hypertension.
BACKGROUND: Alterations in intravascular pressure can affect vascular function and the morphological properties of arteries. Although it has been shown that a transient elevation of blood pressure impairs endothelium-dependent dilation in small arteries, the vascular dilation responses during high intravascular pressure have not yet been investigated. METHODS AND RESULTS: Using pressure myography, the endothelium-dependent and -independent dilation responses of small mesenteric arteries of rats were examined under 3 different intravascular pressure conditions (50, 80 and 120 mmHg). Endothelium-dependent dilation was evaluated by measuring vasodilator responses to increasing doses of acetylcholine (ACh, 10(-9) to 10(-4) mol/L) or increases in intraluminal flow (7-36 microl/min). Endothelium-independent vasodilator function was examined by using sodium nitroprusside (SNP, 10(-9) to 10(-4) mol/L). Flow-mediated dilation was significantly attenuated at 120 mmHg whereas ACh-induced dilation was progressively decreased with increases in intravascular pressure (at 80 and 120 mmHg). Significant attenuation in the vasodilator response to SNP was also observed at 80 and 120 mmHg. CONCLUSION: Endothelium-dependent and-independent dilation responses are progressively attenuated with acute increases in intravascular pressure.
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Gündüz et al. (2008) studied Normotensive (n=30). High intravascular pressure vs. 50 mmHg was evaluated on Endothelium-dependent and -independent dilation responses (sensitivity pD2 to ACh and SNP) (p=<0.001). Acute increases in intravascular pressure to 80 and 120 mmHg progressively and significantly attenuated both endothelium-dependent and -independent dilation responses in rat small mesenteric arteries.
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