Endothelium-dependent basilar and aortic vascular responses in normotensive and coarctation hypertensive rats

Lai, F.M.; Cobuzzi, A.; Shepherd, Cherrie; Tanikella, T.; Hoffman, Aaron; Cervoni, Peter

doi:10.1016/0024-3205(89)90046-5

Cited by 26 publications

(13 citation statements)

References 15 publications

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“…6,7,9,[15][16][17][18] We reported recently that topical application of the rat PAR-2 synthetic tethered ligand sequence, SLIGRL-NH 2 , to the basilar artery in vivo produced dilatation in Sprague-Dawley (normotensive) rats that was blocked by inhibitors of NO synthase or soluble guanylate cyclase. 21 Thus, we concluded that, like acetylcholine, 24,25,27,28 PAR-2 dilator responses of the basilar artery were also mediated by endothelial cell production of NO, which was confirmed in the present study in the WKY strain of rat. In addition, we found that PAR-2-IR was present in endothelial cells of the basilar artery.…”

Section: Mechanism Of Par-2 Vasodilatationsupporting

confidence: 86%

Evidence for Selective Effects of Chronic Hypertension on Cerebral Artery Vasodilatation to Protease-Activated Receptor-2 Activation

Sobey

Moffatt

Cocks

1999

Stroke

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Background and Purpose-Protease-activated receptor-2 (PAR-2) can be activated after proteolysis of the amino terminal of the receptor by trypsin or by synthetic peptides with a sequence corresponding to the endogenous tethered ligand exposed by trypsin (eg, SLIGRL-NH 2 ). PAR-2 mediates nitric oxide (NO)-dependent dilatation in cerebral arteries, but it is unknown whether PAR-2 function is altered in cardiovascular diseases. Since hypertension selectively impairs NO-mediated cerebral vasodilatation in response to acetylcholine and bradykinin, we sought to determine whether PAR-2-mediated vasodilatation is similarly adversely affected by this disease state. Methods-We studied basilar artery responses in Wistar-Kyoto rats (WKY) (normotensive) and spontaneously hypertensive rats (SHR) in vivo (cranial window preparation) and in vitro (isolated arterial rings). The vasodilator effects of acetylcholine, sodium nitroprusside, and activators of PAR-2 and protease-activated receptor-1 (PAR-1) were compared in WKY versus SHR. Immunohistochemical localization of PAR-2 was also assessed in the basilar artery. Results-Increases in basilar artery diameter in response to acetylcholine were 65% to 85% smaller in SHR versus WKY, whereas responses to sodium nitroprusside were not different. In contrast to acetylcholine, vasodilatation in vivo to SLIGRL-NH 2 was largely preserved in SHR, and SLIGRL-NH 2 was Ϸ3-fold more potent in causing vasorelaxation in SHR versus WKY in vitro. In both strains, responses to SLIGRL-NH 2 were abolished by N

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Section: Mechanism Of Par-2 Vasodilatationsupporting

confidence: 86%

Evidence for Selective Effects of Chronic Hypertension on Cerebral Artery Vasodilatation to Protease-Activated Receptor-2 Activation

Sobey

Moffatt

Cocks

1999

Stroke

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“…An immediate decrease in systolic FV coupled with a more variable response of diastolic FV, in which a significant decrease develops with time, strongly suggests that the primary response of basilar artery to L-NAME is an increase of its basal tone and hence a decrease in compliance and increase in resistance [3,4]. The participation of NO in the maintenance of the basal tone of basilar artery supports data obtained in other species using different techniques [7,14,18].…”

Section: Fast Response In the Basilar Artery Blood Flow Velocitysupporting

confidence: 57%

Changes in transcranial Doppler flow velocity waveform following inhibition of nitric oxide synthesis

Richards

Kozniewska²,

Czosnyka

et al. 1997

Acta neurochir

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“…The rationale for proposing blood pressure as an underlying mechanism for vascular limb discrepancies is supported by epidemiological data indicating a strong connection between systemic hypertension and atherosclerotic disease (32, 38). Indeed, chronic increases in blood pressure following coarctation in animals elicit an impairment of the endothelium (2,3,16,19,21), a state that is central in the pathogenesis of atherosclerosis (36). Reciprocally, the improvement in femoral artery endothelial function following bed rest (5) could be explained, at least in part, by the removal of the hydrostatic pressure in the lower extremities.…”

mentioning

confidence: 99%

Impact of acute exposure to increased hydrostatic pressure and reduced shear rate on conduit artery endothelial function: a limb-specific response

Padilla¹,

Sheldon²,

Sitar³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Unlike quadrupeds, humans exhibit a larger hydrostatic pressure in the lower limbs compared with the upper limbs during a major part of the day. It is plausible that repeated episodes of elevated pressure in the legs may negatively impact the endothelium, hence contributing to the greater predisposition of atherosclerosis in the legs. We tested the hypothesis that an acute exposure to increased hydrostatic pressure would induce conduit artery endothelial dysfunction. In protocol 1, to mimic the hemodynamic environment of the leg, we subjected the brachial artery to a hydrostatic pressure gradient ( approximately 15 mmHg) by vertically hanging the arm for 3 h. Brachial artery flow-mediated dilation (FMD) was assessed in both arms before and following the intervention. In protocol 2, we directly evaluated popliteal artery FMD before and after a 3-h upright sitting (pressure gradient approximately 48 mmHg) and control (supine position) intervention. Our arm-hanging model effectively resembled the hemodynamic milieu (high pressure and low shear rate) present in the lower limbs during the seated position. Endothelium-dependent vasodilation at the brachial artery was attenuated following arm hanging (P < 0.05); however, contrary to our hypothesis, upright sitting did not have an impact on popliteal artery endothelial function (P > 0.05). These data suggest an intriguing vascular-specific response to increased hydrostatic pressure and reduced shear rate. Further efforts are needed to determine if this apparent protection of the leg vasculature against an acute hydrostatic challenge is attributable to posture-induced chronic adaptations.

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Endothelium-dependent basilar and aortic vascular responses in normotensive and coarctation hypertensive rats

Cited by 26 publications

References 15 publications

Evidence for Selective Effects of Chronic Hypertension on Cerebral Artery Vasodilatation to Protease-Activated Receptor-2 Activation

Evidence for Selective Effects of Chronic Hypertension on Cerebral Artery Vasodilatation to Protease-Activated Receptor-2 Activation

Changes in transcranial Doppler flow velocity waveform following inhibition of nitric oxide synthesis

Impact of acute exposure to increased hydrostatic pressure and reduced shear rate on conduit artery endothelial function: a limb-specific response

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