Arteriolar reactive hyperemia: modification by inhibitors of prostaglandin synthesis

Messina, Edward J.; Weiner, Richard; Kaley, Gabor

doi:10.1152/ajpheart.1977.232.6.h571

Cited by 27 publications

(19 citation statements)

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“…A continuous dilating effect of prostaglandins in arteriolar vessels in vivo was also found by other investigators in the skeletal muscle of the rat [14,28]. However, indometha cin did not always reduce resting diameters in this partic ular preparation [29], Nevertheless, some results suggest that prostaglandins can contribute directly or indirectly to the control of basal vascular tone in vivo. Inhibition of prostaglandin synthesis resulted in an elevation of blood pressure in awake dogs [30] and in healthy humans [31],…”

Section: Discussionsupporting

confidence: 74%

Mediator Role of Prostaglandins in Acetylcholine-lnduced Vasodilation and Control of Resting Vascular Diameter in the Hamster Cremaster Microcirculation in vivo

Wit

Bismarck

Pohl³

1993

J Vasc Res

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Acetylcholine (ACh) is widely used as a standard test substance for nitric oxide (NO)-mediated vasodilation. However, it also augments the release of prostaglandins, a group of other endothelium-derived smooth muscle relaxants. Using intravital microscopy in the cremaster muscle of anesthetized hamsters, we studied the relative roles of NO and prostaglandins in mediating ACh-induced dilation and in the control of basal vessel tone (253 arterioles in 31 experiments). N^ω-nitro-L-arginine (L·NNA), a competitive inhibitor of NO synthase, significantly reduced ACh-induced vasodilation (by 42-73%), irrespective of whether it was applied intravenously (30 mg/kg) or topically (30 µM). Additional indomethacin (3 µM, topical) nearly abolished the dilator response. In contrast, the vascular responses to the endothelium-independent dilator sodium nitroprusside were not affected. The resting diameters (range: 6–114 µm) were significantly (p < 0.05) reduced after L·NNA or indomethacin by 10.2 and 16.6% of control diameter, respectively. The constriction induced by L·NNA was stronger in larger (>50 µm) than in smaller (<50 µm) vessels, whereas indomethacin was equipotent in both groups. Thus, in addition to NO, dilating prostaglandins are important mediators of the ACh-induced dilation and contribute to the control of resting arteriolar diameter in the hamster cremaster microcirculation in vivo.

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Section: Discussionsupporting

confidence: 74%

Mediator Role of Prostaglandins in Acetylcholine-lnduced Vasodilation and Control of Resting Vascular Diameter in the Hamster Cremaster Microcirculation in vivo

Wit

Bismarck

Pohl³

1993

J Vasc Res

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“…2). Earlier studies in heart and striated muscle preparations have demonstrated heterogeneity in the RH response in microvessels as well as differences between 2A and 3A vessels (2,9,14,22,23,34). The present study demonstrates that differences in shear stress sensitivity underlie branch differences in RH duration, whereas the heterogeneity in recovery times between vessels of the 2A branch are explained by differences in actual shear stress levels at the beginning of RH (Fig.…”

Section: Microvascular Responses During Rhsupporting

confidence: 57%

“…RH responses of second-order (2A) and third-order (3A) vessels were measured in cremaster muscle (15,22,23) of control C57Bl/6 mice and hypercholesterolemic mice. To induce hypercholesterolemia, we placed C57Bl/6 mice and transgenic ApoE3-Leiden mice on a high-fat/high-cholesterol (HFC) diet.…”

mentioning

confidence: 99%

Hypercholesterolemia impairs reactive hyperemic vasodilation of 2A but not 3A arterioles in mouse cremaster muscle

VanTeeffelen¹,

Constantinescu²,

Vink³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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Hypercholesterolemia and atherosclerosis have been associated with changes in the microvasculature, in particular with endothelial dysfunction. In the present study, the impact of atherogenic conditions on arteriolar vasomotor control was determined. Arteriolar [second-order (2A) and third-order (3A) arterioles; diameter range: 9-37 microm] responses during reactive hyperemia (RH) were determined in cremaster muscle of anesthetized mice. C57Bl/6 mice on normal rodent chow were used as controls and high-fat/high-cholesterol (HFC)-fed C57Bl/6 and ApoE3-Leiden mice as hypercholesterolemic mice. The HFC diet resulted in time-dependent increases in plasma cholesterol and triglyceride concentrations (P < 0.001), which were more pronounced in ApoE3-Leiden mice (P < 0.001). In control mice, inhibition of nitric oxide (NO) synthesis with Nomega-nitro-L-arginine (L-NNA) reduced baseline diameter from 17.9 +/- 1.2 to 15.9 +/- 1.3 microm (P < 0.05) and decreased the duration of RH [time to 50% (t50) of recovery: 23.3 +/- 3.6 vs. 12.5 +/- 1.3 s (P = 0.003)]. t50 was longer in 2A versus 3A arterioles (33 +/- 3 vs. 18 +/- 2 s, P < 0.001) and increased with wall shear rate at the beginning of RH in 2A arterioles only. Compared with control mice, RH duration was reduced in 2A arterioles of HFC mice (t50: 11 +/- 2 s, P < 0.001 vs. control) but not affected in 3A vessels. L-NNA did not affect baseline diameter in HFC mice and reduced t50 only in "slow" responders (t50 > or = 10 s). It is concluded that hypercholesterolemia results in an impairment of NO-mediated vasomotor control in 2A but not 3A arterioles during dynamic changes of perfusion like RH. 2A arterioles likely therefore represent the functional locus of endothelial dysfunction during atherogenic conditions.

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“…In normal subjects, the postocclusive hyperemic response has been shown to be blunted by cyclooxygenase inhibitors, which suggests a role for dilating prostaglandins (12)(13)(14).…”

mentioning

confidence: 99%

The post‐occlusive hyperemic response in patients with systemic sclerosis

Wigley

Wise

Mikdashi

et al. 1990

Arthritis & Rheumatism

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We investigated post‐ischemic hyperreactive cutaneous blood flow in patients with primary Raynaud's phenomenon and Raynaud's phenomenon secondary to systemic sclerosis (SSc). Reactive hyperemia was measured over a locally warmed area of skin, using a laser Doppler flowmeter, following 5 minutes of suprasystolic occlusion of blood flow. We found that patients with primary Raynaud's phenomenon had normal post‐ischemic blood flow compared with normal controls. In contrast, patients with SSc had reduced levels of baseline and peak blood flow compared with either the primary Raynaud's phenomenon patients or the normal subjects. Infusion of carbaprostacyclin, a potent prostacyclin analog vasodilator, did not increase blood flow in the SSc patients, nor did it restore the reactive hyperemic response. These findings are consistent with the hypothesis that patients with the nonvasoconstricted condition of SSc have fixed structural defects that limit cutaneous microvascular blood flow.

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Arteriolar reactive hyperemia: modification by inhibitors of prostaglandin synthesis

Cited by 27 publications

References 0 publications

Mediator Role of Prostaglandins in Acetylcholine-lnduced Vasodilation and Control of Resting Vascular Diameter in the Hamster Cremaster Microcirculation in vivo

Mediator Role of Prostaglandins in Acetylcholine-lnduced Vasodilation and Control of Resting Vascular Diameter in the Hamster Cremaster Microcirculation in vivo

Hypercholesterolemia impairs reactive hyperemic vasodilation of 2A but not 3A arterioles in mouse cremaster muscle

The post‐occlusive hyperemic response in patients with systemic sclerosis

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