Hypoxia-induced fetoplacental vasoconstriction in perfused human placental cotyledons

Howard, Randy B.; Hosokawa, Tomokazu; Maguire, M. Helen

doi:10.1016/s0002-9378(87)80307-1

Cited by 99 publications

(42 citation statements)

References 6 publications

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“…Our data suggest that the clearance of contrast from the adjacent labyrinth was slowed in Hpx placentas. Whereas our findings are consistent with the notion that hypoxia influences preplacental vasoconstriction (17), our data illuminate hypoxia-induced changes within the labyrinth, the site of maternal-fetal exchange in the murine placenta (7,32). Finally, we found that the accumulation of contrast in the kidneys of fetuses of Hpx dams was reduced.…”

Section: Discussionsupporting

confidence: 90%

Magnetic resonance imaging of hypoxic injury to the murine placenta

Tomlinson

Garbow

Anderson

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Section: Discussionsupporting

confidence: 90%

Magnetic resonance imaging of hypoxic injury to the murine placenta

Tomlinson

Garbow

Anderson

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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“…However, factors other than hypoxia could act as stimuli in this situation, e.g., reduced supply of nutrients or impaired removal of fetal metabolites. The first direct indication that hypoxia per se causes fetoplacental vasoconstriction was in a study by Howard et al (15). In their experiments on perfused human cotyledons, the increases in perfusion pressure with hypoxia were small (ϳ10% above baseline).…”

Section: Discussionmentioning

confidence: 98%

“…An intact cotyledon that was not damaged (as judged by visual inspection) was chosen for perfusion (14,15,36). The arterial and venous branches supplying the selected cotyledon were injected with heparin (2,500 IU each; Léciva, Prague, Czech Republic) and cannulated within 10 min of the end of the third stage of parturition.…”

Section: Methodsmentioning

confidence: 99%

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Hypoxic fetoplacental vasoconstriction in humans is mediated by potassium channel inhibition

Hampl

Bíbová

Straňák

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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Fetal to maternal blood flow matching in the placenta, necessary for optimal fetal blood oxygenation, may occur via hypoxic fetoplacental vasoconstriction (HFPV). We hypothesized that HFPV is mediated by K+ channel inhibition in fetoplacental vascular smooth muscle, as occurs in several other O2-sensitive tissues. With the use of an isolated human placental cotyledon perfused at a constant flow rate, we found that hypoxia reversibly increased perfusion pressure by >20%. HFPV was unaffected by cyclooxygenase or nitric oxide synthase inhibition. HFPV and 4-aminopyridine, an inhibitor of voltage-dependent K+(Kv) channels, increased pressure in a nonadditive manner, suggesting they act via a common mechanism. Iberiotoxin, a large conductance Ca2+-sensitive K+(BKCa) channel inhibitor, had little effect on normoxic pressure. Immunoblotting and RT-PCR showed expression of several putative O2-sensitive K+ channels in peripheral fetoplacental vessels. In patch-clamp experiments with smooth muscle cells isolated from peripheral fetoplacental arteries, hypoxia reversibly inhibited Kv but not BKCa or ATP-dependent currents. We conclude that human fetoplacental vessels constrict in response to hypoxia. This response is largely mediated by hypoxic inhibition of Kv channels in the smooth muscle of small fetoplacental arteries.

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“…Large amounts of adenosine are released into the foetal effluent from the placenta perfused with Krebs solution in vitro in response to hypoxia, with concomitant foetal vasoconstriction. It has been suggested that adenosine may participate in this response because it can be blocked by the adenosine antagonist, theophylline (Howard et al, 1987;Slegel et al, 1988). Importantly, these studies were performed using placentae with basal foetal vascular tone, which is normally very low (Boura & Walters, 1991).…”

Section: Introductdonmentioning

confidence: 99%

Vascular actions of purines in the foetal circulation of the human placenta

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Boura

Walters

1993

British J Pharmacology

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1 The vasoactive effects of adenosine triphosphate (ATP), adenosine and other purines in the foetal circulation of the human placenta were examined. Single lobules of the placenta were bilaterally perfused in vitro with Krebs buffer (maternal and foetal sides 5 ml min' each, 95% 02:5% CO2, 37°C). Changes in foetal vascular tone were assessed by recording perfusion pressure during constant infusion of each purine. To allow recording of the vasodilator effects, submaximal vasoconstriction was induced by concomitant infusion of prostaglandin F20, (0.7-2.0 ytmolI 1).2 ATP (1.0-1001amoll-1) usually caused concentration-dependent reductions in perfusion pressure.However, biphasic with initial transient increases, or only increases in pressure were sometimes observed. Falls in pressure caused by ATP were significantly reduced by addition to the perfusate of N0-nitro-Larginine (L-NOARG) (100 jamol 1-') but not N0-nitro-D-arginine (D-NOARG) (100 tLmol 1). They were not influenced by addition of indomethacin (I0 lmolI 1) or L-arginine (100 gmol 1').

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Hypoxia-induced fetoplacental vasoconstriction in perfused human placental cotyledons

Cited by 99 publications

References 6 publications

Magnetic resonance imaging of hypoxic injury to the murine placenta

Magnetic resonance imaging of hypoxic injury to the murine placenta

Hypoxic fetoplacental vasoconstriction in humans is mediated by potassium channel inhibition

Vascular actions of purines in the foetal circulation of the human placenta

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