In vitro hypoxia on rat pulmonary artery: effects on contractions to spasmogens and role of KATP channels

Wanstall, Janet C.; O'Brien, Emer

doi:10.1016/0014-2999(96)00110-0

Cited by 7 publications

(9 citation statements)

References 27 publications

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“…In some studies, phase 1 was preceded by a small vasodilation (908,909,1018,1474,1894,1905,1934,2018). Similar results were obtained from prestimulated proximal pulmonary arteries in rabbit (413) and first-and third-order pulmonary arteries in pig (578, 991,1045).…”

Section: Pulmonary Arteriessupporting

confidence: 81%

“…These O 2 concentrations were shifted to higher values when the intensity of prestimulation was increased (1652) or when measurements were made in a rat strain more responsive to hypoxia (1691 656,799,814,900,903,935,991,1043,1045,1131,1151,1413,1430,1651,1652,1691,1896,1961,1976,2018,2089,2185). Moreover, substantial data suggested that the endothelium dependence of phase 1 was caused by an hypoxia-induced decrease in endothelial NO production, leading to smooth muscle contraction (506, 656,814,903,934,935,991,1151,1413,1430,1691,1896,1976,2018). In contrast, other studies reported that removal of endothelium did not eliminate or even enhanced phase 1 HPV (412, 413, 876,1038,1043,1151,1207,1208,1638,2190).…”

Section: Pulmonary Arteriesmentioning

confidence: 96%

“…While some investigators were able to elicit contractile responses to hypoxia under basal conditions (4, 392-394, 412, 413, 799, 1417, 1652, 1715, 1818, 2175), most found that exposure to a contractile stimulus before and during hypoxia was required to obtain measurable, reproducible responses in this preparation. Development of hypoxic responses varied with the increase in isometric force caused by prestimulation ("pretone") (1445,1652), but not the agonist, which included acetylcholine (399), angiotensin II (1652), electrical field stimulation (1818), epinephrine (399), endothelin-1 (394, 1131,2018), histamine (506, 815,1282), KCl (139, 197, 393, 399, 815, 899, 900, 1043KCl (139, 197, 393, 399, 815, 899, 900, , 1652KCl (139, 197, 393, 399, 815, 899, 900, , 1976KCl (139, 197, 393, 399, 815, 899, 900, , 2206KCl (139, 197, 393, 399, 815, 899, 900, -2208, norepinephrine (139,197,198,375,429,814,1043,1056,1652,2018,2206), PGF 2␣ . (126, 413, 908, 909, 1038, 1041, 1043, 1638 -1642, 1894, 1896, 1905), phenylephrine (60, 436, 578, 656,876,896,903,934,935,991,1018,1045,1131,1151,1207,1208,1413,1474,...…”

Section: Pulmonary Arteriesmentioning

confidence: 99%

“…Moreover, basal intracellular [ATP] was estimated to be 2.7 mM in endothelium-denuded pulmonary arteries (1044), and dialysis of PASMC with a pipette solution containing 3 mM ATP abolished the prominent glibenclamide-induced depolarization seen when the pipette solution was ATP free (312,314). In addition, glibenclamide had no effect on resting E m in PASMC (59, 1776,2170), baseline tone in isolated pulmonary arteries (1767,2018,2089) Initial evidence suggested that Cl Ca channels may be encoded by the gene rbCLCA, which is expressed in rat lung (892); however, expression of rbCLCA in PASMC has not been explored. More recent reports indicate that Cl Ca channels may be composed of proteins in the TMEM16/Anocotamin family (255, 1735,2151).…”

Section: Membrane Potentialmentioning

confidence: 99%

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Hypoxic Pulmonary Vasoconstriction

Sylvester

Shimoda

Aaronson

et al. 2012

Physiological Reviews

607

621

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It has been known for more than 60 years, and suspected for over 100, that alveolar hypoxia causes pulmonary vasoconstriction by means of mechanisms local to the lung. For the last 20 years, it has been clear that the essential sensor, transduction, and effector mechanisms responsible for hypoxic pulmonary vasoconstriction (HPV) reside in the pulmonary arterial smooth muscle cell. The main focus of this review is the cellular and molecular work performed to clarify these intrinsic mechanisms and to determine how they are facilitated and inhibited by the extrinsic influences of other cells. Because the interaction of intrinsic and extrinsic mechanisms is likely to shape expression of HPV in vivo, we relate results obtained in cells to HPV in more intact preparations, such as intact and isolated lungs and isolated pulmonary vessels. Finally, we evaluate evidence regarding the contribution of HPV to the physiological and pathophysiological processes involved in the transition from fetal to neonatal life, pulmonary gas exchange, high-altitude pulmonary edema, and pulmonary hypertension. Although understanding of HPV has advanced significantly, major areas of ignorance and uncertainty await resolution.

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Section: Pulmonary Arteriessupporting

confidence: 81%

Section: Pulmonary Arteriesmentioning

confidence: 96%

Section: Pulmonary Arteriesmentioning

confidence: 99%

Section: Membrane Potentialmentioning

confidence: 99%

See 2 more Smart Citations

Hypoxic Pulmonary Vasoconstriction

Sylvester

Shimoda

Aaronson

et al. 2012

Physiological Reviews

607

621

View full text Add to dashboard Cite

show abstract

“…During sustained hypoxia the cellular energy state is balanced by an upregulation of glycolysis [112,116,119]. However, since exposure of PAs to prolonged hypoxia may cause ATP-sensitive potassium channels to open due to ATP depletion, the balance of energy state may be incompletely achieved [120]. This may explain the higher sensitivity of HPV to mitochondrial inhibition during prolonged hypoxia [103].…”

Section: Mitochondria In the Cellmentioning

confidence: 99%

Regulation of hypoxic pulmonary vasoconstriction: basic mechanisms

Sommer¹,

Dietrich²,

Schermuly³

et al. 2008

Eur Respir J

186

142

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Hypoxic pulmonary vasoconstriction (HPV), also known as the von Euler-Liljestrand mechanism, is a physiological response to alveolar hypoxia which distributes pulmonary capillary blood flow to alveolar areas of high oxygen partial pressure.Impairment of this mechanism may result in hypoxaemia. Under conditions of chronic hypoxia generalised vasoconstriction of the pulmonary vasculature in concert with hypoxia-induced vascular remodelling leads to pulmonary hypertension. Although the principle of HPV was recognised decades ago, its exact pathway still remains elusive. Neither the oxygen sensing process nor the exact pathway underlying HPV is fully deciphered yet. The effector pathway is suggested to include L-type calcium channels, nonspecific cation channels and voltagedependent potassium channels, whereas mitochondria and nicotinamide adenine dinucleotide phosphate oxidases are discussed as oxygen sensors. Reactive oxygen species, redox couples and adenosine monophosphate-activated kinases are under investigation as mediators of hypoxic pulmonary vasoconstriction. Moreover, the role of calcium sensitisation, intracellular calcium stores and direction of change of reactive oxygen species is still under debate.In this context the present article focuses on the basic mechanisms of hypoxic pulmonary vasoconstriction and also outlines differences in current concepts that have been suggested for the regulation of hypoxic pulmonary vasoconstriction.

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