Effects of hypoxia upon contractions evoked in isolated rabbit pulmonary artery by potassium and noradrenaline.

Marriott, John; Marshall, Janice M.

doi:10.1113/jphysiol.1990.sp017969

Cited by 15 publications

(5 citation statements)

References 21 publications

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“…Studies of oxygen sensing in carotid body cells by the same group, however, have failed to find an effect on Ca V channel gating (Lopez-Barneo et al , 1993). These results, together with previous reports that relaxation of rabbit pulmonary arteries is usually seen during hypoxic stimulation (Marriott & Marshall, 1990;MacLean et al , 1993;Vadula et al , 1993), suggest that such a mechanism may not play an important role in hypoxic increase in [Ca 2+ ] i . As described above, a number of reports have shown that hypoxic contraction in isolated lungs, PAs and PASMCs are relatively insensitive to multiple Ca V channel blockers (Demiryurek et al , 1993;Jabr et al , 1997;Robertson et al , 2000;Shimoda et al , 2000;Sham et al , 2000;Dipp & Evans, 2001;Kang et al , 2002).…”

Section: Differential Effect Of Hypoxia On Ion Channels In Pulmonasupporting

confidence: 79%

Role of ROS signaling in differential hypoxic Ca2+ and contractile responses in pulmonary and systemic vascular smooth muscle cells

Wang

Zheng

2010

Respiratory Physiology & Neurobiology

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Hypoxia causes a large increase in [Ca2+]i and attendant contraction in pulmonary artery smooth muscle cells (PASMCs), but not in systemic artery SMCs. The different responses meet the respective functional needs in these two distinct vascular myocytes; however, the underlying molecular mechanisms are not well known. We and other investigators have provided extensive evidence to reveal that voltage-dependent K+ (KV) channels, canonical transient receptor potential (TRPC) channels, ryanodine receptor Ca2+ release channels (RyRs), cyclic adenosine diphosphate-ribose, FK506 binding protein 12.6, protein kinase C, NADPH oxidase and reactive oxygen species (ROS) are the essential effectors and signaling intermediates in the hypoxic increase in [Ca2+]i in PASMCs and HPV, but they may not primarily underlie the diverse cellular responses in pulmonary and systemic vascular myocytes. Hypoxia significantly increases mitochondrial ROS generation in PASMCs, which can induce intracellular Ca2+ release by opening RyRs, and may also cause extracellular Ca2+ influx by inhibiting KV channels and activating TRPC channels, leading to a large increase in [Ca2+]i in PASMCs and HPV. In contrast, hypoxia has no or a minor effect on mitochondrial ROS generation in systemic SMCs, thereby causing no change or a negligible increase in [Ca2+]i and contraction. Further preliminary work indicates that Rieske iron–sulfur protein in the mitochondrial complex III may perhaps serve as a key initial molecular determinant for the hypoxic increase in [Ca2+]i in PASMCs and HPV, suggesting its potential important role in different cellular changes to respond to hypoxic stimulation in pulmonary and systemic artery myocytes. All these findings have greatly improved our understanding of the molecular processes for the differential hypoxic Ca2+ and contractile responses in vascular SMCs from distinct pulmonary and systemic circulation systems.

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Section: Differential Effect Of Hypoxia On Ion Channels In Pulmonasupporting

confidence: 79%

Role of ROS signaling in differential hypoxic Ca2+ and contractile responses in pulmonary and systemic vascular smooth muscle cells

Wang

Zheng

2010

Respiratory Physiology & Neurobiology

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“…This may, however, be species-dependent as we have shown potentiation of phenylephrine-induced responses by L-NAME in the rat perfused lung (Shaw et al, 1992) and Liu et al (1991) Marriott & Marshall (1990) also reported that equivalent experimental hypoxia potentiated noradrenaline-evoked contractions in rabbit pulmonary arteries. They concluded, from their studies, that either hypoxia was facilitating noradrenaline-induced influx of calcium through receptor-operated mechanisms or that combined depolarization by hypoxia and noradrenaline may facilitate calcium influx through voltage-operated calcium channels.…”

Section: Discussionmentioning

confidence: 81%

Influences of the endothelium and hypoxia on α₁‐ and α₂‐adrenoceptor‐mediated responses in the rabbit isolated pulmonary artery

MacLean

McCulloch

McGrath

1993

British J Pharmacology

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1 The effects of the inhibitor of nitric oxide synthase, N'0-nitro-L-arginine methylester (L-NAME, i0' M), mechanical disruption of the endothelium and hypoxia on contraction to noradrenaline (al-and x2-adrenoceptor agonist), phenylephrine (a,-adrenoceptor agonist) and UK 14304 (@2-adrenoceptor agonist) were compared in the rabbit isolated pulmonary artery. The effects of the selective antagonists rauwolscine (10-6 M, M2-adrenoceptors) and prazosin (10-' M, ax-adrenoceptors) on the contractions to noradrenaline before and after exposure to L-NAME were also assessed. 2 Noradrenaline, phenylephrine and UK 14304 all produced concentration-dependent increases in vascular tone. The responses to noradrenaline were sensitive to both rauwolscine and prazosin (effect of prazosin > > rauwolscine). L-NAME increased the potency of both noradrenaline and UK 14304, and also the maximum tension achieved. It had no effect on the responses to phenylephrine. After L-NAME, contractions to noradrenaline, although still sensitivie to both rauwolscine and prazosin, were now more sensitive to inhibition by rauwolscine. 3 Endothelium removal augmented the potency and maximum contractions to noradrenaline, phenylephrine and UK 14304. 4 Hypoxia decreased both the potency of phenylephrine and its maximum contractile response, but increased the maximum response to noradrenaline without effecting responses to UK 14304. 5 In conclusion, in the rabbit pulmonary artery, augmentation of contractile responses to noradrenaline by L-NAME involves a potentiation of a2-adrenoceptor-mediated contraction probably through an effect on the synthesis of endothelium-derived nitric oxide. Experimental hypoxia had differential effects on all three agonists and did not mimic the effect of nitric oxide synthase inhibition.

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“…When administered at basal tension, 5,6-EET did not increase active tension in main PA at any concentration administered. The differential responses to 5,6-EET observed in these rings from main and intralobar rabbit PA mimic the differential response to hypoxia observed in large and small rabbit PA. Hypoxia was reported to decrease contraction in large isolated PA vessel segments (4,7,17) and to increase it in small PA (7,16). It has been suggested that this differential response may provide a compensatory mechanism for modulation of the pulmonary arterial blood pressure, i.e., as small PA segments contract in response to hypoxia, large segments relax (4).…”

Section: Discussionmentioning

confidence: 99%

Differential effects of 5,6-EET on segmental pulmonary vasoactivity in the rabbit

Stephenson

Sprague

Losapio

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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In the rabbit, 5,6-epoxyeicosatrienoic acid (EET) was reported both to dilate and to constrict pulmonary blood vessels. We propose that these seemingly contradictory results could be explained by differences in responses to 5,6-EET in large-conductance pulmonary arteries (PA) compared with smaller PA and resistance vessels. Thus we found that in rings of extralobar PA [>2-mm outside diameter (OD)], in which active tension had been increased with PGF(2alpha), 5,6-EET produced relaxation in a concentration- and cyclooxygenase (COX)-dependent manner. In contrast, 5,6-EET increased tension in intralobar (1- to 2-mm OD) PA. Small extralobar PA (2- to 2.5-mm OD) exhibited intermediate responses. In the intact lung, the net effect of 5,6-EET (1 x 10(-8)-1 x 10(-5) M) was an increase in pulmonary vascular resistance (PVR) from 13.0 +/- 0.5 to 47.8 +/- 4.6 mmHg. 100 ml(-1) x min(-1) (EC(50) 5.9 +/- 1.7 x 10(-7) M). The increase in PVR was accompanied by a 10-fold increase in perfusate thromboxane (TX)B(2) concentration. The 5,6-EET-induced increase in PVR was prevented with indomethacin (100 microM), a cyclooxygenase inhibitor, or ONO-3708 (20 microM), a TX/PGH(2) (TP) receptor antagonist, but not with OKY-046 (700 microM), a TX synthase inhibitor. These results demonstrate that although 5,6-EET dilates large extralobar PA segments in a COX-dependent manner, in the intact rabbit lung 5,6-EET produces constriction that requires synthesis of a COX-dependent agonist of the TP receptor other than TX.

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Effects of hypoxia upon contractions evoked in isolated rabbit pulmonary artery by potassium and noradrenaline.

Cited by 15 publications

References 21 publications

Role of ROS signaling in differential hypoxic Ca2+ and contractile responses in pulmonary and systemic vascular smooth muscle cells

Role of ROS signaling in differential hypoxic Ca2+ and contractile responses in pulmonary and systemic vascular smooth muscle cells

Influences of the endothelium and hypoxia on α₁‐ and α₂‐adrenoceptor‐mediated responses in the rabbit isolated pulmonary artery

Differential effects of 5,6-EET on segmental pulmonary vasoactivity in the rabbit

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Effects of hypoxia upon contractions evoked in isolated rabbit pulmonary artery by potassium and noradrenaline.

Cited by 15 publications

References 21 publications

Role of ROS signaling in differential hypoxic Ca2+ and contractile responses in pulmonary and systemic vascular smooth muscle cells

Role of ROS signaling in differential hypoxic Ca2+ and contractile responses in pulmonary and systemic vascular smooth muscle cells

Influences of the endothelium and hypoxia on α1‐ and α2‐adrenoceptor‐mediated responses in the rabbit isolated pulmonary artery

Differential effects of 5,6-EET on segmental pulmonary vasoactivity in the rabbit

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Influences of the endothelium and hypoxia on α₁‐ and α₂‐adrenoceptor‐mediated responses in the rabbit isolated pulmonary artery