Contribution of prostaglandins in hypoxia-induced vasodilatation in isolated rabbit hearts. Relation to adenosine and KATP channels

Nakhostine, Nabil; Lamontagne, Daniel

doi:10.1007/bf00374574

Cited by 46 publications

(44 citation statements)

References 34 publications

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“…Because prostacyclin is a hyperpolarizing vasodilator that acts via the adenylyl cyclase system (22,25,32) and enhanced prostacyclin release is a crucial mediator of hypoxic dilation of MCA of rats on normal salt diet (20), it is likely that a similar impairment of this pathway may contribute to loss of the vasodilator response to iloprost (and to reduced PO 2 ) that we observed in arteries of animals on a high-salt diet. In this respect, the present report provides the initial evidence that high-salt diet can also lead to an impaired coupling between membrane receptors and the ultimate electrophysiological response to reduced PO 2 in cerebral resistance arteries.…”

Section: Effect Of High-salt Diet On Electrical and Mechanical Responmentioning

confidence: 88%

High-salt diet impairs vascular relaxation mechanisms in rat middle cerebral arteries

Lombard

Sylvester

Phillips

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

132

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. High-salt diet impairs vascular relaxation mechanisms in rat middle cerebral arteries. Am J Physiol Heart Circ Physiol 284: H1124-H1133, 2003. First published November 27, 2002 10.1152/ajpheart.00835. 2002-Male Sprague-Dawley rats were maintained on a low-salt (LS) diet (0.4% NaCl) or a high-salt (HS) diet (4% NaCl) for 3 days or 4 wk. PO2 reduction to 40-45 mmHg, the stable prostacyclin analog iloprost (10 pg/ml), and stimulatory G protein activation with cholera toxin (1 ng/ml) caused vascular smooth muscle (VSM) hyperpolarization, increased cAMP production, and dilation in cerebral arteries from rats on a LS diet. Arteries from rats on a HS diet exhibited VSM depolarization and constriction in response to hypoxia and iloprost, failed to dilate or hyperpolarize in response to cholera toxin, and cAMP production did not increase in response to hypoxia, iloprost, or cholera toxin. Low-dose angiotensin II infusion (5 ng ⅐ kg Ϫ1 ⅐ min Ϫ1 iv) restored normal responses to reduced PO2 and iloprost in arteries from animals on a HS diet. These observations suggest that angiotensin II suppression with a HS diet leads to impaired relaxation of cerebral arteries in response to vasodilator stimuli acting at the cell membrane. salt intake; hypertension; angiotensin; hypoxia; vascular smooth muscle; endothelium PREVIOUS STUDIES (8,11,19) have demonstrated that both chronic (4-8 wk) volume expanded hypertension caused by reduced renal mass (RRM) with exposure to a high-salt diet and chronic exposure of normotensive rats to a high-salt diet lead to structural changes in arterioles, reductions in microvessel density, and an impaired relaxation of skeletal muscle resistance vessels in response to a variety of vasodilator stimuli, including reduced PO 2 , the stable prostacyclin analog iloprost, and acetylcholine. Subsequent studies demonstrated that alterations in microvessel structure, density, and reactivity in normotensive animals and RRM hypertensive rats on a high-salt diet develop quite rapidly. For example, Hansen-Smith et al. (15) demonstrated that microvascular rarefaction and profound ultrastructural alterations occur in arterioles of RRM hypertensive rats and normotensive animals after only 3 days on a high-salt diet. Other studies (10)(11)(12)38) have demonstrated that vasodilator responses to reduced PO 2 , acetylcholine, and iloprost are also impaired after short-term exposure to high-salt diet. The microvascular rarefaction and the reduced relaxation of resistance arteries to vasodilator stimuli in animals on a high-salt diet may be related to the angiotensin II (ANG II) suppression that occurs in response to elevated dietary salt intake because both the reduction of cremasteric microvessel density (16) and the impaired dilation of skeletal muscle resistance arteries in response to acetylcholine, iloprost, and reduced PO 2 in animals on a high-salt diet can be prevented by infusion of a low dose of ANG II (37,38).To date, the majority of studies investigating changes in vascular control mechanisms with a highsa...

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Section: Effect Of High-salt Diet On Electrical and Mechanical Responmentioning

confidence: 88%

High-salt diet impairs vascular relaxation mechanisms in rat middle cerebral arteries

Lombard

Sylvester

Phillips

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

132

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“…Nakhostine and Lamontagne [29] showed that glibenclamide, a K + ATP channel antagonist, significantly attenuated hypoxia-and adenosine-induced vasodilation in isolated rabbit hearts. Kirsch et al [30] recently reported that adenosine activates an ATP-sensitive K + current in neonatal rat ventricular myocytes.…”

Section: Discussionmentioning

confidence: 99%

Adenosine and ATP CauseNitric Oxide-Dependent PulmonaryVasodilation in Fetal Lambs

Konduri¹,

Mital²

2000

Neonatology

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We investigated the hypothesis that the purine nucleotide ATP and its nucleoside adenosine cause pulmonary vasodilation in fetal lambs by the release of nitric oxide (NO). We also investigated the potential role of K⁺_ATP channels in mediating the effects of ATP and adenosine on NO. We surgically prepared 28 fetal lambs to measure pulmonary and systemic pressures and pulmonary flow. We investigated the effects of glibenclamide and pinacidil (inhibitor and agonist, respectively, for K⁺_ATP channels), N-nitro-L-arginine (N-LA) and its methyl ester, N-nitro-L-arginine methyl ester (L-NAME) (inhibitors of endothelium-derived NO synthesis), and U46619 (a thromboxane mimetic) on pulmonary vasodilation caused by adenosine and ATP. Adenosine decreased the pulmonary artery pressure and pulmonary vascular resistance (PVR) at doses of 0.08–2.5 μM/kg/min and increased the left pulmonary flow at doses of 0.3–2.5 μM/kg/min in control experiments. N-LA, L-NAME and glibenclamide attenuated the effects of adenosine at doses of < 2.5 μM/ kg/min and pinacidil potentiated its effects. ATP decreased the pulmonary artery pressure and PVR and increased the pulmonary flow at doses of 0.15–2.5 μM/kg/min in control experiments. N-LA and L-NAME attenuated the effects of ATP at doses of < 2.5 μM/kg/min, whereas glibenclamide and pinacidil had no effect on the response to ATP. U46619 increased the basal pulmonary vascular tone, but did not significantly alter the vasodilative responses to ATP and adenosine. In conclusion, adenosine and ATP cause NO-dependent pulmonary vasodilation in fetal lambs. The activation of K⁺_ATP channels plays a role in adenosine-induced pulmonary vasodilation. The mechanism by which ATP causes NO release and pulmonary vasodilation requires further investigation.

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“…inwardly rectifying K ϩ current; coronary vasodilation; protein kinase A; Kir2.1 CORONARY VASCULAR SMOOTH MUSCLE in guinea pig, rabbit, and rat hearts relaxes in response to acute hypoxia or a decrease in PO 2 (7,27,30,37). Vasodilation in response to hypoxia in coronary vascular smooth muscle is likely a protective response to increase blood flow to areas of low PO 2 .…”

mentioning

confidence: 99%

Activation of inward rectifier K⁺channels by hypoxia in rabbit coronary arterial smooth muscle cells

Park¹,

Han²,

Kim³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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Contribution of prostaglandins in hypoxia-induced vasodilatation in isolated rabbit hearts. Relation to adenosine and KATP channels

Cited by 46 publications

References 34 publications

High-salt diet impairs vascular relaxation mechanisms in rat middle cerebral arteries

High-salt diet impairs vascular relaxation mechanisms in rat middle cerebral arteries

Adenosine and ATP CauseNitric Oxide-Dependent PulmonaryVasodilation in Fetal Lambs

Activation of inward rectifier K⁺channels by hypoxia in rabbit coronary arterial smooth muscle cells

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Contribution of prostaglandins in hypoxia-induced vasodilatation in isolated rabbit hearts. Relation to adenosine and KATP channels

Cited by 46 publications

References 34 publications

High-salt diet impairs vascular relaxation mechanisms in rat middle cerebral arteries

High-salt diet impairs vascular relaxation mechanisms in rat middle cerebral arteries

Adenosine and ATP CauseNitric Oxide-Dependent PulmonaryVasodilation in Fetal Lambs

Activation of inward rectifier K+channels by hypoxia in rabbit coronary arterial smooth muscle cells

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Activation of inward rectifier K⁺channels by hypoxia in rabbit coronary arterial smooth muscle cells