Role of endothelin and vasopressin in DOCA‐salt hypertension

Yu, Ming Chih; Gopalakrishnan, Venkat; McNeill, J. Robert

doi:10.1038/sj.bjp.0703958

Cited by 22 publications

(15 citation statements)

References 28 publications

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“…The total peripheral resistance (TPR) is increased in the DOCA-salt rat model [54]. In the present study, Up 4 A-induced contraction was similar in thoracic aorta, which has a small contribution to TPR, from control and DOCA-salt rats.…”

Section: Discussionsupporting

confidence: 52%

Alterations in vasoconstrictor responses to the endothelium-derived contracting factor uridine adenosine tetraphosphate are region specific in DOCA-salt hypertensive rats

Matsumoto

Tostes

Webb

2012

Pharmacological Research

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Uridine adenosine tetraphosphate (Up4A) has been recently identified as a novel and potent endothelium-derived contracting factor and contains both purine and pyrimidine moieties, which activate purinergic P2X and P2Y receptors. The present study was designed to compare contractile responses to Up4A and other nucleotides such as ATP (P2X/P2Y agonist), UTP (P2Y2/P2Y4 agonist), UDP (P2Y6 agonist), and α,β-methylene ATP (P2X1 agonist) in different vascular regions [thoracic aorta, basilar, small mesenteric, and femoral arteries] from deoxycorticosterone acetate-salt (DOCA-salt) and control rats. In DOCA-salt rats [vs. control uninephrectomized (Uni) rats]: (1) in thoracic aorta, Up4A-, ATP-, and UTP-induced contractions were unchanged; (2) in basilar artery, Up4A-, ATP-, UTP- and UDP-induced contractions were increased, and expression for P2X1, but not P2Y2 or P2Y6 was decreased; (3) in small mesenteric artery, Up4A-induced contraction was decreased and UDP-induced contraction was increased; expression of P2Y2 and P2X1 was decreased whereas P2Y6 expression was increased; (4) in femoral artery, Up4A-, UTP-, and UDP-induced contractions were increased, but expression of P2Y2, P2Y6 and P2X1 was unchanged. The α,β-methylene ATP-induced contraction was bell-shaped and the maximal contraction was reached at a lower concentration in basilar and mesenteric arteries from Uni rats, compared to arteries from DOCA-salt rats. These results suggest that Up4A-induced contraction is heterogenously affected among various vascular beds in arterial hypertension. P2Y receptor activation may contribute to enhancement of Up4A-induced contraction in basilar and femoral arteries. These changes in vascular reactivity to Up4A may be adaptive to the vascular alterations produced by hypertension.

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Section: Discussionsupporting

confidence: 52%

Alterations in vasoconstrictor responses to the endothelium-derived contracting factor uridine adenosine tetraphosphate are region specific in DOCA-salt hypertensive rats

Matsumoto

Tostes

Webb

2012

Pharmacological Research

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“…BPs were recorded by a radiotelemetry method in conscious unrestrained rats with a computer‐driven data acquisition system (Data Science, Minneapolis, MN, U.S.A.). Details for this method are described elsewhere in this journal ( Yu et al , 2001a ). After 3 weeks of DOCA or SHAM treatment, BP was monitored for 4 h and readings from the last hour were analyzed to establish the baseline BP.…”

Section: Methodsmentioning

confidence: 99%

Role of oxidative stress and nitric oxide in regulation of spontaneous tone in aorta of DOCA‐salt hypertensive rats

Ghosh

Wang

McNeill

2004

British J Pharmacology

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1 The roles of nitric oxide (NO), superoxide anion (O 2 À ), and hydrogen peroxide (H 2 O 2 ) in the modulation of spontaneous tone were investigated in isolated aorta from deoxycorticosterone acetate (DOCA)-salt hypertensive rats. 2 Increases in preload from 1 to 5 g were accompanied by increases in spontaneous tone in aortic rings from DOCA-salt hypertensive rats but not from SHAM-normotensive rats. 3 Tone was higher in endothelium-denuded aortic rings than in endothelium-intact vessels. Inhibition of nitric oxide synthase (NOS) with 300 mM N G -nitro-L-arginine methyl ester (L-NAME) increased spontaneous tone. 4 Basal O 2 À generation was higher in aortic rings from DOCA-salt hypertensive rats than in those from SHAM-normotensive rats. Stretch increased O 2 À levels even further in the DOCA-salt group. In rings isolated from DOCA-salt hypertensive rats, administration of the O 2 À scavenger, superoxide dismutase (SOD, 150 U ml À1 ), or the nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase inhibitor, apocynin (100 mM), completely abolished the development of spontaneous tone in endothelium-intact aortic rings but not in endothelium-denuded or in L-NAME-treated rings. SOD and apocynin decreased the generation of O 2 À in endothelium-intact, endothelium-denuded, and L-NAME-treated aortic rings. 5 Oral treatment of DOCA-salt hypertensive rats with the O 2 À scavengers, tempol or tiron, or with apocynin for 3 weeks prevented the development of hypertension and abolished the increases in O 2 À generation and spontaneous tone. 6 Administration of catalase (1000 U ml À1 ) to aortic rings increased spontaneous tone in vessels from DOCA-salt hypertensive rats. 7 Administration of the cyclooxygenase (COX) inhibitor, valeroyl salicylate, or the thromboxane/ prostaglandin antagonist, SQ 29548, to aortic rings abolished tone. 8 The results suggest that NO plays a major role in preventing the generation of spontaneous tone in isolated aortic rings from DOCA-salt hypertensive rats. NADPH-oxidase-derived O 2 À enhanced spontaneous tone by inactivating NO. Endogenous H 2 O 2 appears to mitigate the increase in tone. In addition, a COX component may also contribute to spontaneous tone.

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“…[12][13][14]22,24,25 . Brain and plasma levels of vasopressin mRNA and the peptide are increased in rats after DOCA-salt treatment, 26,27 and V1-vasopressin receptor antagonists reduce blood pressure in DOCA-salt hypertension.…”

Section: Discussionmentioning

confidence: 99%

Vasopressin Induces Vascular Superoxide Via Endothelin-1 in Mineralocorticoid Hypertension

Galligan

Fink

et al. 2003

Hypertension

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Abstract-We have recently reported that endothelin-1 (ET-1), which is increased in the arteries of deoxycorticosterone acetate (DOCA)-salt hypertensive rats, stimulates superoxide production. However, the humoral mechanisms responsible for ET-1-induced superoxide formation in low-renin models of hypertension, such as DOCA-salt hypertension, remain undefined. Vasopressin is known to upregulate vascular preproET-1 gene expression in DOCA-salt rats, an effect that is absent in vasopressin-deficient Brattleboro rats treated with DOCA-salt. The present study tested the hypothesis that vasopressin contributes to ET-1-induced vascular superoxide production in DOCA-salt hypertensive rats. Carotid arterial segments of DOCA, sham (uninephrectomized), or normal (untreated) rats were used for the study. In vitro vasopressin treatment of carotid arteries from normal rats for 24 hours, but not 4 hours, increased both ET-1 and superoxide levels. The increase of vasopressin-induced superoxide was reduced by pretreatment of the vessels with ABT627, a selective ET A receptor antagonist ABT627. Vasopressin, ET-1, and superoxide levels were significant elevated in carotid arteries of DOCA-salt rats compared with sham controls. The selective V1-vasopressin receptor antagonist (␤-Mercapto-␤, ␤-cyclopentamethylenepropiony 1 , O-Me-Tyr 2 , Arg 8 vasopressin, ME-AVP), decreased superoxide both in vasopressin-treated vessels of normal rats and in vessels of DOCA-salt rats, with a concomitant reduction of ET-1 content. These results suggest that vasopressin increases vascular superoxide levels by stimulating ET-1 formation in mineralocorticoid hypertension, and that V1-vasopressin receptors play an important role in this process. Ϫ is produced in activated endothelial cells, 4 smooth muscle cells, 5 and adventitial fibroblasts. 6 Vascular dysfunction is manifested as impaired endothelium-dependent NO-mediated relaxation, 1-3 adhesion molecule expression, 7 low-density lipoprotein oxidation, 8 and cell proliferation. 9 However, the detailed mechanisms responsible for O 2 Ϫ production under different pathophysiological circumstances remain to be defined.We have recently shown that arterial endothelin-1 (ET-1) levels are elevated in deoxycorticosterone acetate (DOCA)-salt hypertension, 10 and that this resulted in increased O 2 Ϫ production 7,10 via ET A receptor activation 10 in this low-renin hypertension model. 11 However, the mechanisms contributing to increased ET-1 are unknown. The peptide hormone 8-argininevasopressin (AVP) is able to stimulate preproendothenlin-1 mRNA expression in arteries and cultured endothelial cells. [12][13][14] Furthermore, the enhanced endothelin gene expression observed in DOCA-salt rats was absent in vasopressin-deficient Brattleboro rats treated with DOCA-salt, 13 suggesting a functional link between vasopressin and ET-1 gene expression.The biological effects of vasopressin are mediated through 2 AVP receptor subtypes, the V 1 and V 2 receptors. 15-17 V 1 receptors mediate vasoconstriction, proliferation, ...

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Role of endothelin and vasopressin in DOCA‐salt hypertension

Cited by 22 publications

References 28 publications

Alterations in vasoconstrictor responses to the endothelium-derived contracting factor uridine adenosine tetraphosphate are region specific in DOCA-salt hypertensive rats

Alterations in vasoconstrictor responses to the endothelium-derived contracting factor uridine adenosine tetraphosphate are region specific in DOCA-salt hypertensive rats

Role of oxidative stress and nitric oxide in regulation of spontaneous tone in aorta of DOCA‐salt hypertensive rats

Vasopressin Induces Vascular Superoxide Via Endothelin-1 in Mineralocorticoid Hypertension

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