Atrial natriuretic peptide relaxes arterial basal tone induced by coarctation hypertension

Brunoa, M Peral de; Romano, Liliana; Proto, Maria; Coviello, Alfredo

doi:10.1016/s0196-9781(99)00030-3

Cited by 13 publications

(12 citation statements)

References 26 publications

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“…After 13-14 weeks of second surgery, creatinine clearance (Ccr) (Wiener Lab, Argentina) and microalbuminuria (BioSystem kit, Spain) were measured in metabolic cage by 24 hours. Mean arterial pressure (MAP) was measured by direct method through cannulation of right carotid with a catheter connected to a pressure transductor [12]. In all surgical procedures the animals were anesthetized with sodium pentobarbital (45 mg/kg intraperitoneal).…”

Section: Methodsmentioning

confidence: 99%

“…To evaluate the spontaneous basal tone, the endothelium-independent agent (SNP) was added to rings not previously exposed to any vasoactive agent [12]. For this purpose, SNP was used to maximal dose (10 −5 M), which was found to be the optimal concentration for SNP-induced relaxation (100%) of the precontracted rings with norepinephrine (NE).…”

Section: Methodsmentioning

confidence: 99%

“…Accordingly, we previously demonstrated that arterial vessels from SHR [11] and coarctation-hypertensive rats [12] showed increased basal tone. This increased basal tone was evidenced by a relaxant response to sodium nitroprusside (SNP) and atrial natriuretic peptide.…”

Section: Introductionmentioning

confidence: 99%

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Antioxidant Treatment Reverts Increased Arterial Basal Tone and Oxidative Stress in Nephrectomized (5/6) Hypertensive Rats

Marañón

Turoni

Karbiner

et al. 2013

International Journal of Hypertension

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Nonischemic 5/6 nephrectomized rat (NefR) is a model of chronic kidney disease. However, little is known about vascular dysfunction and its relation with hypertension in NefR. Aims. To evaluate possible alterations of endothelial function, NO-bioavailability, and basal tone in aorta from NefR and the role of oxidative stress. Sprague Dawley rats were divided into sham rats (SR), NefR, and NefR treated with tempol (NefR-T). Mean arterial pressure (MAP) and renal function were determined. In isolated aortic rings the following was measured: 1-endothelial function, 2-basal tone, 3-NO levels, 4-membrane potential (MP), and 5-oxidative stress. NefR increased MAP (SR: 119 ± 4 mmHg; n = 7; NefR: 169 ± 6; n = 8; P < 0.001). Tempol did not modify MAP (NefR-T: 168 ± 10; n = 6; P < 0.001). NefR showed endothelial dysfunction, increased basal tone and decreased NO levels (SR: 32 ± 2 nA; n = 7, NefR: 10 ± 2; n = 8; P < 0.001). In both in vitro and in vivo tempol improves basal tone, NO levels, and MP. Oxidative stress in NefR was reverted in NefR-T. We described, for the first time, that aorta from NefR presented increased basal tone related to endothelial dysfunction and decreased NO-bioavailability. The fact that tempol improves NO-contents and basal tone, without decrease MAP, indicates that oxidative stress could be implicated early and independently to hypertension, in the vascular alterations.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Antioxidant Treatment Reverts Increased Arterial Basal Tone and Oxidative Stress in Nephrectomized (5/6) Hypertensive Rats

Marañón

Turoni

Karbiner

et al. 2013

International Journal of Hypertension

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“…NO can activate calcium-activated potassium channels dependently of cGMP in arteries of pig (Miyoshi and Nakaya, 1994), rabbit (Robertson et al, 1993), and rat (Peral de Bruno et al, 1999). Activation of protein kinases by cGMP can result in phosphorylation of potassium channels (Robertson et al, 1993).…”

Section: No Desensitizes Relaxations To Natriuretic Peptides 229mentioning

confidence: 99%

Endothelium-Derived Nitric Oxide Inhibits the Relaxation of the Porcine Coronary Artery to Natriuretic Peptides by Desensitizing Big Conductance Calcium-Activated Potassium Channels of Vascular Smooth Muscle

Liang

Au²,

Leung³

et al. 2010

J Pharmacol Exp Ther

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The present experiments investigated whether endothelium-derived mediators modulate the effect of natriuretic peptides in porcine coronary arteries. Rings with and without endothelium were suspended in organ chambers for isometric tension recording. Concentrationrelaxation curves to C-type natriuretic peptide (CNP) and atrial natriuretic peptide (ANP) were obtained during contractions to endothelin-1. Removal of the endothelium potentiated relaxations to both CNP and ANP. N thelium. CNP-induced relaxations were reduced by 8-bromoguanosine 3Ј,5Ј-cGMP (8-bromo-cGMP) to the same extent in rings with and without endothelium. There was no significant difference between the increased cGMP content caused by CNP in porcine coronary arteries with or without endothelium. In patch-clamp studies in porcine coronary arterial smooth muscle cells, the natriuretic peptide-mediated enhancement of the IBTX-sensitive big conductance calcium-activated potassium channel (BK Ca ) amplitude was reversed by SNP and 8-bromo-cGMP. These findings demonstrate that, in the porcine coronary artery, the opening of BK Ca and ATP-dependent potassium channels of the vascular smooth muscle contributes to CNP-mediated relaxations. Endothelium-derived and exogenous NO inhibit the direct relaxing effect of natriuretic peptides by desensitizing the response of the BK Ca s of the vascular smooth muscle to the generation of cGMP.

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“…The vasorelaxant responses to ANP in thoracic aortas of both coartation hypertensive and sham-operated rats were investigated in the presence of endothelium, with or without pretreatment with L-NAME (nitric oxide synthase inhibitor) [38]. L-NAME significantly potentiated the responses to ANP only in hypertensive rats.…”

Section: Atrial Natriuretic Peptide Modulation Of Vascular Function Imentioning

confidence: 99%

Atrial natriuretic peptide and regulation of vascular function in hypertension and heart failure

Rubattu¹,

Calvieri²,

Pagliaro³

et al. 2013

Journal of Hypertension

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Atrial natriuretic peptide (ANP) plays a pivotal role in modulation of vascular function and it is also involved in the pathophysiology of several cardiovascular diseases. We provide an updated overview of the current appraisal of ANP vascular effects in both animal models and humans. We describe the physiological implications of ANP vasomodulatory properties as well as the involvement of ANP, through its control of vascular function, in hypertension and heart failure. The principal molecular mechanisms underlying regulation of vascular tone, that is natriuretic peptide receptor type A/cyclic guanylate monophosphate, natriuretic peptide receptor type C, nitric oxide system, are discussed. We review the literature on therapeutic implications of ANP in hypertension and heart failure, examining the potential use of ANP analogues, neutral endopeptidase (NEP) inhibitors, ACE/NEP inhibitors, angiotensin receptor blocker (ARB)/NEP inhibitors, the new dual endothelin-converting enzyme (ECE)/NEP inhibitors and ANP-based gene therapy. The data discussed support the role of ANP in different pathological conditions through its vasomodulatory properties. They also indicate that ANP may represent an optimal therapeutic agent in cardiovascular diseases.

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Atrial natriuretic peptide relaxes arterial basal tone induced by coarctation hypertension

Cited by 13 publications

References 26 publications

Antioxidant Treatment Reverts Increased Arterial Basal Tone and Oxidative Stress in Nephrectomized (5/6) Hypertensive Rats

Antioxidant Treatment Reverts Increased Arterial Basal Tone and Oxidative Stress in Nephrectomized (5/6) Hypertensive Rats

Endothelium-Derived Nitric Oxide Inhibits the Relaxation of the Porcine Coronary Artery to Natriuretic Peptides by Desensitizing Big Conductance Calcium-Activated Potassium Channels of Vascular Smooth Muscle

Atrial natriuretic peptide and regulation of vascular function in hypertension and heart failure

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