Role of cardiovascular nitric oxide system in C-type natriuretic peptide effects

Costa, María A.; Elesgaray, Rosana; Caniffi, Carolina; Fellet, Andrea L.; Arranz, Cristina

doi:10.1016/j.bbrc.2007.05.095

Cited by 24 publications

(27 citation statements)

References 29 publications

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“…In addition, in our previous studies we showed that the peptide also increases endothelial NO synthase (eNOS) activity through NPR-C-coupled Gi protein activation in aorta of spontaneously hypertensive rats (SHR). The response of the NO system to CNP is lower in hypertensive than in normotensive rats [6,7]. It is well documented that endothelial production of NO causes vasorelaxation primarily by activating soluble guanylyl cyclase (sGC) in smooth muscle cells and by increasing intracellular cGMP, which in turn activates protein kinase G to induce vasorelaxation by decreasing cytosolic Ca 2+ concentration [8,9].…”

Section: Introductionmentioning

confidence: 99%

Vascular Tone Regulation Induced by C-Type Natriuretic Peptide: Differences in Endothelium-Dependent and -Independent Mechanisms Involved in Normotensive and Spontaneously Hypertensive Rats

et al. 2016

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Given that the role of C-type natriuretic peptide (CNP) in the regulation of vascular tone in hypertensive states is unclear, we hypothesized that impaired response of the nitric oxide system to CNP in spontaneously hypertensive rats (SHR) could affect vascular relaxation induced by the peptide in this model of hypertension, and that other endothelial systems or potassium channels opening could also be involved. We examined the effect of CNP on isolated SHR aortas, and the hindlimb vascular resistance (HVR) in response to CNP administration compared to normotensive rats. Aortas were mounted in an isometric organ bath and contracted with phenylephrine. CNP relaxed arteries in a concentration-dependent manner but was less potent in inducing relaxation in SHR. The action of CNP was diminished by removal of the endothelium, inhibition of nitric oxide synthase by Nω-nitro-L-arginine methyl ester, and inhibition of soluble guanylyl cyclase by 1H-[1,2,4]oxadiazolo[4,3-alpha]quinoxalin-1-one in both groups. In contrast, blockade of cyclooxygenase or subtype 2 bradykinin receptor increased CNP potency only in SHR. In both Wistar and SHR, CNP relaxation was blunted by tetraethylammonium and partially inhibited by BaCl2 and iberiotoxin, indicating that it was due to opening of the Kir and BKCa channels. However, SHR seem to be more sensitive to Kir channel blockade and less sensitive to BKCa channel blockade than normotensive rats. In addition, CNP decreases HVR in Wistar and SHR, but the effect of CNP increasing blood flow was more marked in SHR. We conclude that CNP induces aorta relaxation by activation of the nitric oxide system and opening of potassium channels, but the response to the peptide is impaired in conductance vessel of hypertensive rats.

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Section: Introductionmentioning

confidence: 99%

Vascular Tone Regulation Induced by C-Type Natriuretic Peptide: Differences in Endothelium-Dependent and -Independent Mechanisms Involved in Normotensive and Spontaneously Hypertensive Rats

et al. 2016

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“…A third natriuretic receptor subtype, NPR-C, has been proposed primarily as a clearance receptor removing natriuretic peptides from the circulation, but now other biological functions have also been reported (2,4,5). In this regard, NPR-C is coupled to adenylyl cyclase through an inhibitory guanine nucleotide-regulatory protein (G i ) and/or to activation of phospholipase C (PLC) (2,30).…”

mentioning

confidence: 98%

Renal actions of atrial natriuretic peptide in spontaneously hypertensive rats: the role of nitric oxide as a key mediator

Elesgaray

Caniffi

Savignano

et al. 2012

American Journal of Physiology-Renal Physiology

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Atrial natriuretic peptide (ANP) is an important regulator of blood pressure (BP). One of the mechanisms whereby ANP impacts BP is by stimulation of nitric oxide (NO) production in different tissues involved in BP control. We hypothesized that ANP-stimulated NO is impaired in the kidneys of spontaneously hypertensive rats (SHR) and this contributes to the development and/or maintenance of high levels of BP. We investigated the effects of ANP on the NO system in SHR, studying the changes in renal nitric oxide synthase (NOS) activity and expression in response to peptide infusion, the signaling pathways implicated in the signaling cascade that activates NOS, and identifying the natriuretic peptide receptors (NPR), guanylyl cyclase receptors (NPR-A and NPR-B) and/or NPR-C, and NOS isoforms involved. In vivo, SHR and Wistar-Kyoto rats (WKY) were infused with saline (0.05 ml/min) or ANP (0.2 μg·kg(-1)·min(-1)). NOS activity and endothelial (eNOS), neuronal (nNOS), and inducible (iNOS) NOS expression were measured in the renal cortex and medulla. In vitro, ANP-induced renal NOS activity was determined in the presence of iNOS and nNOS inhibitors, NPR-A/B blockers, guanine nucleotide-regulatory (G(i)) protein, and calmodulin inhibitors. Renal NOS activity was higher in SHR than in WKY. ANP increased NOS activity, but activation was lower in SHR than in WKY. ANP had no effect on expression of NOS isoforms. ANP-induced NOS activity was not modified by iNOS and nNOS inhibitors. NPR-A/B blockade blunted NOS stimulation via ANP in kidney. The renal NOS response to ANP was reduced by G(i) protein and calmodulin inhibitors. We conclude that ANP interacts with NPR-C, activating Ca-calmodulin eNOS through G(i) protein. NOS activation also involves NPR-A/B. The NOS response to ANP was diminished in kidneys of SHR. The impaired NO system response to ANP in SHR participates in the maintenance of high blood pressure.

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“…[3,14] Moreover, CNP also shows anti-atherogenic properties on vessel walls with the inhibition of leukocyte migration and suppression of P-selectin expression. [14,15] Furthermore, Costa et al [16] demonstrated that infusion of CNP increases inducible nitric oxide synthase (iNOS) expression. Interestingly, some researchers have also claimed that CNP has a vaso-relaxant impact through the increased production of endothelial NO via elevated iNOS activity.…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, some researchers have also claimed that CNP has a vaso-relaxant impact through the increased production of endothelial NO via elevated iNOS activity. [16,17] Several studies have investigated NPR-B as it relates to inducible ischemia types. [5,18] Staub et al [5] suggested that it might have diagnostic value in the determination of inducible myocardial ischemia, and Kumakura et al [7] reported that high NPR-B levels correlated with a number of affected distal arteries in critical limb ischemia.…”

Section: Discussionmentioning

confidence: 99%

Use of C-type natriuretic peptide as an indicator in detection of inducible peripheral ischemia

Çalışkan¹

2014

Turk Gogus Kalp Dama

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Role of cardiovascular nitric oxide system in C-type natriuretic peptide effects

Cited by 24 publications

References 29 publications

Vascular Tone Regulation Induced by C-Type Natriuretic Peptide: Differences in Endothelium-Dependent and -Independent Mechanisms Involved in Normotensive and Spontaneously Hypertensive Rats

Vascular Tone Regulation Induced by C-Type Natriuretic Peptide: Differences in Endothelium-Dependent and -Independent Mechanisms Involved in Normotensive and Spontaneously Hypertensive Rats

Renal actions of atrial natriuretic peptide in spontaneously hypertensive rats: the role of nitric oxide as a key mediator

Use of C-type natriuretic peptide as an indicator in detection of inducible peripheral ischemia

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