EFFECTS OF ARGININE VASOPRESSIN, ANGIOTENSIN II AND ENDOTHELIN-1 ON THE RELEASE OF BRAIN NATRIURETIC PEPTIDE IN VIVO AND IN VITRO

Angiotensin II potentiates methacholine-evoked bronchoconstriction both in bovine airways in vitro and in asthmatic patients in vivo. Angiotensin II also potentiates endothelin-1-evoked contractions in vitro, but fails to alter such contractions in vivo. One possible confounding factor in patients is their use of inhaled corticosteroids. Accordingly the present study examined the effects of hydrocortisone (cortisol) on contractions evoked by methacholine and endothelin-1 in the presence and absence of angiotensin II. Contractions of rings of isolated bovine airways were measured isometrically in organ baths. Concentration–response curves were obtained for endothelin-1 or methacholine in the presence and absence of angiotensin II, hydrocortisone and a combination of angiotensin II and hydrocortisone. Hydrocortisone abolished the angiotensin II-mediated potentiation of endothelin-1-evoked, but not methacholine-evoked, contractions. Hydrocortisone alone evoked the enhancement of methacholine responses, similar to the effect produced by angiotensin II. While species differences may exist, our present results suggest that the use of corticosteroids can have a profound effect on the interaction between angiotensin II and endothelin-1. Accordingly, the presence of inhaled corticosteroids might explain the differences between the results obtained in vitro and in vivo.

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Angiotensin II (Ang II) stimulates endothelin-1 (ET-1) secretion in vitro but does not regulate circulating endothelin-1 levels in vivo.

American Journal of Hypertension ◽

10.1016/0895-7061(96)81710-9 ◽

1996 ◽

Vol 9 (4) ◽

pp. 78A

Author(s):

G DESIDERI

Keyword(s):

Angiotensin Ii ◽

Ang Ii ◽

Endothelin 1

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Abstract 325: Brain Natriuretic Peptide During Coronary Intervention Prevents Endothelial Dysfunction Post PCI via NP-cGMP Activation

Circulation Research ◽

10.1161/res.111.suppl_1.a325 ◽

2012 ◽

Vol 111 (suppl_1) ◽

Author(s):

Aviva Peleg ◽

Yonathan Hasin

Keyword(s):

Endothelial Dysfunction ◽

Brain Natriuretic Peptide ◽

Natriuretic Peptide ◽

Kidney Injury ◽

Coronary Intervention ◽

Control Group ◽

Estimate Glomerular Filtration Rate ◽

And Control

Background: Contrast media (CM) administrated during percutaneous coronary intervention (PCI) is associated with endothelial dysfunction (ED) and systemic vascular injury. Brain natriuretic peptide (BNP) administration 24 hours post PCI decreases ED. Aims: To evaluate 1.The ability of human BNP (hBNP) infusion during PCI, to prevent ED in acute coronary syndrome's (ACS) patients post the PCI. 2. The effect of CM on human coronary microvascular endothelial cells (HCMEC).3. Explain ED by invitro study. Methods and results (in vivo): Non-ST elevation ACS patients who underwent PCI (111) were randomized into 2 groups: an hBNP group who received hBNP infusion during the procedure (n=44), and control group who received nitroglycerin (n=67). Flow mediated dilatation (FMD) (by ≥2.5%), BNP, corin, serum creatinine (sCr) and estimate Glomerular Filtration Rate (eGFR), before and 24 hr after operative were recorded, starting with the same baseline. The post PCI FMD and eGFR were significantly reduced in the control group (p=0.05, 0.002) but not in the hBNP group (p=0.16, 0.4). BNP, corin and sCr increased significantly in the control group (p=0.001, 0.003, 0.0002 respectively) but not in hBNP group (p=0.09, 0.07, 0.18). Methods and results (in vitro): HCMEC were treated with CM (10%) in the presence and absence of BNP. eNOS, corin and cGMP levels were measured by ELISA and the results were compared to untreated cells. In both treatments eNOS was significantly reduced (p=0.001) and corin was significantly increased (p=0.002). cGMP was not affected by CM treatment (p=0.278), but was increased significantly (p=0.001) by hBNP combination. cGMP immuno-flourescence staining of HCMEC showed distorted cellular cGMP appearance by CM treatment, that was corrected in the combination with hBNP with accentuated subsarcolemmal staining. Conclusions: CM reduces eNOS level in HCMEC. Therefore, reduced in NO-cGMP pathway's products, probably is the mechanism that induces ED in-vivo. BNP treatment reduces FMD diminution and kidney injury post PCI. A compensatory rise in corin that increases BNP as well as the hBNP administration, invivo and invitro, maintains cytosolic cGMP via NP-cGMP pathway, and compensates for NO-cGMP loss, (reduced sGC) and thus prevents ED.

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Effects of atrial natriuretic peptide, dopamine, and ouabain on aldosterone synthesis

Acta Endocrinologica ◽

10.1530/acta.0.1150057 ◽

1987 ◽

Vol 115 (1) ◽

pp. 57-62 ◽

Cited By ~ 7

Author(s):

Sadao Nakajima ◽

Hiromichi Suzuki ◽

Ikuo Saito ◽

Takao Saruta

Keyword(s):

Angiotensin Ii ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

In Vivo Study ◽

Stimulatory Action ◽

Related Substances ◽

Natriuretic Factors ◽

Atrial Natriuretic

Abstract. This study was undertaken to examine the effects of atrial natriuretic peptide (ANP), dopamine, and ouabain, which each are considered to be a kind of natriuretic factor, on aldosterone synthesis in vivo and in vitro. In the in vivo experiments, during infusion of one of the natriuretic factors, ANP (64 pmol · min−1 · kg−1), dopamine (20 nmol · min−1 · kg−1) or ouabain (684 pmol · min−1 · kg−1), the stimulatory action of angiotensin II (20 pmol · min−1 · kg−1) or adrenocorticotropin (ACTH, 7 pmol · min−1 · kg−1) on aldosterone synthesis was investigated in 36 anaesthetized (pentobarbital, 40 mg/kg, iv) female rabbits. In the basal condition, aldosterone synthesis was suppressed slightly by each of the natriuretic factors. The stimulatory actions of angiotensin II and ACTH on aldosterone synthesis were significantly attenuated by pre-treatment with ANP and dopamine. However, ouabain infusion did not induce any changes in the synthesis of aldosterone, 18-hydroxycorticosterone (18-OHB), and corticosterone (B) in either the basal or the stimulated conditions. For the in vitro experiments, rabbit adrenal glomerulosa cells (105 cells/tube) were used. The effects of ANP and dopamine on the aldosterone synthesis revealed results identical to those from the in vivo study. However, in contrast to the in vivo study, ouabain completely inhibited the synthesis of aldosterone, 18-OHB and B. The above results obtained in vivo and in vitro suggest that ANP inhibits corticosterone methyloxidase II activity and dopamine inhibits corticosterone methyloxidase I activity. However, from the present study we were unable to specify the action of ouabain on the synthesis of aldosterone and its related substances.

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Angiotensin II increases the release of endothelin-I from human cultured endothelial cells but does not regulate its circulating levels

Clinical Science ◽

10.1042/cs0960261 ◽

1999 ◽

Vol 96 (3) ◽

pp. 261-270 ◽

Cited By ~ 1

Author(s):

Claudio FERRI ◽

Giovambattista DESIDERI ◽

Roberta BALDONCINI ◽

Cesare BELLINI ◽

Marco VALENTI ◽

...

Keyword(s):

Endothelial Cells ◽

Protein Synthesis ◽

Angiotensin Ii ◽

At1 Receptor ◽

Dependent Manner ◽

Synthesis Inhibitor ◽

Endothelin 1 ◽

Cultured Endothelial Cells

We investigated the effect of angiotensin II on endothelin-1 secretion in vitro and in vivo. In vivo, angiotensin II was given intravenously to 23 essential hypertensive and 8 control subjects according to different protocols: Study A, 1.0 ngċmin-1ċkg-1 and 3.0 ngċmin-1ċkg-1 angiotensin II for 30 min each; Study B, 1.0 ngċmin-1ċkg-1 and 3.0 ngċmin-1ċkg-1 angiotensin II for 120 min each; Study C, 3.0 ngċmin-1ċkg-1 angiotensin II for 30 min followed by a dose increment of 3.0 ngċmin-1ċkg-1 every 30 min until mean blood pressure levels increased by 25 mmHg; Study D, 1.0 ngċmin-1ċkg-1 followed by 3.0 ngċmin-1ċkg-1 angiotensin II for 60 min each on two different NaCl diets (either 20 mmol NaCl/day or 220 mmol NaCl/day, both for 1 week). In all in vivo studies neither plasma nor urine endothelin-1 levels changed with angiotensin II infusion. In contrast, angiotensin II (10-9, 10-8, 10-7 mol/l) stimulated endothelin-1 secretion from cultured human vascular endothelial cells derived from umbilical cord veins in a time- and dose-dependent manner. The in vitro angiotensin II effects were abolished by candesartan cilexetil, an inhibitor of the membrane-bound AT1 receptor, and also by actinomycin D, an RNA synthesis inhibitor, and cycloheximide, a protein synthesis inhibitor, indicating that endothelin-1 release depended on AT1 receptor subtype and de novo protein synthesis. Our findings indicate that angiotensin II regulates endothelin-1 release by cultured endothelial cells through an AT1 receptor-dependent pathway, but does not influence circulating endothelin-1 levels in vivo.

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Angiotensin II and Atrial Natriuretic Peptide in the Cow Oviductal Contraction In Vitro: Direct Effect and Local Secretion of Prostaglandins, Endothelin-1, and Angiotensin II

Biology of Reproduction ◽

10.1095/biolreprod65.3.799 ◽

2001 ◽

Vol 65 (3) ◽

pp. 799-804 ◽

Cited By ~ 24

Author(s):

Missaka P.B. Wijayagunawardane ◽

Akio Miyamoto ◽

Yuhji Taquahashi ◽

Tomas J. Acosta ◽

Masakazu Nishimura ◽

...

Keyword(s):

Angiotensin Ii ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Direct Effect ◽

Endothelin 1 ◽

Atrial Natriuretic

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Dietary Glycine Prevents FOLFOX Chemotherapy-Induced Heart Injury: A Colorectal Cancer Liver Metastasis Treatment Model in Rats

Nutrients ◽

10.3390/nu12092634 ◽

2020 ◽

Vol 12 (9) ◽

pp. 2634

Author(s):

Juste Maneikyte ◽

Augustinas Bausys ◽

Bettina Leber ◽

Nicole Feldbacher ◽

Gerald Hoefler ◽

...

Keyword(s):

Liver Metastasis ◽

Brain Natriuretic Peptide ◽

Natriuretic Peptide ◽

Myocardial Fibrosis ◽

Pcr Analysis ◽

Type I ◽

Fatty Acid Binding ◽

Folfox Chemotherapy

Introduction: FOLFOX chemotherapy (CTx) is used for the treatment of colorectal liver metastasis (CRLM). Side effects include rare cardiotoxicity, which may limit the application of FOLFOX. Currently, there is no effective strategy to prevent FOLFOX-induced cardiotoxicity. Glycine has been shown to protect livers from CTx-induced injury and oxidative stress, and it reduces platelet aggregation and improves microperfusion. This study tested the hypothesis of glycine being cardioprotective in a rat model of FOLFOX in combination with CRLM. Materials and Methods: The effect of glycine was tested in vitro on human cardiac myocytes (HCMs). To test glycine in vivo Wag/Rij rats with induced CRLM were treated with FOLFOX ±5% dietary glycine. Left ventricle ejection fraction (LVEF), myocardial fibrosis, and apoptosis, also heart fatty acid binding protein (h-FABP) and brain natriuretic peptide levels were monitored. PCR analysis for Collagen type I, II, and brain natriuretic peptide (BNP) in the heart muscle was performed. Results: In vitro glycine had no effect on HCM cell viability. Treatment with FOLFOX resulted in a significant increase of h-FABP levels, increased myocardial fibrosis, and apoptosis as well as increased expression of type I Collagen. Furthermore, FOLFOX caused a decrease of LVEF by 10% (p = 0.028). Dietary glycine prevented FOLFOX-induced myocardial injury by preserving the LVEF and reducing the levels of fibrosis (p = 0.012) and apoptosis (p = 0.015) in vivo. Conclusions: Data presented here demonstrate for the first time that dietary glycine protects the heart against FOLFOX-induced injury during treatment for CRLM.

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