Interaction of ANP with endothelin on cardiovascular, renal, and endocrine function

Ota, Kozo; Kimura, Tomohiko; Miyake, Shoji; Inoue, Minoru; Sato, Kazutoshi; Ohta, Makoto; Yamamoto, Takeki; Tsunoda, Kazuo; Abe, Keishi; Yoshinaga, Kaoru

doi:10.1152/ajpendo.1992.262.2.e135

Cited by 15 publications

(14 citation statements)

References 3 publications

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“…Experimental data have shown that plasma ANP rises after infusion of ET-1 but it remains uncertain to what extent the concomitant rise in blood pressure after ET-1 infusion or a direct stimulatory action of ET-1 on ANP release of cardiomyocytes is responsible for this increase (25). In the present study no correlation between plasma ET-1 and ANP could be found.…”

Section: Discussioncontrasting

confidence: 76%

Oxygen-mediated pulmonary vasodilation and plasma levels of endothelin-1, atrial natriuretic peptide and cyclic GMP in patients with left-to-right shunt and pulmonary hypertension

Gorenflo¹,

Bettendorf

He³

et al. 2000

Z Kardiol

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This study was performed to evaluate the role of endogenous endothelin-1 (ET-1), atrial natriuretic peptide (ANP) and cyclic guanosine monophosphate (cGMP) in patients with left-to-right shunt and pulmonary hypertension. Further objectives were to study a possible feedback mechanism between ANP and ET-1 and to examine the influence of ANP on cGMP plasma levels. Finally, the role of these hormones in oxygen-mediated pulmonary vasodilation was examined. Plasma concentrations of ET-1, ANP and cGMP were studied in 39 patients with congenital heart disease and left-to-right shunt. Blood samples were taken from the pulmonary artery and pulmonary vein at cardiac catheterization at baseline and after breathing oxygen for 20 min. Patients were grouped according to the presence or absence of pulmonary hypertension (defined as mean Pp/Ps > or = 0.5). Patients with pulmonary hypertension (n = 18) were found to have significantly higher plasma ANP (665 [59-1358] versus 267 [47-832] pg/ml) and cGMP (21.5 [3.6-82.2] versus 7.8 [0-14.6] nM/L) levels than patients without pulmonary hypertension (n = 21). Pulmonary venous ET-1 plasma concentrations were above normal limits in one patient only. ANP plasma levels were not related to ET-1 and cGMP concentrations. There was no transpulmonary gradient for any of the factors. Pulmonary vasodilation in response to oxygen was found in 7 of 18 patients with PH, but was not associated with significant changes in ET-1, ANP or cGMP plasma concentrations. Patients with congenital heart disease and PH show an increase both in vasoconstrictive and vasodilating factors. The mechanism of oxygen-mediated vasodilation in these patients remains to be elucidated.

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Section: Discussioncontrasting

confidence: 76%

Oxygen-mediated pulmonary vasodilation and plasma levels of endothelin-1, atrial natriuretic peptide and cyclic GMP in patients with left-to-right shunt and pulmonary hypertension

Gorenflo¹,

Bettendorf

He³

et al. 2000

Z Kardiol

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“…4F). It is known that the endothelin system not only stimulates the secretion of Nppa (52) but that they also counteract each other in some cardiovascular, renal, and endocrine functions (53). Furthermore, previous studies have also demonstrated that Nppa secretion occurs via an EDNRB-mediated pathway involving the MAPK signaling pathway (54), and MAPK along with PI3K pathways regulate the hypoxia-induced Nppa secretion by controlling HIF-1α (55).…”

Section: Discussionmentioning

confidence: 99%

Endothelin receptor B, a candidate gene from human studies at high altitude, improves cardiac tolerance to hypoxia in genetically engineered heterozygote mice

Stobdan

Zhou

Ao-Ieong

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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To better understand human adaptation to stress, and in particular to hypoxia, we took advantage of one of nature's experiments at high altitude (HA) and studied Ethiopians, a population that is well-adapted to HA hypoxic stress. Using whole-genome sequencing, we discovered that EDNRB (Endothelin receptor type B) is a candidate gene involved in HA adaptation. To test whether EDNRB plays a critical role in hypoxia tolerance and adaptation, we generated EdnrB knockout mice and found that when EdnrB −/+ heterozygote mice are treated with lower levels of oxygen (O 2 ), they tolerate various levels of hypoxia (even extreme hypoxia, e.g., 5% O 2 ) very well. For example, they maintain ejection fraction, cardiac contractility, and cardiac output in severe hypoxia. Furthermore, O 2 delivery to vital organs was significantly higher and blood lactate was lower in EdnrB −/+ compared with wild type in hypoxia. Tissue hypoxia in brain, heart, and kidney was lower in EdnrB −/+ mice as well. These data demonstrate that a lower level of EDNRB significantly improves cardiac performance and tissue perfusion under various levels of hypoxia. Transcriptomic profiling of left ventricles revealed three specific genes [natriuretic peptide type A (Nppa), sarcolipin (Sln), and myosin light polypeptide 4 (Myl4)] that were oppositely expressed (q < 0.05) between EdnrB −/+ and wild type. Functions related to these gene networks were consistent with a better cardiac contractility and performance. We conclude that EDNRB plays a key role in hypoxia tolerance and that a lower level of EDNRB contributes, at least in part, to HA adaptation in humans.is often referred to as a biosignature, a chemical marker in the atmosphere closely associated with life, and in a complex organism, such as humans, various physiological systems have evolved to maintain an optimal O 2 homeostasis. Arguably, humans living at high altitude (HA) for thousands of years ought to have undergone a significant level of natural selection to adjust to the challenging hypoxic condition. Human adaptation to HA hypoxia, which can be protective to tissues, can potentially be harnessed for better therapeutic modalities for sea-level diseases that involve hypoxia and ischemia in their pathogenesis. Indeed, lessons from such an "experiment in nature" can be derived from HA adaptation and can advance lowaltitude medicine (1). With the advent of newer technology including next-generation sequencing (seq), this idea has recently led to intensive efforts, and a number of publications have appeared on studies of human populations living at HA (2-4). These studies also draw added significance not only to sea-level human diseases but also to more than 140 million people living at an altitude above 2,500 m, where the hypoxic condition presents a major challenge for survival (5). Although a number of laboratory methods that mimic hypoxia adaptation using model organisms (6) have been used as tools to identify causative genetic pathways (7,8), studies in human populations living at different H...

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“…Angiotensin II downregulates NP receptors [24] to decrease cGMP production evoked by ANP [25] . Infusion of a high dose of endothelin after ANP infusion curtails the response to ANP, and induces a fall in renal blood flow and GFR [26] . Furthermore, the synthesis of angiotensin II and endothelin was increased in the cortex in GM-induced nephropathy [27,28] .…”

Section: Discussionmentioning

confidence: 99%

Gentamicin Decreases Guanylyl Cyclase Activity in Rat Glomerulus

Bae¹,

Park³

et al. 2007

Kidney Blood Press Res

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Background: Effects of gentamicin (GM) on the local natriuretic peptide (NP) and nitric oxide (NO) systems in the kidney were investigated. Methods: Male Sprague-Dawley rats (180–200 g) were intramuscularly injected with GM (100 mg/kg/day) for 5 days. The expression of NO synthase (NOS) isoforms was determined by Western blot analysis, and that of NPs by real-time polymerase chain reaction. The activity of guanylyl cyclase was also determined by the amount of guanosine 3′,5′-cyclic monophosphate (cGMP) generated in responses to atrial natriuretic peptide (ANP) or sodium nitroprusside (SNP). Results: GM treatment resulted in renal failure in association with increases in urinary flow and the fractional excretion of sodium. Accordingly, the expression of inducible NOS was increased in the cortex, while that of endothelial NOS remained unchanged. The urinary excretion of NO metabolites was increased. The expression of ANP, brain natriuretic peptide and C-type natriuretic peptide mRNA was increased in the kidney. The cGMP production provoked by either ANP or SNP was decreased in the glomerulus, but not in the papilla. Conclusion: GM-induced nephropathy may be causally related with decreased guanylyl cyclase activities in the glomerulus.

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Interaction of ANP with endothelin on cardiovascular, renal, and endocrine function

Cited by 15 publications

References 3 publications

Oxygen-mediated pulmonary vasodilation and plasma levels of endothelin-1, atrial natriuretic peptide and cyclic GMP in patients with left-to-right shunt and pulmonary hypertension

Oxygen-mediated pulmonary vasodilation and plasma levels of endothelin-1, atrial natriuretic peptide and cyclic GMP in patients with left-to-right shunt and pulmonary hypertension

Endothelin receptor B, a candidate gene from human studies at high altitude, improves cardiac tolerance to hypoxia in genetically engineered heterozygote mice

Gentamicin Decreases Guanylyl Cyclase Activity in Rat Glomerulus

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