LIVIVO - Search results -

Search results

Result 1 - 10 of total 18

Search options

Article ; Online: Renal venous congestion and renal function in congestive heart failure.

Joles, Jaap A / Bongartz, Lennart G / Gaillard, Carlo A / Braam, Branko

Journal of the American College of Cardiology

2009 Volume 54, Issue 17, Page(s) 1632; author reply 1632–3

MeSH term(s)	Glomerular Filtration Rate ; Heart Failure/complications ; Heart Failure/physiopathology ; Humans ; Kidney/physiopathology ; Kidney Diseases/etiology ; Kidney Diseases/physiopathology ; Venous Insufficiency/physiopathology
Language	English
Publishing date	2009-10-20
Publishing country	United States
Document type	Comment ; Letter
ZDB-ID	605507-2
ISSN	1558-3597 ; 0735-1097
ISSN (online)	1558-3597
ISSN	0735-1097
DOI	10.1016/j.jacc.2009.05.068
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1846: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 196: Show issues

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: 5/6th nephrectomy in combination with high salt diet and nitric oxide synthase inhibition to induce chronic kidney disease in the Lewis rat.

van Koppen, Arianne / Verhaar, Marianne C / Bongartz, Lennart G / Joles, Jaap A

Journal of visualized experiments : JoVE

2013 , Issue 77, Page(s) e50398

Abstract: Chronic kidney disease (CKD) is a global problem. Slowing CKD progression is a major health priority. Since CKD is characterized by complex derangements of homeostasis, integrative animal models are necessary to study development and progression of CKD. ... ...

Abstract	Chronic kidney disease (CKD) is a global problem. Slowing CKD progression is a major health priority. Since CKD is characterized by complex derangements of homeostasis, integrative animal models are necessary to study development and progression of CKD. To study development of CKD and novel therapeutic interventions in CKD, we use the 5/6th nephrectomy ablation model, a well known experimental model of progressive renal disease, resembling several aspects of human CKD. The gross reduction in renal mass causes progressive glomerular and tubulo-interstitial injury, loss of remnant nephrons and development of systemic and glomerular hypertension. It is also associated with progressive intrarenal capillary loss, inflammation and glomerulosclerosis. Risk factors for CKD invariably impact on endothelial function. To mimic this, we combine removal of 5/6th of renal mass with nitric oxide (NO) depletion and a high salt diet. After arrival and acclimatization, animals receive a NO synthase inhibitor (NG-nitro-L-Arginine) (L-NNA) supplemented to drinking water (20 mg/L) for a period of 4 weeks, followed by right sided uninephrectomy. One week later, a subtotal nephrectomy (SNX) is performed on the left side. After SNX, animals are allowed to recover for two days followed by LNNA in drinking water (20 mg/L) for a further period of 4 weeks. A high salt diet (6%), supplemented in ground chow (see time line Figure 1), is continued throughout the experiment. Progression of renal failure is followed over time by measuring plasma urea, systolic blood pressure and proteinuria. By six weeks after SNX, renal failure has developed. Renal function is measured using 'gold standard' inulin and para-amino hippuric acid (PAH) clearance technology. This model of CKD is characterized by a reduction in glomerular filtration rate (GFR) and effective renal plasma flow (ERPF), hypertension (systolic blood pressure>150 mmHg), proteinuria (> 50 mg/24 hr) and mild uremia (>10 mM). Histological features include tubulo-interstitial damage reflected by inflammation, tubular atrophy and fibrosis and focal glomerulosclerosis leading to massive reduction of healthy glomeruli within the remnant population (<10%). Follow-up until 12 weeks after SNX shows further progression of CKD.
MeSH term(s)	Animals ; Disease Models, Animal ; Glomerular Filtration Rate ; Male ; Nephrectomy ; Nitric Oxide Synthase/antagonists & inhibitors ; Nitroarginine/pharmacology ; Rats ; Rats, Inbred Lew ; Renal Insufficiency, Chronic/etiology ; Renal Insufficiency, Chronic/physiopathology ; Sodium Chloride, Dietary/administration & dosage
Chemical Substances	Sodium Chloride, Dietary ; Nitroarginine (2149-70-4) ; Nitric Oxide Synthase (EC 1.14.13.39)
Language	English
Publishing date	2013-07-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Video-Audio Media
ZDB-ID	2259946-0
ISSN	1940-087X ; 1940-087X
ISSN (online)	1940-087X
ISSN	1940-087X
DOI	10.3791/50398
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: The cardiorenal syndrome a classification into 4 groups?

van der Putten, Karien / Bongartz, Lennart G / Braam, Branko / Gaillard, Carlo A J M

Journal of the American College of Cardiology

2009 Volume 53, Issue 15, Page(s) 1340; author reply 1340–1

MeSH term(s)	Heart Failure/classification ; Heart Failure/complications ; Humans ; Renal Insufficiency/classification ; Renal Insufficiency/complications ; Syndrome
Language	English
Publishing date	2009-04-14
Publishing country	United States
Document type	Comment ; Letter
ZDB-ID	605507-2
ISSN	1558-3597 ; 0735-1097
ISSN (online)	1558-3597
ISSN	0735-1097
DOI	10.1016/j.jacc.2008.12.042
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1846: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 196: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: The cardiorenal connection.

Bongartz, Lennart G / Cramer, Maarten Jan M / Braam, Branko

Hypertension (Dallas, Tex. : 1979)

2004 Volume 43, Issue 4, Page(s) e14

MeSH term(s)	Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/etiology ; Feedback, Physiological ; Heart Failure/complications ; Heart Failure/physiopathology ; Humans ; Inflammation ; Kidney Failure, Chronic/complications ; Kidney Failure, Chronic/physiopathology ; Models, Biological ; Oxidative Stress ; Renin-Angiotensin System/physiology ; Risk Factors ; Sympathetic Nervous System/physiopathology ; Syndrome
Language	English
Publishing date	2004-04
Publishing country	United States
Document type	Comment ; Letter
ZDB-ID	423736-5
ISSN	1524-4563 ; 0194-911X ; 0362-4323
ISSN (online)	1524-4563
ISSN	0194-911X ; 0362-4323
DOI	10.1161/01.HYP.0000118521.06245.b8
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1488: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: 5/6th nephrectomy in combination with high salt diet and nitric oxide synthase inhibition to induce chronic kidney disease in the lewis rat

van Koppen, Arianne / Verhaar, Marianne C / Bongartz, Lennart G / Joles, Jaap A

Journal of visualized experiments. 2013 July 03, , no. 77

2013

Abstract	Chronic kidney disease (CKD) is a global problem. Slowing CKD progression is a major health priority. Since CKD is characterized by complex derangements of homeostasis, integrative animal models are necessary to study development and progression of CKD. To study development of CKD and novel therapeutic interventions in CKD, we use the 5/6th nephrectomy ablation model, a well known experimental model of progressive renal disease, resembling several aspects of human CKD. The gross reduction in renal mass causes progressive glomerular and tubulo-interstitial injury, loss of remnant nephrons and development of systemic and glomerular hypertension. It is also associated with progressive intrarenal capillary loss, inflammation and glomerulosclerosis. Risk factors for CKD invariably impact on endothelial function. To mimic this, we combine removal of 5/6th of renal mass with nitric oxide (NO) depletion and a high salt diet. After arrival and acclimatization, animals receive a NO synthase inhibitor (NG-nitro-L-Arginine) (L-NNA) supplemented to drinking water (20 mg/L) for a period of 4 weeks, followed by right sided uninephrectomy. One week later, a subtotal nephrectomy (SNX) is performed on the left side. After SNX, animals are allowed to recover for two days followed by LNNA in drinking water (20 mg/L) for a further period of 4 weeks. A high salt diet (6%), supplemented in ground chow (see time line Figure 1), is continued throughout the experiment. Progression of renal failure is followed over time by measuring plasma urea, systolic blood pressure and proteinuria. By six weeks after SNX, renal failure has developed. Renal function is measured using 'gold standard' inulin and para-amino hippuric acid (PAH) clearance technology. This model of CKD is characterized by a reduction in glomerular filtration rate (GFR) and effective renal plasma flow (ERPF), hypertension (systolic blood pressure>150 mmHg), proteinuria (> 50 mg/24 hr) and mild uremia (>10 mM). Histological features include tubulo-interstitial damage reflected by inflammation, tubular atrophy and fibrosis and focal glomerulosclerosis leading to massive reduction of healthy glomeruli within the remnant population (<10%). Follow-up until 12 weeks after SNX shows further progression of CKD.
Keywords	acclimation ; animal models ; atrophy ; diet ; drinking water ; enzyme inhibition ; enzyme inhibitors ; fibrosis ; glomerular filtration rate ; hippuric acid ; histology ; homeostasis ; humans ; hypertension ; inflammation ; inulin ; nephrons ; nitric oxide ; nitric oxide synthase ; proteinuria ; rats ; renal failure ; risk factors ; systolic blood pressure ; therapeutics ; urea ; uremia
Language	English
Dates of publication	2013-0703
Size	p. e50398.
Publishing place	Journal of Visualized Experiments
Document type	Article
ZDB-ID	2259946-0
ISSN	1940-087X
ISSN	1940-087X
DOI	10.3791/50398
Database	NAL-Catalogue (AGRICOLA)

Order via subito

Article: Neuronal nitric oxide synthase-dependent amelioration of diastolic dysfunction in rats with chronic renocardiac syndrome.

Bongartz, Lennart G / Soni, Siddarth / Cramer, Maarten-Jan / Steendijk, Paul / Gaillard, Carlo A J M / Verhaar, Marianne C / Doevendans, Pieter A / van Veen, Toon A / Joles, Jaap A / Braam, Branko

Cardiorenal medicine

2015 Volume 5, Issue 1, Page(s) 69–78

Abstract: We have recently described the chronic renocardiac syndrome (CRCS) in rats with renal failure, cardiac dysfunction and low nitric oxide (NO) availability by combining subtotal nephrectomy and transient low-dose NO synthase (NOS) inhibition. Cardiac gene ... ...

Abstract	We have recently described the chronic renocardiac syndrome (CRCS) in rats with renal failure, cardiac dysfunction and low nitric oxide (NO) availability by combining subtotal nephrectomy and transient low-dose NO synthase (NOS) inhibition. Cardiac gene expression of the neuronal isoform of NOS (nNOS) was induced. Hence, we studied the role of nNOS, in vivo cardiac function and β-adrenergic response in our CRCS model by micromanometer/conductance catheter. Left ventricular (LV) hemodynamics were studied during administration of dobutamine (dobu), the highly specific irreversible inhibitor of nNOS L-VNIO [L-N5-(1-Imino-3-butenyl)-ornithine], or both at steady state and during preload reduction. Rats with CRCS showed LV systolic dysfunction at baseline, together with prolonged diastolic relaxation and rightward shift of the end-systolic pressure-volume relationships. After L-VNIO infusion, diastolic relaxation of CRCS rats further prolonged. The time constant of active relaxation (tau) increased by 25 ± 6% from baseline (p < 0.05), and the maximal rate of pressure decrease was 36 ± 7% slower (p < 0.001). These variables did not change in controls. In our CRCS model, nNOS did not seem to affect systolic dysfunction. In summary, in this model of CRCS, blockade of nNOS further worsens diastolic dysfunction and L-VNIO does not influence inherent contractility and the response to dobu stress.
Language	English
Publishing date	2015-02
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2595659-0
ISSN	1664-5502 ; 1664-3828
ISSN (online)	1664-5502
ISSN	1664-3828
DOI	10.1159/000370052
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Details ▾
- Full text online
- Order with fees

Article ; Online: Target organ cross talk in cardiorenal syndrome: animal models.

Bongartz, Lennart G / Braam, Branko / Gaillard, Carlo A / Cramer, Maarten J / Goldschmeding, Roel / Verhaar, Marianne C / Doevendans, Pieter A / Joles, Jaap A

American journal of physiology. Renal physiology

2012 Volume 303, Issue 9, Page(s) F1253–63

Abstract: The combination of chronic kidney disease (CKD) and heart failure (HF) is associated with an adverse prognosis. Although clinical studies hint at a specific bidirectional interaction between HF and CKD, insight into the pathogenesis of cardiorenal ... ...

Abstract	The combination of chronic kidney disease (CKD) and heart failure (HF) is associated with an adverse prognosis. Although clinical studies hint at a specific bidirectional interaction between HF and CKD, insight into the pathogenesis of cardiorenal syndrome (CRS) remains limited. We review available evidence on cardiorenal interactions from animal models of CKD and HF and discuss several studies that employed a "double-hit" model to research organ cross talk between the heart and kidneys. Regarding cardiac changes in CKD models, parameters of cardiac remodeling are equivocal and cardiac systolic function generally remains preserved. Structural changes include hypertrophy, fibrosis, and microvasculopathy. In models of HF, data on renal pathology are mostly limited to functional hemodynamic changes. Most double-hit models were unable to show that combined renal and cardiac injury induces additive damage to both organs, perhaps because of the short study duration or absence of organ failure. Because of this lack of "dual-failure" models, we have developed two rat models of combined CKD and HF in which renal dysfunction induced by a subtotal nephrectomy preceded cardiac dysfunction. Cardiac dysfunction was induced either functionally by nitric oxide depletion or structurally by myocardial infarction. In both models, we found that cardiac remodeling and failure were worse in CKD rats compared with controls undergoing the same cardiac insult. Variables of renal damage, like glomerulosclerosis and proteinuria, were also further worsened by combined cardiorenal injury. These studies show that target organ cross talk does occur in CRS. These models may be useful for interventional studies in rats.
MeSH term(s)	Animals ; Cardio-Renal Syndrome/pathology ; Cardio-Renal Syndrome/physiopathology ; Disease Models, Animal ; Heart/physiopathology ; Heart Failure/pathology ; Heart Failure/physiopathology ; Kidney/pathology ; Kidney/physiopathology ; Myocardium/pathology ; Rats ; Renal Insufficiency, Chronic/pathology ; Renal Insufficiency, Chronic/physiopathology
Language	English
Publishing date	2012-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00392.2012
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.89: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Cardiac Hepcidin Expression Associates with Injury Independent of Iron.

van Breda, G Fenna / Bongartz, Lennart G / Zhuang, Wenqing / van Swelm, Rachel P L / Pertijs, Jeanne / Braam, Branko / Cramer, Maarten-Jan / Swinkels, Dorine W / Doevendans, Pieter A / Verhaar, Marianne C / Masereeuw, Roos / Joles, Jaap A / Gaillard, Carlo A J M

American journal of nephrology

2016 Volume 44, Issue 5, Page(s) 368–378

Abstract: Background: Hepcidin regulates systemic iron homeostasis by downregulating the iron exporter ferroportin. Circulating hepcidin is mainly derived from the liver but hepcidin is also produced in the heart. We studied the differential and local regulation ... ...

Abstract	Background: Hepcidin regulates systemic iron homeostasis by downregulating the iron exporter ferroportin. Circulating hepcidin is mainly derived from the liver but hepcidin is also produced in the heart. We studied the differential and local regulation of hepcidin gene expression in response to myocardial infarction (MI) and/or chronic kidney disease (CKD). We hypothesized that cardiac hepcidin gene expression is induced by and regulated to severity of cardiac injury, either through direct (MI) or remote (CKD) stimuli, as well as through increased local iron content. Methods: Nine weeks after subtotal nephrectomy (SNX) or sham surgery (CON), rats were subjected to coronary ligation (CL) or sham surgery to realize 4 groups: CON, SNX, CL and SNX + CL. In week 16, the gene expression of hepcidin, iron and damage markers in cardiac and liver tissues was assessed by quantitative polymerase chain reaction and ferritin protein expression was studied by immunohistochemistry. Results: Cardiac hepcidin messenger RNA (mRNA) expression was increased 2-fold in CL (p = 0.03) and 3-fold in SNX (p = 0.01). Cardiac ferritin staining was not different among groups. Cardiac hepcidin mRNA expression correlated with mRNA expression levels of brain natriuretic peptide (β = 0.734, p < 0.001) and connective tissue growth factor (β = 0.431, p = 0.02). In contrast, liver hepcidin expression was unaffected by SNX and CL alone, while it had decreased 50% in SNX + CL (p < 0.05). Hepatic ferritin immunostaining was not different among groups. Conclusions: Our data indicate differences in hepcidin regulation in liver and heart and suggest a role for injury rather than iron as the driving force for cardiac hepcidin expression in renocardiac failure.
MeSH term(s)	Animals ; Bone Morphogenetic Protein 6/metabolism ; CCAAT-Enhancer-Binding Protein-alpha/metabolism ; Cation Transport Proteins/metabolism ; Connective Tissue Growth Factor/metabolism ; Cytokines/metabolism ; Gene Expression Regulation ; Heme Oxygenase (Decyclizing)/metabolism ; Hepcidins/metabolism ; Iron/metabolism ; Liver/metabolism ; Male ; Myocardial Infarction/metabolism ; Myocardium/metabolism ; Natriuretic Peptide, Brain/metabolism ; Rats, Inbred Lew ; Renal Insufficiency, Chronic/metabolism
Chemical Substances	Bmp6 protein, rat ; Bone Morphogenetic Protein 6 ; CCAAT-Enhancer-Binding Protein-alpha ; CCN2 protein, rat ; Cation Transport Proteins ; Cytokines ; Hepcidins ; metal transporting protein 1 ; Natriuretic Peptide, Brain (114471-18-0) ; Connective Tissue Growth Factor (139568-91-5) ; Iron (E1UOL152H7) ; Heme Oxygenase (Decyclizing) (EC 1.14.14.18) ; Hmox1 protein, rat (EC 1.14.14.18)
Language	English
Publishing date	2016-10-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	604540-6
ISSN	1421-9670 ; 0250-8095
ISSN (online)	1421-9670
ISSN	0250-8095
DOI	10.1159/000449419
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 1635: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article: Arrhythmogenic Remodeling in Murine Models of Deoxycorticosterone Acetate-Salt-Induced and 5/6-Subtotal Nephrectomy-Salt-Induced Cardiorenal Disease.

Fontes, Magda S C / Papazova, Diana A / van Koppen, Arianne / de Jong, Sanne / Korte, Sanne M / Bongartz, Lennart G / Nguyen, Tri Q / Bierhuizen, Marti F A / de Boer, Teun P / van Veen, Toon A B / Verhaar, Marianne C / Joles, Jaap A / van Rijen, Harold V M

Cardiorenal medicine

2015 Volume 5, Issue 3, Page(s) 208–218

Abstract: Background: Renal failure is associated with adverse cardiac remodeling and sudden cardiac death. The mechanism leading to enhanced arrhythmogenicity in the cardiorenal syndrome is unclear. The aim of this study was to characterize electrophysiological ... ...

Abstract	Background: Renal failure is associated with adverse cardiac remodeling and sudden cardiac death. The mechanism leading to enhanced arrhythmogenicity in the cardiorenal syndrome is unclear. The aim of this study was to characterize electrophysiological and tissue alterations correlated with enhanced arrhythmogenicity in two distinct mouse models of renal failure. Methods: Thirty-week-old 129Sv mice received a high-salt diet and deoxycorticosterone acetate (DOCA) for 8 weeks, followed by an additional period of high-salt diet for 27 weeks (DOCA-salt aged model). Adult CD-1 mice were submitted to 5/6-subtotal nephrectomy (SNx) and treated for 11 weeks with a high-salt diet (SNx-salt adult model). Vulnerability to arrhythmia as well as conduction velocities (CVs) of the hearts were determined ex vivo with epicardial mapping. Subsequently, the hearts were characterized for connexin 43 (Cx43) and fibrosis. Results: DOCA-salt and SNx-salt mice developed renal dysfunction characterized by albuminuria. Heart, lung and kidney weights were increased in DOCA-salt mice. Both DOCA-salt and SNx-salt mice were highly susceptible to ventricular arrhythmias. DOCA-salt mice had a significant decrease in both longitudinal and transversal CV in the left ventricle. Histological analysis revealed a significant reduction in Cx43 expression as well as an increase in interstitial fibrosis in both DOCA-salt and SNx-salt mice. Conclusion: DOCA-salt and SNx-salt treatment induced renal dysfunction, which resulted in structural and electrical cardiac remodeling and enhanced arrhythmogenicity. The reduced Cx43 expression and increased fibrosis levels in these hearts are likely candidates for the formation of the arrhythmogenic substrate.
Language	English
Publishing date	2015-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2595659-0
ISSN	1664-5502 ; 1664-3828
ISSN (online)	1664-5502
ISSN	1664-3828
DOI	10.1159/000430475
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Details ▾
- Full text online
- Order with fees

Article: The severe cardiorenal syndrome: 'Guyton revisited'.

Bongartz, Lennart G / Cramer, Maarten Jan / Doevendans, Pieter A / Joles, Jaap A / Braam, Branko

European heart journal

2005 Volume 26, Issue 1, Page(s) 11–17

Abstract: The incidence of cardiac failure and chronic renal failure is increasing and it has now become clear that the co-existence of the two problems has an extremely bad prognosis. We propose the severe cardiorenal syndrome (SCRS), a pathophysiological ... ...

Abstract	The incidence of cardiac failure and chronic renal failure is increasing and it has now become clear that the co-existence of the two problems has an extremely bad prognosis. We propose the severe cardiorenal syndrome (SCRS), a pathophysiological condition in which combined cardiac and renal dysfunction amplifies progression of failure of the individual organ, so that cardiovascular morbidity and mortality in this patient group is at least an order of magnitude higher than in the general population. Guyton has provided an excellent framework describing the physiological relationships between cardiac output, extracellular fluid volume control, and blood pressure. While this model is also sufficient to understand systemic haemodynamics in combined cardiac and renal failure, not all aspects of the observed accelerated atherosclerosis, structural myocardial changes, and further decline of renal function can be explained. Since increased activity of the renin-angiotensin system, oxidative stress, inflammation, and increased activity of the sympathetic nervous system seem to be cornerstones of the pathophysiology in combined chronic renal disease and heart failure, we have explored the potential interactions between these cardiorenal connectors. As such, the cardiorenal connection is an interactive network with positive feedback loops, which, in our view, forms the basis for the SCRS.
MeSH term(s)	Blood Pressure/physiology ; Coronary Artery Disease/etiology ; Heart Failure/complications ; Heart Failure/physiopathology ; Humans ; Kidney Failure, Chronic/complications ; Kidney Failure, Chronic/physiopathology ; Nephritis/etiology ; Nitric Oxide/physiology ; Oxidative Stress/physiology ; Reactive Oxygen Species/metabolism ; Renin-Angiotensin System/physiology ; Syndrome
Chemical Substances	Reactive Oxygen Species ; Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2005-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	603098-1
ISSN	1522-9645 ; 0195-668X
ISSN (online)	1522-9645
ISSN	0195-668X
DOI	10.1093/eurheartj/ehi020
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1563: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 640: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito