Database: Ovid MEDLINE(R) <1996 to April Week 4 2010>
Search Strategy:
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1 *Kidney Diseases/pp [Physiopathology] (1285)
2 *Heart/ph, pp [Physiology, Physiopathology] (8642)
3 1 and 2 (5)
4 limit 3 to (english language and humans) (4)
5 *heart/ and 1 (5)
6 limit 5 to (english language and humans) (4)
7 kidney diseases/pp and heart/ (23)
8 limit 7 to (english language and humans) (16)
9 from 8 keep 1-16 (16)
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<1>
Unique Identifier
11694220
Status
MEDLINE
Authors
Dzau VJ. Bernstein K. Celermajer D. Cohen J. Dahlof B. Deanfield J. Diez J. Drexler H. Ferrari R. van Gilst W. Hansson L. Hornig B. Husain A. Johnston C. Lazar H. Lonn E. Luscher T. Mancini J. Mimran A. Pepine C. Rabelink T. Remme W. Ruilope L. Ruzicka M. Schunkert H. Swedberg K. Unger T. Vaughan D. Weber M. Working Group on Tissue Angiotensin-converting enzyme, International Society of Cardiovascular Pharmacotherapy.
Authors Full Name
Dzau, V J. Bernstein, K. Celermajer, D. Cohen, J. Dahlof, B. Deanfield, J. Diez, J. Drexler, H. Ferrari, R. van Gilst, W. Hansson, L. Hornig, B. Husain, A. Johnston, C. Lazar, H. Lonn, E. Luscher, T. Mancini, J. Mimran, A. Pepine, C. Rabelink, T. Remme, W. Ruilope, L. Ruzicka, M. Schunkert, H. Swedberg, K. Unger, T. Vaughan, D. Weber, M. Working Group on Tissue Angiotensin-converting enzyme, International Society of Cardiovascular Pharmacotherapy.
Institution
Department of Medicine, Brigham Women's Hospital, 75 Francis Street, Boston, MA 02115, USA.
Title
The relevance of tissue angiotensin-converting enzyme: manifestations in mechanistic and endpoint data. [Review] [160 refs]
Source
American Journal of Cardiology. 88(9A):1L-20L, 2001 Nov 8.
Abstract
Angiotensin-converting enzyme (ACE) is primarily localized (>90%) in various tissues and organs, most notably on the endothelium but also within parenchyma and inflammatory cells. Tissue ACE is now recognized as a key factor in cardiovascular and renal diseases. Endothelial dysfunction, in response to a number of risk factors or injury such as hypertension, diabetes mellitus, hypercholesteremia, and cigarette smoking, disrupts the balance of vasodilation and vasoconstriction, vascular smooth muscle cell growth, the inflammatory and oxidative state of the vessel wall, and is associated with activation of tissue ACE. Pathologic activation of local ACE can have deleterious effects on the heart, vasculature, and the kidneys. The imbalance resulting from increased local formation of angiotensin II and increased bradykinin degradation favors cardiovascular disease. Indeed, ACE inhibitors effectively reduce high blood pressure and exert cardio- and renoprotective actions. Recent evidence suggests that a principal target of ACE inhibitor action is at the tissue sites. Pharmacokinetic properties of various ACE inhibitors indicate that there are differences in their binding characteristics for tissue ACE. Clinical studies comparing the effects of antihypertensives (especially ACE inhibitors) on endothelial function suggest differences. More comparative experimental and clinical studies should address the significance of these drug differences and their impact on clinical events. [References: 160]
Publication Type
Consensus Development Conference. Journal Article. Research Support, Non-U.S. Gov't. Review.
<2>
Unique Identifier
9074770
Status
MEDLINE
Authors
Matsusaka T. Ichikawa I.
Authors Full Name
Matsusaka, T. Ichikawa, I.
Institution
Vanderbilt University Medical Center, Nashville, Tennessee 37232-2584, USA.
Title
Biological functions of angiotensin and its receptors. [Review] [99 refs]
Source
Annual Review of Physiology. 59:395-412, 1997.
Abstract
Angiotensin receptors are present in a number of organs and systems including heart, kidney, gonad, and placenta; pituitary and adrenal glands; the peripheral vessels, and the central nervous system. This octapeptide exerts diverse effects that include induction of cell hypertrophy and/or hyperplasia and a stimulation of hormone synthesis and ion transport in the heart, kidney, and adrenal, primarily through type 1 (AT1) receptors. In the kidney, several heterogeneous cell populations--endothelial, epithelial, and vascular--carry AT1 receptors. Some studies suggest that AT2 receptors are also functional, but the cell type carrying this receptor and the nature of its specific function have not been fully elucidated. Although studies indicate that AT1 receptors are affected in response to physiological and pathophysiological manipulations, the functional significance of these modulations remains largely uncertain. Nevertheless, recent human genetic studies indicate that polymorphisms in AT1 receptors, as well as in other angiotensin-related genes, have significant impact on organ remodeling processes of the heart and the kidney. [References: 99]
Publication Type
Journal Article. Research Support, Non-U.S. Gov't. Research Support, U.S. Gov't, P.H.S.. Review.
<3>
Unique Identifier
15629009
Status
MEDLINE
Authors
Nakas-Icindic E. Zaciragic A. Hadzovic A. Avdagic N.
Authors Full Name
Nakas-Icindic, Emina. Zaciragic, Asija. Hadzovic, Almira. Avdagic, Nesina.
Institution
Institute of Physiology and Biochemistry, University of Sarajevo, School of Medicine, Bosnia and Herzegovina.
Title
Endothelin in health and disease. [Review] [25 refs]
Source
Bosnian Journal of Basic Medical Sciences. 4(3):31-4, 2004 Jul.
Abstract
Endothelin is a recently discovered peptide composed of 21 amino acids. There are three endothelin isomers: endothelin-1 (ET-1), endothelin-2 (ET-2) and endothelin- 3 (ET-3). In humans and animals levels of ET-1, ET-2, ET-3 and big endothelin in blood range from 0,3 to 3 pg/ml. ET-1, ET-2 and ET-3 act by binding to receptors. Two main types of the receptors for endothelins exist and they are referred to as A and B type receptors. Different factors can stimulate or inhibit production of endothelin by endothelial cells. Mechanical stimulation of endothelium, thrombin, calcium ions, epinephrine, angiotensin II, vasopressin, dopamine, cytokines, growth factors stimulate the production of endothelin whereas nitric oxide, cyclic guanosine monophosphate, atrial natriuretic peptide, prostacyclin, bradykinin inhibit its production. Endothelins have different physiological roles in human body but at the same time their actions are involved in the pathogenesis of many diseases. The aim of this review was to present some of, so far, the best studied physiological roles of endothelin and to summarize evidence supporting the potential role of ET in the pathogenesis of certain diseases. [References: 25]
Publication Type
Journal Article. Review.
<4>
Unique Identifier
16783414
Status
MEDLINE
Authors
Zhu YC. Zhu YZ. Moore PK.
Authors Full Name
Zhu, Yi-Chun. Zhu, Yi-Zhun. Moore, Philip Keith.
Institution
Department of Physiology and Pathophysiology, Fudan University Shanghai Medical College, Shanghai, China.
Title
The role of urotensin II in cardiovascular and renal physiology and diseases. [Review] [97 refs]
Source
British Journal of Pharmacology. 148(7):884-901, 2006 Aug.
Other ID
Source: NLM. PMC1751922
Abstract
Urotensin II (U-II) is a cyclic neuropeptide that was first isolated from teleost fish some 35 years ago. Mammalian U-II is a powerful vasoconstrictor with a potency greater than that of endothelin-1.Nevertheless, unlike endothelin-1, which constricts all or nearly all vascular beds, the vasoactive effects of U-II are reported to be dependent both on the species and on the regional vascular bed examined. Typical regional variability occurs in the rat in which vasoconstriction to U-II is most robust in thoracic aorta proximal to the aortic arch and decreases gradually towards the distal peripheral arteries. As small peripheral arteries but not larger arteries such as the aorta play a major role in regulating peripheral resistance and consequent blood pressure as well as workload on the heart, doubts have been raised concerning the importance of this peptide in cardiovascular physiology. Moreover, an interaction between U-II and other endogenous vasoactive molecules may add a level of complexity to the vascular actions of U-II.On the other hand, recent experimental and clinical studies have revealed increased expression of U-II and urotensin receptor (UT receptor) in animals with experimentally induced myocardial infarction, heart failure, and in patients with hypertension, atherosclerosis, and diabetic nephropathy, which suggests a potential role for U-II in both cardiovascular and renal diseases. A series of peptidic and nonpeptidic UT receptor ligands have been shown to be effective in antagonizing the effects of U-II in the cardiorenal system. This article aims to review recent advances in our understanding of the physiology and pathophysiology of U-II with particular references to its role in cardiovascular health and disease. [References: 97]
Publication Type
Journal Article. Research Support, Non-U.S. Gov't. Review.
<5>
Unique Identifier
9861294
Status
MEDLINE
Authors
Moreau P.
Authors Full Name
Moreau, P.
Institution
Faculty of Pharmacy, Universite de Montreal, Quebec, Canada.
Title
Endothelin in hypertension: a role for receptor antagonists?. [Review] [81 refs]
Source
Cardiovascular Research. 39(3):534-42, 1998 Sep.
Abstract
The rapid development of endothelin-receptor antagonists has made the endothelin pathway a new therapeutic target in the treatment of cardiovascular diseases, only ten years after the report of its discovery. While the first clinical trials will help to position this new family of compounds in our therapeutic armament for the treatment of essential or secondary forms of hypertension, several preclinical chronic studies already provide a picture of what we can expect from these drugs. Endothelin-receptor antagonists are not effective in all experimental models of hypertension, but those that respond present hypertrophy of small arteries, secondary to a local overexpression of the peptide. Although angiotensin II seems to represent a stimulus for endothelin overexpression in some models, other, as yet undetermined, stimuli are likely in others. Besides their narrow spectrum of antihypertensive activity, endothelin-receptor antagonists may also protect from complications of hypertension by improving end-organ function in a pressure-independent manner. This seems to be the case for the structure and reactivity of resistance arteries, as well as for renal damage. However, it is not clear at this point if cardiac structure and function are improved beyond the benefits produced by blood pressure reduction. The first results in essential hypertensive subjects suggest some degree of efficacy of endothelin-receptor antagonists. Other clinical trials will help to determine if secondary forms of the disease benefit equally or more from this new class of drugs, and if end-organ damage can be reduced beyond blood-pressure reduction. [References: 81]
Publication Type
Journal Article. Research Support, Non-U.S. Gov't. Review.
<6>
Unique Identifier
16292049
Status
MEDLINE
Authors
Lewis MJ.
Authors Full Name
Lewis, Michael J.
Institution
Department of Sports Science, University of Wales-Swansea, Singleton Park, Swansea SA2 8PP, Wales, UK.
Title
Heart rate variability analysis: a tool to assess cardiac autonomic function.
Source
CIN: Computers, Informatics, Nursing. 23(6):335-41, 2005 Nov-Dec.
Abstract
Heart rate monitoring is commonly used to provide an acute indicator of an individual's cardiovascular status and responsiveness. An increasingly popular technique involves quantifying the very small amounts by which the heart rate changes from one cardiac cycle to the next. This "heart rate variability (HRV) analysis" provides a substantial amount of additional information about the cardiovascular system and enables quantification of cardiac regulatory influences on the autonomic nervous system. The autonomic nervous system consists of two main components: the sympathetic system and the parasympathetic system. The relative influence of these two components on the sino-atrial node of the heart determines the heart rate. A number of physiological factors, including blood pressure and respiratory rate, can have a profound effect on this autonomic "balance." HRV analysis therefore provides a noninvasive method for investigating the dynamic influence of changing physiological parameters on cardiac regulation.
Publication Type
Journal Article.
<7>
Unique Identifier
11934826
Status
MEDLINE
Authors
Tsuruda T. Burnett JC Jr.
Authors Full Name
Tsuruda, Toshihiro. Burnett, John C Jr.
Title
Adrenomedullin: an autocrine/paracrine factor for cardiorenal protection.
Comments
Comment on: Circ Res. 2002 Apr 5;90(6):657-63; PMID: 11934832]
Source
Circulation Research. 90(6):625-7, 2002 Apr 5.
Publication Type
Comment. Editorial.
<8>
Unique Identifier
9146979
Status
MEDLINE
Authors
Bianchi G.
Authors Full Name
Bianchi, G.
Title
Pathophysiology of hypertension.
Comments
Comment on: Curr Opin Nephrol Hypertens. 1997 Mar;6(2):199-204; PMID: 9146984], Comment on: Curr Opin Nephrol Hypertens. 1997 Mar;6(2):184-91; PMID: 9146982], Comment on: Curr Opin Nephrol Hypertens. 1997 Mar;6(2):169-76; PMID: 9146980], Comment on: Curr Opin Nephrol Hypertens. 1997 Mar;6(2):177-83; PMID: 9146981]
Source
Current Opinion in Nephrology & Hypertension. 6(2):167-8, 1997 Mar.
Publication Type
Comment. Editorial.
<9>
Unique Identifier
17329915
Status
MEDLINE
Authors
Sasatomi Y. Sato H. Chiba Y. Abe Y. Takeda S. Ogahara S. Murata T. Kaneoka H. Takebayashi S. Iwasaki H. Saito T.
Authors Full Name
Sasatomi, Yoshie. Sato, Hiroshi. Chiba, Yoshiro. Abe, Yasuhiro. Takeda, Seiji. Ogahara, Satoru. Murata, Toshiaki. Kaneoka, Hidetoshi. Takebayashi, Shigeo. Iwasaki, Hiroshi. Saito, Takao.
Institution
Division of Nephrology & Rheumatology, Department of Internal Medicine, Fukuoka University School of Medicine, Fukuoka, Japan.
Title
Prognostic factors for renal amyloidosis: a clinicopathological study using cluster analysis.
Source
Internal Medicine. 46(5):213-9, 2007.
Abstract
OBJECTIVE: There is no standardized therapy for renal amyloidosis, which shows rapid progression and poor prognosis. Here, we used cluster analysis to examine the correlation between amyloid-related renal damage and prognosis, and determined the clinicopathological prognostic factors for renal amyloidosis. METHODS AND PATIENTS: We analyzed 125 patients with renal amyloidosis (men/women: 43/82; mean age at renal biopsy: 58.811.1 years, SD; range: 21-78 years). Cluster analysis was performed using clinical parameters, renal histological findings, type of renal amyloidosis, and follow-up data. We also analyzed survival data. RESULTS: We divided 125 cases (prognosis was checked in 97 [77.6%] cases) into three groups by cluster analysis. In the cluster groups, accelerated progression correlated with serum creatinine (s-Cr) levels at renal biopsy and histological grade of renal damage by amyloid deposition (p<0.0001). The most important prognostic factors were glomerular, tubulointerstitial, and vascular lesions induced by amyloid deposition at biopsy (p<0.0001). We also found that amyloid-A (AA) type amyloidosis correlated is more significantly with amyloid-mediated vascular (P=0.0010) and tubulointerstitial lesions (p=0.0705) than with amyloid-L (AL) type amyloidosis. Proteinuria and nephrotic syndrome were more severe in AL than AA amyloidosis (p=0.0836). The 10-year individual survival rate was about 20%, and most deaths were due to cardiovascular disease and infection. CONCLUSION: Our results indicate that the quantity of amyloid deposition in the kidney, and the extent of glomerular, tubulointerstitial, and vascular damage are significant renal prognostic factors in amyloidosis.
Publication Type
Comparative Study. Journal Article. Research Support, Non-U.S. Gov't.
<10>
Unique Identifier
12673184
Status
MEDLINE
Authors
Perazella MA. Setaro JF.
Authors Full Name
Perazella, Mark A. Setaro, John F.
Institution
Department of Internal Medicine, Yale University School of Medicine, New Haven, Conn. 06520-8017, USA.
Title
Renin-angiotensin-aldosterone system: fundamental aspects and clinical implications in renal and cardiovascular disorders. [Review] [111 refs]
Source
Journal of Nuclear Cardiology. 10(2):184-96, 2003 Mar-Apr.
Abstract
The renin-angiotensin-aldosterone system (RAAS) exerts a principal influence in maintaining vascular tone, optimal salt and water homeostasis, and forward cardiac output in human beings. Overactivity of the RAAS can lead to pathologic consequences in states of diabetic nephropathy, hypertension, renal artery stenosis, left ventricular hypertrophy, coronary atherosclerosis, myocardial infarction, and congestive heart failure. In addition to fluid and hemodynamic effects, the RAAS may have a critical role in the activation of the sympathetic nervous system, the progression of atherosclerosis, the dysregulation of endothelial function, and the inhibition of the fibrinolytic system. Accumulated basic and clinical evidence supports the use of inhibitors of the RAAS, including aldosterone antagonists, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers, in treating hypertension, improving diabetic nephropathy, preventing or ameliorating congestive heart failure, and optimizing the prognosis after myocardial infarction. [References: 111]
Publication Type
Journal Article. Review.
<11>
Unique Identifier
19148149
Status
MEDLINE
Authors
Breidthardt T. Mebazaa A. Mueller CE.
Authors Full Name
Breidthardt, Tobias. Mebazaa, Alexandre. Mueller, Christian E.
Institution
Department of Internal Medicine, University Hospital, Basel, Switzerland.
Title
Predicting progression in nondiabetic kidney disease: the importance of cardiorenal interactions.[Erratum appears in Kidney Int. 2009 Jul;76(1):121]
Comments
Comment on: Kidney Int. 2009 Feb;75(3):312-6; PMID: 19002217]
Source
Kidney International. 75(3):253-5, 2009 Feb.
Abstract
The interplay between the heart and the kidneys has received widespread attention in recent years. A novel five-class definition of cardiorenal syndromes has been proposed. The ability of two markers of cardiac dysfunction to predict progression of primary kidney disease, described by Dieplinger and his co-workers, highlights the prognostic importance of the chronic cardiorenal (types 2 and 4) syndromes.
Publication Type
Comment. Journal Article.
<12>
Unique Identifier
15698440
Status
MEDLINE
Authors
Bavanandan S. Ajayi S. Fentum B. Paul SK. Carr SJ. Robinson TG.
Authors Full Name
Bavanandan, Sunita. Ajayi, Samuel. Fentum, Barbara. Paul, Sanjoy K. Carr, Susan J. Robinson, Thompson G.
Institution
Department of Nephrology, Leicester Warwick Medical Schools, United Kingdom.
Title
Cardiac baroreceptor sensitivity: a prognostic marker in predialysis chronic kidney disease patients?.
Source
Kidney International. 67(3):1019-27, 2005 Mar.
Abstract
BACKGROUND: Small, uncontrolled studies of dialysis-dependent chronic kidney disease (CKD) patients have demonstrated abnormalities of cardiovascular autonomic control and vascular compliance, which may contribute to adverse cardiovascular morbidity in this population. However, there is little information utilizing newer, noninvasive techniques in predialysis patients with increasing degrees of uremia. METHODS: One hundred and five nondialysis CKD patients with a median GFR of 23 mL/min/1.73 m(2) (range: 6 to 102) at baseline were studied. Cardiac baroreceptor sensitivity (BRS) was recorded by time- and frequency-domain techniques, and its relationship with increasing degrees of uremia studied. During a mean follow-up period of 42 months (range: 3 to 70), primary (death, dialysis, transplantation) and secondary (fatal and nonfatal cardiovascular events) outcome measures were recorded. The importance of cardiac BRS in comparison to other important renal and cardiovascular prognostic variables in predicting outcome was assessed. RESULTS: Median cardiac BRS by time domain analysis at baseline was 8.85 msec/mm Hg (interquartile range: 6.85), and impaired cardiac BRS was related to reduced GFR, increasing age, and hypertension on quantile regression analysis. 'Impaired' cardiac BRS was associated with a trend toward increased likelihood of both primary and secondary outcomes, and may act as a surrogate measure of other cardiovascular risk factors, including age, hyperlipidemia, hypertension, previous cardiovascular disease, and doubling of creatinine. CONCLUSION: Nondialysis-dependent CKD patients have impaired cardiac BRS, and this was related to decreasing GFR. There was a trend toward poorer prognosis in patients with impaired cardiac BRS that requires further study. Cardiac BRS may provide a simple, bedside, noninvasive assessment of overall cardiovascular risk in this population.