A Reassessment of the Pathophysiology of Progressive Cardiorenal Disorders

Ré, Richard N.

doi:10.1016/j.mcna.2016.08.007

Cited by 6 publications

(24 citation statements)

References 65 publications

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“…Notably, the yearly increase in the number of new patients is estimated at 50% [1][2][3][4][5]. Despite an array of therapeutic approaches available, the prognosis of patients with CHF is poor, especially when CHF is associated with impairment of renal hemodynamics and sodium excretion [4,[6][7][8]. Unfortunately, the current therapeutic regimes usually fail to prevent the development of renal dysfunction in patients with CHF [4,8,9].…”

Section: Introductionmentioning

confidence: 99%

“…Despite an array of therapeutic approaches available, the prognosis of patients with CHF is poor, especially when CHF is associated with impairment of renal hemodynamics and sodium excretion [4,[6][7][8]. Unfortunately, the current therapeutic regimes usually fail to prevent the development of renal dysfunction in patients with CHF [4,8,9]. Therefore new treatment strategies targeting renal dysfunction are urgently needed.…”

Section: Introductionmentioning

confidence: 99%

“…It is well recognized that a decrease in renal blood flow (RBF) is a common finding in patients with CHF, and it is detected already at a relatively early stage [4,6,8,10,11]. Since adequate, stable perfusion of the kidneys is essential for normal renal function [12,13], the decrease in RBF is the harbinger of renal dysfunction in CHF.…”

Section: Introductionmentioning

confidence: 99%

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The Role of Renal Vascular Reactivity in the Development of Renal Dysfunction in Compensated and Decompensated Congestive Heart Failure

Krátký

Kopkan

Kikerlová

et al. 2018

Kidney Blood Press Res

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Background/Aims: Reduction of renal blood flow (RBF) is commonly thought to be a causative factor of renal dysfunction in congestive heart failure (CHF), but the exact mechanism of the renal hypoperfusion is not clear. Apart from the activation of neurohormonal systems controlling intrarenal vascular tone, the cause might be altered reactivity of the renal vasculature to endogenous vasoactive agents. Methods: To evaluate the role of this mechanism, we assessed by an ultrasonic transient-time flow probe maximum RBF responses to renal artery infusion of angiotensin II (ANG II), norepinephrine (NE) and acetylcholine (Ach) in healthy male rats and animals with compensated and decompensated CHF. CHF was induced by volume overload achieved by the creation of the aorto-caval fistula (ACF) in Hannover Sprague-Dawley rats. Results: Maximum responses in RBF to ANG II were similar in rats studied five weeks (compensated phase) and 20 weeks (decompensated phase) after ACF creation when compared to sham-operated rats. On the other hand, NE elicited larger maximum decreases in RBF in rats with CHF (five and 20 weeks post-ACF) than in sham-operated controls. We observed greater maximum vasodilatory responses to Ach only in rats with a compensated stage of CHF (five weeks post-ACF). Conclusion: Greater renal vasoconstrictor responsiveness to ANG II or reduced renal vasodilatation in response to Ach do not play a decisive role in the development of renal dysfunction in ACF rats with compensated and decompensated CHF. On the other hand, exaggerated renal vascular responsiveness to NE may be here a contributing causative factor, active in either CHF phase.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The Role of Renal Vascular Reactivity in the Development of Renal Dysfunction in Compensated and Decompensated Congestive Heart Failure

Krátký

Kopkan

Kikerlová

et al. 2018

Kidney Blood Press Res

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“…Population aging is associated with increasing prevalence of a variety of chronic degenerative diseases. Included in this number are progressive renal insufficiency (often secondary to diabetes mellitus and/or to hypertension), systolic congestive heart failure, heart failure with preserved ejection fraction (diastolic heart failure), age‐related macular degeneration, and a variety of neurodegenerative diseases such as Parkinson disease, Alzheimer disease, and amyotrophic lateral sclerosis . Each of these is the subject of intense investigation, and considerable information regarding their pathogenesis has been developed.…”

mentioning

confidence: 99%

“…It is intriguing, however, that in the case of the nonneurological diseases pathogenesis is associated with the upregulation of specific signaling proteins, many of which can operate in paracrine, autocrine, or intracrine modes. In fact, in some of these disorders, the same factors are upregulated, albeit often against a background of the upregulation of other disease‐specific factors, and this suggests the possibility that a commonality of pathogenesis could link these disorders . In the neurological disorders other intracellular proteins are upregulated, but these proteins also traffic between cells .…”

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confidence: 99%

A Pathogenic Mechanism Potentially Operative in Multiple Progressive Diseases and Its Therapeutic Implications

Ré

2017

The Journal of Clinical Pharma

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A variety of peptide signaling moieties that we have termed intracrines can act in the interiors of their cells of synthesis or of target cells after internalization. These intracrine factors are known to be upregulated in such disorders as diabetic nephropathy, systolic heart failure, and age-related macular degeneration. Indeed, a similar set of intracrines is upregulated in each of these disorders, suggesting a commonality of mechanism. In addition, several chronic neurodegenerative disorders such as Alzheimer disease and Parkinson disease involve intercellular trafficking of intracellular disease-causing proteins. These disorders can be considered intracrine-like. Here the mechanistic and therapeutic implications of these observations, and of the relevant modes of intracrine action, are discussed, including the possibility that similar therapeutic approaches could be effective in multiple progressive disorders and the implications of these observations for intracrine pharmacology in general.

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Altered Renal Vascular Responsiveness to Vasoactive Agents in Rats with Angiotensin II-Dependent Hypertension and Congestive Heart Failure

Vacková¹,

Kikerlová²,

Melenovský³

et al. 2019

Kidney Blood Press Res

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Objective: We evaluated the hypothesis that the development of renal dysfunction and congestive heart failure (CHF) caused by volume overload in rats with angiotensin II (ANG II)-dependent hypertension is associated with altered renal vascular responsiveness to ANG II and to epoxyeicosatrienoic acids (EETs). Methods: Ren-2 transgenic rats (TGRs) were used as a model of ANG II-dependent hypertension. CHF was induced by volume overload achieved by the creation of the aorto-caval fistula (ACF). Renal blood flow (RBF) responses were determined to renal arterial administration of ANG II, native 11,12-EET, an analog of 14,15-EETs (EET-A), norepinephrine (NE), acetylcholine (Ach) and bradykinin (Bk) in healthy (i.e., sham-operated) TGR and ACF TGR (5 weeks after ACF creation). Results: Selective intrarenal administration of neither vasoactive drug altered mean arterial pressure in any group. Administration of ANG II caused greater decreases in RBF in ACF TGR than in sham-operated TGR, whereas after administration of NE the respective decreases were comparable in the 2 groups. Administration of Ach and Bk elicited significantly higher RBF increases in ACF TGR as compared with sham-operated TGR. In contrast, administration of 11,12-EET and EET-A caused significantly smaller RBF increases in ACF TGR than in sham-operated TGR. Conclusion: The findings show that 5 weeks after creation of ACF, the TGR exhibit exaggerated renal vasoconstrictor responses to ANG II and reduced renal vasodilatory responses to EETs, suggesting that both these alterations might play an important role in the development of renal dysfunction in this model of CHF.

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A Reassessment of the Pathophysiology of Progressive Cardiorenal Disorders

Cited by 6 publications

References 65 publications

The Role of Renal Vascular Reactivity in the Development of Renal Dysfunction in Compensated and Decompensated Congestive Heart Failure

The Role of Renal Vascular Reactivity in the Development of Renal Dysfunction in Compensated and Decompensated Congestive Heart Failure

A Pathogenic Mechanism Potentially Operative in Multiple Progressive Diseases and Its Therapeutic Implications

Altered Renal Vascular Responsiveness to Vasoactive Agents in Rats with Angiotensin II-Dependent Hypertension and Congestive Heart Failure

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