Hyperkalemia, Renal Failure, and Converting-Enzyme Inhibition

García, Néstor H.; Baigorria, Sandra T.; Juncos, Luis I.

doi:10.1161/hy09t1.095762

Cited by 12 publications

(11 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Central administration of TRH increases blood pressure and heart rate (HR) [12,13,14,15] and may contribute to leptin-induced hypertension [16]. Central TRH infusion also stimulates brown adipose tissue thermogenesis [17, 18].…”

Section: Introductionmentioning

confidence: 99%

Central Thyrotropin-Releasing Hormone Infusion Opposes Cardiovascular and Metabolic Suppression during Caloric Restriction

Knight¹,

Swoap

Parsons

et al. 2006

Neuroendocrinology

View full text Add to dashboard Cite

Inhibition of hypothalamic thyrotropin-releasing hormone (TRH) neuronal activity is a well-established adaptation to caloric restriction (CR) that suppresses pituitary secretion of thyroid-stimulating hormone, but may also participate in modulation of autonomic function. Thus, we hypothesized that decreased hypothalamic TRH activity contributes to CR-induced bradycardia and decreased metabolic rate. To test this hypothesis, male Sprague-Dawley rats were instrumented with telemetry devices for measurement of heart rate (HR) and blood pressure (BP) and a lateral intracerebroventricular (i.c.v.) guide cannula for central infusions. After recovery, rats were housed in metabolic chambers and given either ad libitum(ad-lib) or CR treatments for 7 days; half of each diet group was then given continuous i.c.v. infusions of TRH (25 nmol/h) or saline (0.25 µl/h) for 7 days via osmotic pump. This dose of TRH did not significantly alter peripheral free T₄ levels. In ad-lib rats, TRH infusion produced small reductions in food intake and small increases in HR and BP over saline-infused controls. In CR rats, TRH infusion resulted in an increase in HR and also energy expenditure over saline-infused controls. These results support the hypothesis that suppression of central TRH activity contributes to the homeostatic suppression of energy expenditure and HR observed during CR.

show abstract

Section: Introductionmentioning

confidence: 99%

Central Thyrotropin-Releasing Hormone Infusion Opposes Cardiovascular and Metabolic Suppression during Caloric Restriction

Knight¹,

Swoap

Parsons

et al. 2006

Neuroendocrinology

View full text Add to dashboard Cite

show abstract

“…Atorvastatin was mixed into the rat chow to achieve a dose of 30 mg·kg Ϫ1 day Ϫ1 (58). After 1 wk of acclimation in the metabolic cages and after 6 wk on their respective regimens, we measured body weight, urinary sodium excretion, and systolic blood pressure by the tail-cuff method (16). Briefly, for 7 days the rats were acclimated to restraint and tail-cuff inflation.…”

Section: Animalsmentioning

confidence: 99%

“…Body weights were measured once a week. Twenty-four-hour urine was collected for the determination of urinary excretion of protein, creatinine, and sodium as described previously (16).…”

Section: Animalsmentioning

confidence: 99%

Statins reverse renal inflammation and endothelial dysfunction induced by chronic high salt intake

Fiore

Jiménez

Cremonezzi

et al. 2011

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

Fiore MC, Jimenez PM, Cremonezzi D, Juncos LI, García NH. Statins reverse renal inflammation and endothelial dysfunction induced by chronic high salt intake. Am J Physiol Renal Physiol 301: F263-F270, 2011. First published May 4, 2011 doi:10.1152/ajprenal.00109.2010.-High salt intake (HS) is a risk factor for cardiovascular and kidney disease. Indeed, HS may promote blood-pressure-independent tissue injury via inflammatory factors. The lipid-lowering 3-hydroxy 3-methylglutaryl-coenzyme A (HMGCoA) reductase inhibitors exert beneficial lipid-independent effects, reducing the expression and synthesis of inflammatory factors. We hypothesized that HS impairs kidney structure and function in the absence of hypertension, and these changes are reversed by atorvastatin. Four groups of rats were treated for 6 wk in metabolic cages with their diets: normal salt (NS); HS, NS plus atorvastatin and HS plus atorvastatin. We measured basal and final body weight, urinary sodium and protein excretion (UProtV), and systolic blood pressure (SBP). At the end of the experimental period, cholesterolemia, creatinine clearance, renal vascular reactivity, glomerular volume, cortical and glomerular endothelial nitric oxide synthase (eNOS), and transforming growth factor (TGF)-␤1 expression were measured. We found no differences in SBP, body weight, and cholesterolemia. HS rats had increased creatinine clearence, UProtV, and glomerular volume at the end of the study. Acetylcholine-induced vasodilatation decreased by 40.4% in HS rats (P Ͻ 0.05). HS decreased cortical and glomerular eNOS and caused mild glomerular sclerosis, interstitial mononuclear cell infiltration, and increased cortical expression of TGF-␤1. All of these salt-induced changes were reversed by atorvastatin. We conclude that long-term HS induces inflammatory and hemodynamic changes in the kidney that are independent of SBP. Atorvastatin corrected all, suggesting that the nitric oxide-oxidative stress balance plays a significant role in the earlier stages of salt induced kidney damage.atrovastatin; blood pressure; kidney injury HIGH SALT (sodium chloride) intake, an established habit in industrialized nations, is an important risk factor for cardiovascular (27) and kidney disease (42). Indeed, clinical and experimental studies have shown an independent association between increased dietary salt intake and left ventricular hypertrophy, urine protein excretion, and renal fibrosis and disease progression (9, 23). These associations could be of great significance as proteinuria and renal disease have been implicated as independent risk factors for cardiovascular mortality in hypertensive and diabetic patients and in the elderly (18).Although a high-salt (HS) diet increases blood pressure in susceptible humans and in experimental animals (19,34,40), it can also cause tissue injury independently of blood pressure. For instance, salt promotes kidney and myocardial fibrosis along with increased transforming growth factor (TGF)-␤ 1 expression and abnormal microvascular function, all...

show abstract

“…As a result of the safe therapeutic profile of ACE inhibitors and ARBs the proposed intensified RAS inhibition should cause no significant intolerance [García et al 2001]. …”

Section: Introductionmentioning

confidence: 99%

Combination therapy in chronic kidney disease?

Juncos¹,

Joaquin²

2015

Therapeutic Advances in Cardiovascular Disease

Self Cite

View full text Add to dashboard Cite

The renin-angiotensin system (RAS) plays a fundamental role in preserving the circulation and yet, it may be injurious to heart and blood vessels and may also allow, and sometimes hasten, kidney disease progression. Thus, effective RAS inhibition may be a major pharmacologic necessity to control hypertension, to decrease cardiovascular complication, and to inhibit kidney disease progression. Unfortunately, the beneficial effects attained in the management of renal disease sometimes are incomplete. The reasons for these inadequate outcomes may include angiotensin escape or excessive local angiotensin production. Two pharmacologic strategies have been proposed to overcome this drawback including higher than recommended doses of RAS inhibitors and the combination of two different RAS inhibitors. However, three large studies have shown that these more intensive pharmacologic approaches should be treated with caution when applied to high-risk patients, as organ perfusion may fall to critical levels that may cause severe complications. Nevertheless, intensive RAS inhibition (including combination therapy) may be the sole alternative in patients with chronic kidney disease (CKD) in whom other therapeutics options have failed. In these cases, adequate precautions including close clinical and laboratory follow up should prevent major complications.

show abstract

Hyperkalemia, Renal Failure, and Converting-Enzyme Inhibition

Cited by 12 publications

References 30 publications

Central Thyrotropin-Releasing Hormone Infusion Opposes Cardiovascular and Metabolic Suppression during Caloric Restriction

Central Thyrotropin-Releasing Hormone Infusion Opposes Cardiovascular and Metabolic Suppression during Caloric Restriction

Statins reverse renal inflammation and endothelial dysfunction induced by chronic high salt intake

Combination therapy in chronic kidney disease?

Contact Info

Product

Resources

About