scholarly journals Effects of Low Salt Diet on Gene Expression in Dog Heart

2017 ◽  
Vol 20 (9) ◽  
pp. A495-A496
Author(s):  
X Ren ◽  
R Zhang
Keyword(s):  
Gene Expression ◽  
Salt Diet ◽  
Dog Heart ◽  
Low Salt

Role of renal nerves in stimulation of renin, COX-2, and nNOS in rat renal cortex during salt deficiency

2002 ◽  
Vol 282 (3) ◽  
pp. F478-F484 ◽  
Author(s):  
K. Höcherl ◽  
M. Kammerl ◽  
F. Kees ◽  
B. K. Krämer ◽  
H. F. Grobecker ◽  
...  
Keyword(s):  
Gene Expression ◽  
Renal Denervation ◽  
Juxtaglomerular Apparatus ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Mrna Levels ◽  
Salt Diet ◽  
Low Salt ◽  
Cox 2 ◽  
Nnos Expression ◽  
Stimulation Of

We investigated a possible involvement of the sympathetic nervous system in the parallel increase of renin, cyclooxygenase-2 (COX-2), and neuronal nitric oxide synthase (nNOS) gene expression in the juxtaglomerular apparatus of rat kidneys induced by salt deficiency. Therefore, we determined the effects of renal denervation and the β-adrenoreceptor antagonist metoprolol (50 mg/kg body wt po, twice a day) on renocortical expression of renin, COX-2, and nNOS in rats fed a low-salt (0.02% wt/wt) diet or treated for 1 wk with ramipril (10 mg/kg body wt) in combination with a low-salt diet. We found that a low-salt diet in combination with ramipril strongly increased renocortical mRNA levels of renin, COX-2, and nNOS 9-, 7-, and 2.5-fold, respectively. Treatment with metoprolol did not change basal expression of the three genes or induction of renin and COX-2 gene expression, while induction of nNOS expression was clearly attenuated. Similarly, unilateral renal denervation attenuated induction of nNOS expression but had no effect on all other parameters. These findings suggest that β-adrenergic stimulation is not required for stimulation of renin and COX-2 gene expression in the juxtaglomerular apparatus during salt deficiency. However, β-adrenoreceptor activity or renal nerve activity appears to be required for the full stimulation of nNOS expression by low salt intake or combined with angiotensin-converting enzyme inhibition.

scholarly journals Urea and NaCl regulate UT-A1 urea transporter in opposing directions via TonEBP pathway during osmotic diuresis

2009 ◽  
Vol 296 (1) ◽  
pp. F67-F77 ◽  
Author(s):  
Yu-Mi Kim ◽  
Wan-Young Kim ◽  
Hyun-Wook Lee ◽  
Jin Kim ◽  
H. Moo Kwon ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Plasma Osmolality ◽  
Urea Concentration ◽  
Urea Transporter ◽  
Osmotic Diuresis ◽  
High Salt Diet ◽  
Salt Diet ◽  
Low Protein ◽  
Low Salt ◽  
Urine Concentrating Ability

In our previous studies of varying osmotic diuresis, UT-A1 urea transporter increased when urine and inner medullary (IM) interstitial urea concentration decreased. The purposes of this study were to examine 1) whether IM interstitial tonicity changes with different urine urea concentrations during osmotic dieresis and 2) whether the same result occurs even if the total urinary solute is decreased. Rats were fed a 4% high-salt diet (HSD) or a 5% high-urea diet (HUD) for 2 wk and compared with the control rats fed a regular diet containing 1% NaCl. The urine urea concentration decreased in HSD but increased in HUD. In the IM, UT-A1 and UT-A3 urea transporters, CLC-K1 chloride channel, and tonicity-enhanced binding protein (TonEBP) transcription factor were all increased in HSD and decreased in HUD. Next, rats were fed an 8% low-protein diet (LPD) or a 0.4% low-salt diet (LSD) to decrease the total urinary solute. Urine urea concentration significantly decreased in LPD but significantly increased in LSD. Rats fed the LPD had increased UT-A1 and UT-A3 in the IM base but decreased in the IM tip, resulting in impaired urine concentrating ability. The LSD rats had decreased UT-A1 and UT-A3 in both portions of the IM. CLC-K1 and TonEBP were unchanged by LPD or LSD. We conclude that changes in CLC-K1, UT-A1, UT-A3, and TonEBP play important roles in the renal response to osmotic diuresis in an attempt to minimize changes in plasma osmolality and maintain water homeostasis.

scholarly journals Renal effects of the serine protease inhibitor aprotinin in healthy conscious mice

2021 ◽  
Author(s):  
Stefan Wörner ◽  
Bernhard N. Bohnert ◽  
Matthias Wörn ◽  
Mengyun Xiao ◽  
Andrea Janessa ◽  
...  
Keyword(s):  
Protease Inhibitor ◽  
Serine Protease ◽  
Kidney Injury ◽  
Serine Protease Inhibitor ◽  
Tubular Function ◽  
Proteolytic Activation ◽  
Salt Diet ◽  
Low Salt ◽  
Proximal Tubular ◽  
Proximal Tubular Function

AbstractTreatment with aprotinin, a broad-spectrum serine protease inhibitor with a molecular weight of 6512 Da, was associated with acute kidney injury, which was one of the reasons for withdrawal from the market in 2007. Inhibition of renal serine proteases regulating the epithelial sodium channel ENaC could be a possible mechanism. Herein, we studied the effect of aprotinin in wild-type 129S1/SvImJ mice on sodium handling, tubular function, and integrity under a control and low-salt diet. Mice were studied in metabolic cages, and aprotinin was delivered by subcutaneously implanted sustained release pellets (2 mg/day over 10 days). Mean urinary aprotinin concentration ranged between 642 ± 135 (day 2) and 127 ± 16 (day 8) µg/mL . Aprotinin caused impaired sodium preservation under a low-salt diet while stimulating excessive hyperaldosteronism and unexpectedly, proteolytic activation of ENaC. Aprotinin inhibited proximal tubular function leading to glucosuria and proteinuria. Plasma urea and cystatin C concentration increased significantly under aprotinin treatment. Kidney tissues from aprotinin-treated mice showed accumulation of intracellular aprotinin and expression of the kidney injury molecule 1 (KIM-1). In electron microscopy, electron-dense deposits were observed. There was no evidence for kidney injury in mice treated with a lower aprotinin dose (0.5 mg/day). In conclusion, high doses of aprotinin exert nephrotoxic effects by accumulation in the tubular system of healthy mice, leading to inhibition of proximal tubular function and counterregulatory stimulation of ENaC-mediated sodium transport.

A2714 The efficacy of low-salt diet education in hypertensive patients

2018 ◽  
Vol 36 ◽  
pp. e280
Author(s):  
Iryna Voloshyna ◽  
Vitaliy Krivenko ◽  
Vadym Vizir ◽  
Vladislav Ponomarenko
Keyword(s):  
Salt Diet ◽  
Hypertensive Patients ◽  
Low Salt

Does a low-salt diet exert a protective effect on endothelial function in normal rats?

2001 ◽  
Vol 138 (3) ◽  
pp. 200-205 ◽  
Author(s):  
A.H. Boonstra ◽  
S. Gschwend ◽  
M.J.A. Kocks ◽  
H. Buikema ◽  
D. de Zeeuw ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Protective Effect ◽  
Salt Diet ◽  
Low Salt

Impact of Low-Salt Diet

2017 ◽  
pp. 1-16
Author(s):  
Flávia Ramos de Siqueira ◽  
Karin Carneiro de Oliveira ◽  
Joel Claudio Heimann ◽  
Luzia Naôko Shinohara Furukawa
Keyword(s):  
Salt Diet ◽  
Low Salt

scholarly journals Low-salt Diet for Congestive Heart Failure

BMJ ◽  
1951 ◽  
Vol 1 (4719) ◽  
pp. 1349-1353
Author(s):  
A. L. Nielsen ◽  
P. Bechgaard ◽  
H. O. Bang
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Salt Diet ◽  
Low Salt

Drug Interactions and Reactions Update

1982 ◽  
Vol 16 (12) ◽  
pp. 925-929 ◽  
Keyword(s):  
Elderly Patient ◽  
Drug Interactions ◽  
The Elderly ◽  
Salt Diet ◽  
The Past ◽  
Inadequate Knowledge ◽  
Or Groups ◽  
Low Salt ◽  
Nonsteroidal Antiinflammatory Agents ◽  
Extreme Care

Elderly patients take a large number of drugs, especially psychoactive agents, and polypharmacy seems to be the rule in acute hospital settings and in institutions alike. Knowledge about alteration in drug response, with aging, is still at a preliminary and investigational stage, and the problem is compounded by the fact that there are relatively few drugs for which a special geriatric dosage is recommended. It appears to be common practice to keep the elderly in “chemical strait jackets” in some institutions, with emphasis on the use of antipsychotic and sedative/hypnotic combinations. Use of these agents has reached such proportions in Britain and America that it has become necessary to warn that antipsychotic drugs should be used only to treat acute behavior disorders in such patients. The potential for drug-drug interactions in the elderly patient is, therefore, large, and, in the community, the most common categories of prescribed drugs taken by the elderly are psychotropics, diuretics, and antipyretic/analgesics. In addition, analgesics and laxatives are often taken as nonprescribed medicines. Poor compliance with medication instructions, hoarding of drugs, and inadequate knowledge of the purpose of medication are very common. The eventual sequel to these factors is hospitalization; diuretics, hypotensives, antiparkinsonian agents, and psychotropics carry the greatest risk of evoking serious adverse drug reactions. Some specific drugs or groups of drugs present peculiar problems to the aged patient; these agents are relatively few in number and include digoxin, hypotensives, diuretics, nonsteroidal antiinflammatory agents, benzodiazepines, phenothiazines, lithium, and other psychoactive drugs. Currently, lithium and the antirheumatoid agent benoxaprofen are causing much concern in regard to the elderly. With lithium, there are adverse effects suggestive of neurotoxicity, and interactions with concurrent neuroleptic and/or antidepressant therapy, diuretics, and low salt diet are involved. As for benoxaprofen, reports in the past few months have causally linked this drug with fatal cholestatic jaundice and other serious reactions; this drug has now been withdrawn from clinical use. Health professionals must use extreme care when treating an elderly patient with drugs.

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