Regulation of Arterial Tone in Rats
Fed a Long-Term High-Salt Diet

Lobov, G. I.; Ivanova, Galina

doi:10.1134/s0022093021010142

Cited by 2 publications

(2 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It acts via relaxing the vascular smooth muscle cell (VSMC) through putative potassium channels and desensitizes the cell to vasoconstrictor stimuli ( Chen and Suzuki, 1990 ). Notably, reserved EDHF protection may serve as a compensatory vasodilatory mechanism in the disease state ( Katz and Krum, 2001 ; Quek et al, 2016 ; Lobov and Ivanova, 2020 ). Reports have demonstrated the presence of extensive interaction between NO and EDHF, and that EDHF activity might be enhanced or depressed depending on the state of hypertension, vessel studied, and species ( Luksha et al, 2009 ; Lobov and Ivanova, 2020 ).…”

Section: Pathogenesis Of Hypertension In Chronic Kidney Diseasementioning

confidence: 99%

“…Notably, reserved EDHF protection may serve as a compensatory vasodilatory mechanism in the disease state ( Katz and Krum, 2001 ; Quek et al, 2016 ; Lobov and Ivanova, 2020 ). Reports have demonstrated the presence of extensive interaction between NO and EDHF, and that EDHF activity might be enhanced or depressed depending on the state of hypertension, vessel studied, and species ( Luksha et al, 2009 ; Lobov and Ivanova, 2020 ). For example, EDHF responses were shown to be preserved in mesenteric arteries from the LPK ( Quek et al, 2016 ) and one kidney-one clip Sprague-Dawley rat model of renovascular hypertension ( Christensen et al, 2007 ), yet diminished in the mesenteric arteries from Wistar rats of the same renal failure model ( Vettoretti et al, 2006 ).…”

Section: Pathogenesis Of Hypertension In Chronic Kidney Diseasementioning

confidence: 99%

See 1 more Smart Citation

Hypertension in chronic kidney disease: What lies behind the scene

Ameer

2022

Front. Pharmacol.

View full text Add to dashboard Cite

Hypertension is a frequent condition encountered during kidney disease development and a leading cause in its progression. Hallmark factors contributing to hypertension constitute a complexity of events that progress chronic kidney disease (CKD) into end-stage renal disease (ESRD). Multiple crosstalk mechanisms are involved in sustaining the inevitable high blood pressure (BP) state in CKD, and these play an important role in the pathogenesis of increased cardiovascular (CV) events associated with CKD. The present review discusses relevant contributory mechanisms underpinning the promotion of hypertension and their consequent eventuation to renal damage and CV disease. In particular, salt and volume expansion, sympathetic nervous system (SNS) hyperactivity, upregulated renin–angiotensin–aldosterone system (RAAS), oxidative stress, vascular remodeling, endothelial dysfunction, and a range of mediators and signaling molecules which are thought to play a role in this concert of events are emphasized. As the control of high BP via therapeutic interventions can represent the key strategy to not only reduce BP but also the CV burden in kidney disease, evidence for major strategic pathways that can alleviate the progression of hypertensive kidney disease are highlighted. This review provides a particular focus on the impact of RAAS antagonists, renal nerve denervation, baroreflex stimulation, and other modalities affecting BP in the context of CKD, to provide interesting perspectives on the management of hypertensive nephropathy and associated CV comorbidities.

show abstract

Section: Pathogenesis Of Hypertension In Chronic Kidney Diseasementioning

confidence: 99%

Section: Pathogenesis Of Hypertension In Chronic Kidney Diseasementioning

confidence: 99%

Hypertension in chronic kidney disease: What lies behind the scene

Ameer

2022

Front. Pharmacol.

View full text Add to dashboard Cite

show abstract

Influence of excessive salt consumption on the functional state of microvascular vessels of the skin of rats with renal dysfunction

Ivanova,

Khasun,

Parastaeva

et al. 2024

Nefrologiâ (St.-Peterbg.)

View full text Add to dashboard Cite

Background. Cardiovascular complications are common in chronic kidney disease (CKD). The relationship between the cardiovascular system and the kidneys is complex and diverse, but the question of the mechanisms of the influence of excess NaCl consumption on the functional state of blood vessels during renal dysfunction remains relevant.The aim: to evaluate the effect of a high-salt diet on the functional state of microcirculatory vessels (MCR) of the skin in rats at an early stage of renal dysfunction.Material and Methods. The study was conducted on Wistar rats. The first SO group included animals subjected to sham surgery (SO) and receiving a standard diet (0.34% NaCl); in the second, HS group – animals that also underwent a sham operation, but received a high-salt diet (4% NaCl); in the third, NE group – rats subjected to ¾ nephrectomy (NE) and receiving a standard diet; the fourth, HS+ NE group included rats subjected to ¾ NE and fed a high-salt diet (4% NaCl). Blood pressure (BP) was measured in the tail using the cuff method (Sistola, Russia), MCR was assessed using laser Doppler flowmetry (LDF). The reactivity of skin microvessels was assessed by changes in the MCR index before and after iontophoresis of acetylcholine (ACh) and sodium nitroprusside (NP). Based on the assessment of the spectral characteristics of fluctuations in the MCR index obtained using Wavelet analysis, the value of endothelial, neurogenic and myogenic microvascular tone was calculated.Results. 4 months after ¾ NE, rats showed a decrease in the excretory function of the kidneys. In rats on a highsalt diet, an increase in blood urea levels was noted. The blood pressure in rats of the SO+HS group did not significantly differ from the control animals of the SO group (131 ± 8 and 125 ± 4 mmHg, respectively, NS), NE led to a significant increase in blood pressure (135 ± 5 mmHg in rats of the NE group, and 145 ± 7 mmHg – in the NE+HS group). The average MCR was higher in rats receiving a high-salt diet (SO+HS and NE+HS groups), compared with animals of the corresponding group receiving a standard diet. The combination of NE and high-salt load has an inhibitory effect on the amplitude of fluctuations in the intensity of perfusion in all studied ranges: endothelial, neurogenic and myogenic, while the calculated value of skin microvascular tone in three ranges was the highest in NE+HS group rats. In all experimental groups, the reactivity to AH was reduced compared with the SO group, and after NP iontophoresis, the average perfusion rate significantly decreased only in groups of animals receiving a high-salt diet: SO+HS and NE+HS.Conclusion. A high-salt diet in rats with an initial stage of renal dysfunction contributes to an increase in blood pressure and a decrease in natriuresis compared with animals with NE who received a standard diet. With excessive consumption of table salt in rats after NE, the intensity of cutaneous MCR increases, while reducing the variability of the MCR index. A high-salt diet in rats with NE modifies the characteristics of the spectral components of fluctuations in the MCR index, indicating an increase in tonic effects on skin microvessels in the endothelial, neurogenic and myogenic ranges. With hypernatrial load, animals with ¾ NE have a decrease in the reactivity of cutaneous microvessels to AH and NP, which is mediated by both a decrease in endothelial NO production and a decrease in MMC sensitivity to NO.

show abstract

Regulation of Arterial Tone in Rats Fed a Long-Term High-Salt Diet

Cited by 2 publications

References 40 publications

Hypertension in chronic kidney disease: What lies behind the scene

Hypertension in chronic kidney disease: What lies behind the scene

Influence of excessive salt consumption on the functional state of microvascular vessels of the skin of rats with renal dysfunction

Contact Info

Product

Resources

About