Effects of salt loading on sympathetic activity and blood pressure in anesthetized two-kidney, one clip hypertensive rats

Özaykan, Besim; Doğan, Alper

doi:10.17305/bjbms.2011.2555

Cited by 6 publications

(3 citation statements)

References 48 publications

(50 reference statements)

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“…Despite the lack of differences in baseline ABP of mice fed 0.1% and 4.0% NaCl, a high-salt diet transiently exaggerated 2K1C hypertension during the first 7 days, and ABP normalized thereafter. Other studies report a similar time course or no differences in ABP between high- and low-NaCl groups ( 10 , 15 , 45 , 49 , 51 ). The mechanism(s) by which a high-salt diet transiently exaggerates ABP in 2K1C mice is not known but may include a higher cardiac output due to the dietary salt loading, enhanced cardiovascular reactivity by high salt to surgical stress, or an interaction between high salt and RAAS.…”

Section: Discussionmentioning

confidence: 72%

Excessive dietary salt promotes aortic stiffness in murine renovascular hypertension

DeLalio

Hahn

Katayama

et al. 2020

American Journal of Physiology-Heart and Circulatory Physiology

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Renal artery stenosis is the most common cause of secondary hypertension. The 2‐kidney‐1‐clip (2K1C) model of renal stenosis is associated with elevated arterial blood pressure (ABP), activation of the sympathetic nervous system, and blunted reno‐renal reflexes and natriuretic responses. Excess dietary salt intake has multiple actions on the cardiovascular system and exacerbates ABP in some models of hypertension. The present study tested the hypothesis that 2K1C mice exhibit salt sensitive hypertension and worsening cardiovascular responses to high salt feeding. Male C57Bl6 mice (8–12 weeks) were fed 0.1% NaCl or 4% NaCl diets and ABP was continuously monitored using telemetry. 2K1C hypertension was produced by placing a 0.5mm length of PTFE tubing around the right renal artery. Baseline 24‐h mean ABP was not different between 0.1% versus 4.0% NaCl fed mice (101±1 vs 99±1 mmHg, respectively; n=8/group). 2K1C significantly increased ABP in both groups; however, 24‐h mean ABP at 3 weeks post‐renal clipping was not different between mice fed 0.1% vs 4.0% NaCl (122±3 vs. 124±6 mmHg, respectively; n=8/group). In addition, renal artery stenosis significantly increased arterial pulse pressure (systolic‐diastolic) in 0.1% NaCl (Day 0: 35±1 vs Day 21: 42±1 mmHg, P<0.05) and 4.0% NaCl (Day 0: 36±1 vs Day 21: 49±3 mmHg, P<0.05). Interestingly, the magnitude of the increase in arterial pulse pressure was significantly greater in mice fed 4.0% vs 0.1% NaCl (Δ14±3 vs Δ7±2 mmHg, P<0.05). This suggests dietary salt intake promotes aortic stiffness in the 2K1C model. To test this, endothelial‐dependent vasodilatory responses were measured using myography in sham and 2K1C mice fed 0.1% and 4.0% NaCl diets for 3 weeks. 4.0% NaCl 2K1C mice exhibited significantly blunted aortic vasodilation responses versus 2K1C mice fed 0.1% NaCl or sham mice fed 0.1% or 4.0% NaCl. These effects were not observed in the mesenteric arteries of the same animal. In vivo, pulse wave velocity (PWV) measurements revealed a significantly higher PWV value in 2K1C mice fed 4.0% NaCl versus 2K1C fed 0.1% NaCl (3.97±0.19; n=7 vs. 3.18±0.19; n=8, P<0.01) or sham fed 0.1% or 4.0% NaCl (3.21±0.19; n=7 vs. 3.01±0.19; n=7). We conclude that high dietary salt does not exaggerate the chronic hypertension in 2K1C mice but produces a specific endothelial‐dependent aortic stiffness. Support or Funding Information RO1 HL128388 This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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Section: Discussionmentioning

confidence: 72%

Excessive dietary salt promotes aortic stiffness in murine renovascular hypertension

DeLalio

Hahn

Katayama

et al. 2020

American Journal of Physiology-Heart and Circulatory Physiology

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“…It has been previously reported that even short-term oral or central salt loading increases sympathetic activity, especially when salt is directly infused into the brain stem of rats (21,37). The mechanism by which a HS load activates the sympathetic nervous system has not been completely elucidated, but a recent study (10) has suggested the involvement of oxidative stress.…”

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confidence: 99%

Depressor effect of chymase inhibitor in mice with high salt-induced moderate hypertension

Devarajan

Yahiro

Uehara

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Devarajan S, Yahiro E, Uehara Y, Habe S, Nishiyama A, Miura S, Saku K, Urata H. Depressor effect of chymase inhibitor in mice with high salt-induced moderate hypertension. Am J Physiol Heart Circ Physiol 309: H1987-H1996, 2015. First published October 2, 2015; doi:10.1152/ajpheart.00721.2014.-The aim of the present study was to determine whether long-term high salt intake in the drinking water induces hypertension in wild-type (WT) mice and whether a chymase inhibitor or other antihypertensive drugs could reverse the increase of blood pressure. Eight-week-old male WT mice were supplied with drinking water containing 2% salt for 12 wk (high-salt group) or high-salt drinking water plus an oral chymase inhibitor (TPC-806) at four different doses (25, 50, 75, or 100 mg/kg), captopril (75 mg/kg), losartan (100 mg/kg), hydrochlorothiazide (3 mg/kg), eplerenone (200 mg/kg), or amlodipine (6 mg/kg). Control groups were given normal water with or without the chymase inhibitor. Blood pressure and heart rate gradually showed a significant increase in the high-salt group, whereas a dose-dependent depressor effect of the chymase inhibitor was observed. There was also partial improvement of hypertension in the losartan-and eplerenone-treated groups but not in the captopril-, hydrochlorothiazide-, and amlodipine-treated groups. A high salt load significantly increased chymasedependent ANG II-forming activity in the alimentary tract. In addition, the relative contribution of chymase to ANG II formation, but not actual average activity, showed a significant increase in skin and skeletal muscle, whereas angiotensin-converting enzyme-dependent ANG II-forming activity and its relative contribution were reduced by high salt intake. Plasma and urinary renin-angiotensin system components were significantly increased in the high-salt group but were significantly suppressed in the chymase inhibitor-treated group. In conclusion, 2% salt water drinking for 12 wk caused moderate hypertension and activated the renin-angiotensin system in WT mice. A chymase inhibitor suppressed both the elevation of blood pressure and heart rate, indicating a definite involvement of chymase in salt-sensitive hypertension. mouse; high salt; hypertension; renin-angiotensin system; chymase inhibitor NEW & NOTEWORTHYOur study, for the first time, has provided 1) a new establishment of the salt-sensitive hypertensive mice model, 2) confirmation of direct involvement of chymase-mediated mechanisms proved using a specific chymase inhibitor, and 3) the inhibition of all renin-angiotensin-aldosterone components by a chymase inhibitor.THE ASSOCIATION between high salt (HS) intake and elevated blood pressure has been well established by cross-sectional and longitudinal epidemiological studies. Observational studies and clinical trials performed in the general population have indicated that a higher or lower salt intake is associated with an increase or a decrease of blood pressure, respectively (20, 32). However, the response of blood pressure to changes in salt intake...

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“…For instance, an abnormal baroreflex control of heart rate has been linked to the pathogenesis of essential hypertension [2], [3] and impaired baroreflex sensitivity (BRS) has been demonstrated in salt-sensitive hypertension [4]- [6]. The baroreflex system buffers the changes in BP by the beat-tobeat regulation of the heart rate and peripheral vascular resistance [7].…”

Section: Introductionmentioning

confidence: 99%

High Salt Diet Blunted Baroreflex Sensitivity (BRS) to Bilateral Common Carotid Artery Occlusion (BCCO) in Male Sprague –Dawley Rats – Permissive Effect of Testosterone

Oloyo

Elias

Tom

et al. 2021

EJMED

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Autonomic dysfunction is involved in the onset of salt-sensitive hypertension as baroreflex sensitivity (BRS) is blunted in salt-sensitive hypertension. However, salt sensitivity exhibits sex disparity because in salt-sensitive hypertension, blood pressure (BP) is usually higher in males when compared with females. The mechanism(s) underlying this sexual dimorphism is not clear. We, therefore, designed this study to determine BRS in weanling male Sprague – Dawley rats that were either bilaterally orchidectomized or sham-operated (under ketamine and xylazine anaesthesia (90 mg and 10 mg/kg/body weight i.m) respectively, with or without testosterone replacement (10 mg/kg sustanon 250® i.m once in 3 weeks) and were placed on normal (0.3%) or high (8%) NaCl diet for 6 weeks. Blood pressure (BP) and heart rate (HR) were measured via arterial cannulation under urethane and α-chloralose anesthesia (5 ml/kg body weight i.p). BRS was determined as change in HR per unit change in BP in response to 30 seconds bilateral common carotid artery occlusion (BCCO). Serum concentration of testosterone was measured using enzyme-linked immunosorbent assay (ELISA). High salt diet (HSD) increased both the basal BP and peak BP after BCCO when compared with control. Orchidectomy attenuated but testosterone replacement restored the elevated BP in rats fed HSD. HSD blunted BRS to BCCO. However, this effect of HSD was lost in the absence of testosterone as there was no significant difference in BRS between rat fed a normal or high salt diet. Our results suggest that blunting of the BRS may be one of the mechanisms by which testosterone promotes salt-induced hypertension and serves as one of the bases for sex disparity in salt-sensitive hypertension.

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Effects of salt loading on sympathetic activity and blood pressure in anesthetized two-kidney, one clip hypertensive rats

Cited by 6 publications

References 48 publications

Excessive dietary salt promotes aortic stiffness in murine renovascular hypertension

Excessive dietary salt promotes aortic stiffness in murine renovascular hypertension

Depressor effect of chymase inhibitor in mice with high salt-induced moderate hypertension

High Salt Diet Blunted Baroreflex Sensitivity (BRS) to Bilateral Common Carotid Artery Occlusion (BCCO) in Male Sprague –Dawley Rats – Permissive Effect of Testosterone

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