Altered Structure and Mechanics of Skeletal Muscle Arteries with High-Salt Diet and Reduced Renal Mass Hypertension

Frisbee, Jefferson C.; Weber, David S.; Liu, Y.; DeBruin, Janet; Lombard, Julian H.

doi:10.1006/mvre.1999.2222

Cited by 9 publications

(8 citation statements)

References 11 publications

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“…A final consideration that could affect the degree of vascular relaxation in ANG II–infused rats maintained on a chronic HS diet would be any changes in vessel distensibility or structural remodeling of the vessel that would interfere with vascular relaxation. While structural remodeling of the vessel was not present in the MCA used in the present studies, structural narrowing and reduced vessel distensibility does occur, to some extent, in skeletal muscle resistance arteries 13 55 (although the latter changes are not sufficient to eliminate vasodilator responses to forskolin, SNP, or Ca 2+ ‐free solution 55 ).…”

Section: Discussionmentioning

confidence: 62%

Time‐Course and Mechanisms of Restored Vascular Relaxation by Reduced Salt Intake and Angiotensin II Infusion in Rats Fed a High‐Salt Diet

McEwen¹,

Schmidt²,

Somberg

et al. 2009

Microcirculation

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Objective: This study determined the mechanisms and time-course of recovery of vascular relaxation in middle cerebral arteries (MCA) of salt-fed Sprague-Dawley rats returned to low salt (LS) diet (0.4% NaCl) or infused with low-dose angiotensin II (ANG II).Methods: Rats were fed high salt (HS) diet (4% NaCl) for 3 days or 4 weeks before return to LS diet for various periods. Other rats fed HS diet (HS + ANG II) received a chronic (3 days) i.v. infusion of a low dose of ANG II (5 ng·kg −1 ·min −1 ) to prevent salt-induced ANG II suppression.Results: HS diet eliminated the increase in cerebral blood flow in response to acetylcholine (ACh) infusion and the relaxation of MCA in response to ACh, iloprost, cholera toxin, and reduced PO 2 . Recovery of vascular relaxation was slow, requiring at least 2 weeks of LS diet, regardless of the duration of exposure to HS diet. Hypoxic dilation was mediated by cyclooxygenase metabolites and ACh-induced dilation was mediated via NO in LS rats and in HS rats returned to LS diet or receiving ANG II infusion. Conclusions:Return to LS diet for 2 weeks or chronic 3-day ANG II infusion restore the mechanisms that normally mediate cerebral vascular relaxation.

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Section: Discussionmentioning

confidence: 62%

Time‐Course and Mechanisms of Restored Vascular Relaxation by Reduced Salt Intake and Angiotensin II Infusion in Rats Fed a High‐Salt Diet

McEwen¹,

Schmidt²,

Somberg

et al. 2009

Microcirculation

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“…Dilator agonists. In addition, the dilation of in situ cremasteric arterioles from LZR and OZR were assessed in response to 1) acetylcholine (10 Ϫ9 -10 Ϫ6 M), a receptor-mediated endothelium-dependent dilator agonist; 2) sodium nitroprusside (10 Ϫ9 -10 Ϫ6 M), an endothelium-independent NO donor; 3) aprikalim (10 Ϫ9 -10 Ϫ6 M), an activator of ATPsensitive potassium (KATP) channels; and 4) Ca 2ϩ -free PSS containing 10 Ϫ3 M adenosine, to produce complete relaxation of the microvessel and determine the maximum (passive) arteriolar diameter (10).…”

Section: Methodsmentioning

confidence: 99%

Impaired NO-dependent dilation of skeletal muscle arterioles in hypertensive diabetic obese Zucker rats

Frisbee

Stepp

2001

American Journal of Physiology-Heart and Circulatory Physiology

143

162

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This study determined alterations to nitric oxide (NO)-dependent dilation of skeletal muscle arterioles from obese (OZR) versus lean Zucker rats (LZR). In situ cremaster muscle arterioles from both groups were viewed via television microscopy, and vessel dilation was measured with a video micrometer. Arteriolar dilation to acetylcholine and sodium nitroprusside was reduced in OZR versus LZR, although dilation to aprikalim was unaltered. NO-dependent flow-induced arteriolar dilation (via parallel microvessel occlusion) was attenuated in OZR, impairing arteriolar ability to regulate wall shear rate. Vascular superoxide levels, as assessed by dihydroethidine fluorescence, were elevated in OZR versus LZR. Treatment of cremaster muscles of OZR with the superoxide scavengers polyethylene glycol-superoxide dismutase and catalase improved arteriolar dilation to acetylcholine and sodium nitroprusside and restored flow-induced dilation and microvascular ability to regulate wall shear rate. These results suggest that NO-dependent dilation of skeletal muscle microvessels in OZR is impaired due to increased levels of superoxide. Taken together, these data suggest that the development of diabetes and hypertension in OZR may be associated with an impaired skeletal muscle perfusion via an elevated vascular oxidant stress.

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“…In mammals, it has been reported that a HSD inhibits angiogenesis in response to chronic muscle stimulation and impairs skeletal muscle performance (Petersen and Greene, 2008). A HSD intake acutely impairs muscular exercise ability due to the calcium deficit in muscle cells via the destruction of sodium-calcium exchange homeostasis (Frisbee et al, 2000). In flies, their muscles are used for flying, crawling and climbing.…”

Section: Resultsmentioning

confidence: 99%

Endurance exercise protects agingDrosophilafrom high-salt diet(HSD)-induced climbing capacity decline and lifespan decrease by enhancing antioxidant capacity

et al. 2020

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A high-salt diet (HSD) is a major cause of many chronic and agerelated defects such as myocardial hypertrophy, locomotor impairment and mortality. Exercise training can efficiently prevent and treat many chronic and age-related diseases. However, it remains unclear whether endurance exercise can resist HSDinduced impairment of climbing capacity and longevity in aging individuals. In our study, flies were given exercise training and fed a HSD from 1-week old to 5-weeks old. Overexpression or knockdown of salt and dFOXO were built by UAS/Gal4 system. The results showed that a HSD, salt gene overexpression and dFOXO knockdown significantly reduced climbing endurance, climbing index, survival, dFOXO expression and SOD activity level, and increased malondialdehyde level in aging flies. Inversely, in a HSD aging flies, endurance exercise and dFOXO overexpression significantly increased their climbing ability, lifespan and antioxidant capacity, but they did not significantly change the salt gene expression. Overall, current results indicated that a HSD accelerated the age-related decline of climbing capacity and mortality via upregulating salt expression and inhibiting the dFOXO/SOD pathway. Increased dFOXO/SOD pathway activity played a key role in mediating endurance exercise resistance to the low salt tolerance-induced impairment of climbing capacity and longevity in aging Drosophila.

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Altered Structure and Mechanics of Skeletal Muscle Arteries with High-Salt Diet and Reduced Renal Mass Hypertension

Cited by 9 publications

References 11 publications

Time‐Course and Mechanisms of Restored Vascular Relaxation by Reduced Salt Intake and Angiotensin II Infusion in Rats Fed a High‐Salt Diet

Time‐Course and Mechanisms of Restored Vascular Relaxation by Reduced Salt Intake and Angiotensin II Infusion in Rats Fed a High‐Salt Diet

Impaired NO-dependent dilation of skeletal muscle arterioles in hypertensive diabetic obese Zucker rats

Endurance exercise protects agingDrosophilafrom high-salt diet(HSD)-induced climbing capacity decline and lifespan decrease by enhancing antioxidant capacity

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