Decreased Endothelium-Dependent NO-cGMP Vascular Relaxation and Hypertension in Growth-Restricted Rats on a High-Salt Diet

Payne, Jerry A.; Alexander, Barbara T.; Khalil, Raouf A.

doi:10.1161/01.hyp.0000111832.47667.13

Cited by 32 publications

(28 citation statements)

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“…Interestingly, PE-evoked contraction was largely increased in the two groups of regimen when the endothelium was removed, and the difference between normal and HS groups vanished as reported by Payne et al (18). In addition, the response of denuded rings to KCl, which induces voltageactivated calcium entry from the extracellular space, and to caffeine, which mobilizes calcium from the sarcoplasmic reticulum, was markedly higher in the HS than in NS group.…”

Section: Discussionsupporting

confidence: 73%

“…In contrast, an enhanced influence of nitric oxide (NO) may have a major role in the lack of rise in blood pressure of sodiumresistant rats when fed a HS diet. In the Dahl-resistant strain (16) and more clearly in the Sprague-Dawley rats (18), N Gnitro-L-arginine methyl ester (L-NAME) or 1H- [1,2,4]oxadiazolo [4,3-a]quinoxalin-1-one, a guanylate cyclase inhibitor, enhanced phenylephrine (PE) contraction, and to a greater extent in rats fed an HS than a normal salt (NS) diet. Taken together, these results favor an adaptive response of both the endothelium and the vascular smooth muscle cells to chronic HS intake in adult rats of resistant strains.…”

mentioning

confidence: 99%

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Nitric oxide pathway counteracts enhanced contraction to membrane depolarization in aortic rings of rats on high-sodium diet

Cordaillat¹,

Fort²,

Virsolvy³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Cordaillat M, Fort A, Virsolvy A, Elghozi J-L, Richard S, Jover B. Nitric oxide pathway counteracts enhanced contraction to membrane depolarization in aortic rings of rats on high-sodium diet. Am J Physiol Regul Integr Comp Physiol 292: R1557-R1562, 2007. First published December 21, 2006; doi:10.1152/ajpregu.00624.2006.-Vascular smooth muscle cell contraction and endothelium-dependent relaxation was evaluated in aortic rings isolated from weaned, 5-moold Sprague-Dawley rats fed a normal (NS; 0.8% NaCl) or high (HS; 8% NaCl) sodium diet. Arterial pressure was 140 Ϯ 6 (NS) and 145 Ϯ 6 mmHg (HS). In endothelium-denuded rings, the response to phenylephrine (PE) was not modified by the sodium diet, while that of depolarizing agent KCl and intracellular calcium releasing agent caffeine increased in the HS group. When endothelium was preserved, PE-evoked contraction was reduced in both NS and HS groups, the contraction being yet lower in the HS group. This effect was partially obliterated by addition of N G -nitro-L-arginine methyl ester (L-NAME), independently of the sodium diet. Relaxation to ACh in intact rings and to sodium nitroprusside (SNP) and 8-bromoadenosine 3Ј5Ј cyclic guanosine monophosphate (8-BrcGMP) in the absence of endothelium was enhanced in rings isolated from HS rats. In addition, the dose-response curve to 8-BrcGMP was shifted to the right in the presence of iberiotoxin, an inhibitor of large conductance, voltagedependent, and calcium-sensitive potassium channel (BKCa). However, shift was more marked in rings from HS rats. Present results provide evidence that response of vascular smooth muscle cell to nitric oxide/cGMP-related compounds is increased in HS rings and is associated with a greater activation of the repolarizing BKCa channels. Such changes might counterbalance enhanced contractile response to membrane depolarization and thus participate in maintenance of arterial pressure in the present model of early and long-term HS feeding in rats. vascular smooth muscle cell; endothelial cell; sodium nitroprusside; iberiotoxin.EXCESSIVE CONSUMPTION OF SODIUM is reported to induce cardiac, vascular, and renal alterations in normotensive and hypertensive humans and animals (9, 30). In various strains of rat, a high salt (HS) diet is associated with changes in the reactivity of aortic rings. Many studies conducted in salt-loaded models have shown an increased contraction of vascular smooth muscle cells in response to agonists (1,14). In addition, relaxation evoked by acetylcholine (ACh) or sodium nitroprusside (SNP) was obliterated in aortic rings isolated from adult spontaneously hypertensive and Dalh-sensitive rats fed a 8% NaCl diet for 4 -8 wk (12,14,16). These results suggest that concomitant increase in vascular smooth muscle cell contraction and impaired endothelium-dependent relaxation both participate in the development of hypertension in the salt-sensitive strains. In contrast, an enhanced influence of nitric oxide (NO) may have a major role in the lack of rise in blood pressure of sodiumr...

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Section: Discussionsupporting

confidence: 73%

mentioning

confidence: 99%

Nitric oxide pathway counteracts enhanced contraction to membrane depolarization in aortic rings of rats on high-sodium diet

Cordaillat¹,

Fort²,

Virsolvy³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…In adult IUGR rats, endothelial dysfunction in association with a decrease in activity and expression of endothelial NO synthase was described [226,227] . Others have shown a diminished NO-dependent vasorelaxation [111,138,[228][229][230][231] . Deficiency of NO, induced by exogenous inhibition of NO generation by arginine analogues leads to hypertension [232][233][234] , and increased levels of PRA [234,235] , suggesting a role of RAS activation through endogenous NO inhibition after IUGR.…”

Section: Nitric Oxidementioning

confidence: 99%

Consequences of Intrauterine Growth Restriction for the Kidney

Schreuder

Waal

Wijk

2006

Kidney Blood Press Res

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Low birth weight due to intrauterine growth restriction is associated with various diseases in adulthood, such as hypertension, cardiovascular disease, insulin resistance and end-stage renal disease. The purpose of this review is to describe the effects of intrauterine growth restriction on the kidney. Nephrogenesis requires a fine balance of many factors that can be disturbed by intrauterine growth restriction, leading to a low nephron endowment. The compensatory hyperfiltration in the remaining nephrons results in glomerular and systemic hypertension. Hyperfiltration is attributed to several factors, including the renin-angiotensin system (RAS), insulin-like growth factor (IGF-I) and nitric oxide. Data from human and animal studies are presented, and suggest a faltering IGF-I and an inhibited RAS in intrauterine growth restriction. Hyperfiltration makes the kidney more vulnerable during additional kidney disease, and is associated with glomerular damage and kidney failure in the long run. Animal studies have provided a possible therapy with blockage of the RAS at an early stage in order to prevent the compensatory glomerular hyperfiltration, but this is far from being applicable to humans. Research is needed to further unravel the effect of intrauterine growth restriction on the kidney.

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“…The volume overload triggers suppression of the renin-angiotensin-aldosterone system, leading to increased salt and water excretion and restoration of vascular volume toward normal (10 -12, 23). High dietary sodium may also promote vasoconstriction by changing plasma osmolarity, nuclear localization, and increased nuclear expression of vasoconstrictive stimuli, such as endothelin-1, release of ouabainlike factor, and activation of the sodium/calcium exchange mechanisms (1,2,18,20,28). Other studies have suggested that high dietary sodium may also affect vascular nitric oxide (NO) production (9).…”

mentioning

confidence: 99%

Effect of dietary sodium on vasoconstriction and eNOS-mediated vascular relaxation in caveolin-1-deficient mice

Pojoga

Yao²,

Sinha³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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RA. Effect of dietary sodium on vasoconstriction and eNOS-mediated vascular relaxation in caveolin-1-deficient mice. Am J Physiol Heart Circ Physiol 294: H1258-H1265, 2008. First published January 4, 2008 doi:10.1152/ajpheart.01014.2007.-Changes in dietary sodium intake are associated with changes in vascular volume and reactivity that may be mediated, in part, by alterations in endothelial nitric oxide synthase (eNOS) activity. Caveolin-1 (Cav-1), a transmembrane anchoring protein in the plasma membrane caveolae, binds eNOS and limits its translocation and activation. To test the hypothesis that endothelial Cav-1 participates in the dietary sodium-mediated effects on vascular function, we assessed vascular responses and nitric oxide (NO)-mediated mechanisms of vascular relaxation in Cav-1 knockout mice (Cav-1 Ϫ/Ϫ ) and wild-type control mice (WT; Cav-1 ϩ/ϩ ) placed on a high-salt (HS; 4% NaCl) or low-salt (LS; 0.08% NaCl) diet for 16 days. After the systolic blood pressure was measured, the thoracic aorta was isolated for measurement of vascular reactivity and NO production, and the heart was used for measurement of eNOS expression and/or activity. The blood pressure was elevated in HS mice treated with N G -nitro-L-arginine methyl ester and more so in Cav-1 Ϫ/Ϫ than WT mice and was significantly reduced during the LS diet. Phenylephrine caused vascular contraction that was significantly reduced in Cav-1 Ϫ/Ϫ (maximum 0.25 Ϯ 0.06 g/mg) compared with WT (0.75 Ϯ 0.22 g/mg) on the HS diet, and the differences were eliminated with the LS diet. Also, vascular contraction in response to membrane depolarization by high KCl (96 mM) was reduced in Cav-1 Ϫ/Ϫ (0.27 Ϯ 0.05 g/mg) compared with WT mice (0.53 Ϯ 0.12 g/mg) on the HS diet, suggesting that the reduced vascular contraction is not limited to a particular receptor. Acetylcholine (10 Ϫ5 M) caused aortic relaxation in WT mice on HS (23.6 Ϯ 3.5%) and LS (23.7 Ϯ 5.5%) that was enhanced in Cav-1 Ϫ/Ϫ HS (72.6 Ϯ 6.1%) and more so in Cav-1 Ϫ/Ϫ LS mice (93.6 Ϯ 3.5%). RT-PCR analysis indicated increased eNOS mRNA expression in the aorta and heart, and Western blots indicated increased total eNOS and phosphorylated eNOS in the heart of Cav-1 Ϫ/Ϫ compared with WT mice on the HS diet, and the genotypic differences were less apparent during the LS diet. Thus Cav-1 deficiency during the HS diet is associated with decreased vasoconstriction, increased vascular relaxation, and increased eNOS expression and activity, and these effects are altered during the LS diet. The data support the hypothesis that endothelial Cav-1, likely through an effect on eNOS activity, plays a prominent role in the regulation of vascular function during substantial changes in dietary sodium intake. endothelium; nitric oxide; vascular smooth muscle; blood pressure; hypertension HIGH-SALT (HS) DIET IS OFTEN associated with increased vascular volume (4, 15). The volume overload triggers suppression of the renin-angiotensin-aldosterone system, leading to increased salt and water excretion and restoration of v...

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Decreased Endothelium-Dependent NO-cGMP Vascular Relaxation and Hypertension in Growth-Restricted Rats on a High-Salt Diet

Cited by 32 publications

References 50 publications

Nitric oxide pathway counteracts enhanced contraction to membrane depolarization in aortic rings of rats on high-sodium diet

Nitric oxide pathway counteracts enhanced contraction to membrane depolarization in aortic rings of rats on high-sodium diet

Consequences of Intrauterine Growth Restriction for the Kidney

Effect of dietary sodium on vasoconstriction and eNOS-mediated vascular relaxation in caveolin-1-deficient mice

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