Gender Differences in Vascular Smooth Muscle Reactivity to Increases in Extracellular Sodium Salt

Barron, Laura A.; Green, Gachavis M.; Khalil, Raouf A.

doi:10.1161/hy02t2.102779

Cited by 19 publications

(18 citation statements)

References 44 publications

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“…Periarteriolar [NO], arteriolar diameter, and blood flow velocity were measured for an individual arteriole in the intestine at the control osmolarity of 300 mosM and at 360 mosM before and after the administration of KB-R7943 (50 M). The concentration of KB-R7943 used in this study was based on previously published reports (1,14). The osmolarity of the bathing solution was changed to 360 mosM by adding a 1 osM NaCl solution to the bicarbonate solution flow (5 ml/min) at the rate of 28.125 ml/h.…”

Section: Methodsmentioning

confidence: 99%

Sodium channels are required during in vivo sodium chloride hyperosmolarity to stimulate increase in intestinal endothelial nitric oxide production

Zani

Bohlen

2005

American Journal of Physiology-Heart and Circulatory Physiology

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Section: Methodsmentioning

confidence: 99%

Sodium channels are required during in vivo sodium chloride hyperosmolarity to stimulate increase in intestinal endothelial nitric oxide production

Zani

Bohlen

2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…SM1, 204-kDa myosin heavy chain (MHC) isoform. *Adapted from Barron et al (3). †P Յ 0.01 compared with both normal and ovariectomized groups.…”

Section: Effects Of Estrogenmentioning

confidence: 99%

Effects of sex and estrogen on myosin COOH-terminal isoforms and contractility in rat aorta

Rutgeerts

Bowman²,

Johnson³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Paul RJ, Bowman PS, Johnson J, Martin AF. Effects of sex and estrogen on myosin COOH-terminal isoforms and contractility in rat aorta. Am J Physiol Regul Integr Comp Physiol 292: R751-R757, 2007. First published August 17, 2006; doi:10.1152/ajpregu.00167.2006.-We reported that estrogen treatment of ovariectomized rats increased uterine smooth muscle contractility and the ratio of the COOH-terminal myosin heavy chain isoform SM1 (204 kDa) and SM2 [200 kDa; Hewett TE, Martin AF, Paul RJ. J Physiol (Lond) 460: 351-364, 1993]. We extended this model to study sex and estrogen effects on vascular contractility. Experimental groups included 10-to 14-wk-old male (M), female (F), ovariectomized female (OF), and OF treated with estrogen (OF&E) for 7 days with a subcutaneous pellet delivery system, resulting in 17␤-estradiol of 85 (OF&E) vs. 5 (OF or M) pg/ml. The SM1-to-SM2 ratio increased from 1.8 to 2.6 in thoracic aorta, similar to uterine muscle. Isometric force was measured in 5-mm segments of intact and endothelium-denuded (Ϫendo) aorta. With KCl, the maximum forces were in the order OF Ϸ M Ͼ OF&E, and ED50 OF&E Ͼ OF Ϸ M. Differences in ED50 with estrogen persisted after endothelial denudation. The decreased force in Ϫendo OF aorta was not seen in OF&E, suggesting that estrogen altered an endothelium-dependent effect. No differences in maximum forces were noted with norepinephrine: ED50 OF Ͼ OF&E Ͼ M. Estrogen treatment, in contrast to KCl, increased sensitivity. Endothelial denudation increased sensitivity but reduced the differences between groups. With ACh relaxation, males were more sensitive than females, and estrogen had no effect. In the abdominal aorta, there were no changes in SM1/SM2 with 17␤-estradiol, and differences in contractility were blunted. In summary, estrogen treatment decreased responses to KCl but increased sensitivity to norepinephrine; male rats always demonstrated the highest contractility. An increase in the COOH-terminal myosin heavy chain isoform SM1-to-SM2 ratio with 17␤-estradiol treatment may underlie the changes observed in contractility.estrogen; vascular sensitivity; isometric force; myosin isoforms; ovariectomy THE OCCURRENCE OF CARDIOVASCULAR diseases is greater in men aged 30 -50 yr compared with women of similar age (15, 16). The incidence of cardiovascular diseases is also greater in postmenopausal compared with premenopausal women, and vascular protective effects of female sex hormones have been proposed (15,16,18,31). Currently, estrogen replacement therapy to postmenopausal women is in widespread use, but its validity is questioned (14,17,23,27,34,36). The mechanism by which sex and/or estrogen may affect the heart is unknown; it is likely to be multifactorial and has been reviewed in detail (30, 40). Estrogen receptors have been identified on both vascular endothelial (4, 10) and smooth muscle cells (5, 21, 22, 29), providing two potential pathways by which estrogen could affect vascular function. In addition, non-receptor-mediated mechanisms may play a role (35). Estroge...

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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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Gender Differences in Vascular Smooth Muscle Reactivity to Increases in Extracellular Sodium Salt

Cited by 19 publications

References 44 publications

Sodium channels are required during in vivo sodium chloride hyperosmolarity to stimulate increase in intestinal endothelial nitric oxide production

Sodium channels are required during in vivo sodium chloride hyperosmolarity to stimulate increase in intestinal endothelial nitric oxide production

Effects of sex and estrogen on myosin COOH-terminal isoforms and contractility in rat aorta

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

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