Estrogen Induces Nitric Oxide-Mediated Vasodilation of Human Mammary Arteriesin Vitro

Nechmad, Allon; Merin, Gideon; Schwalb, Herzl; Shimon, D; Borman, Joseph B.; Milgalter, Eli; Mosseri, Morris

doi:10.1006/niox.1998.0202

Cited by 21 publications

(11 citation statements)

References 37 publications

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“…OVX was not associated with changes in NOS expression or activity in either strain regardless of the diet. Female sex hormones consistently increase NO production in vitro (32), although in vivo studies have yielded conflicting results (11). Consistent with our current results, we have previously published that manipulation of female sex hormones in SHR does not alter NOS enzymatic activity or expression in the renal IM (45) or cortex (44).…”

Section: Intact Ns Intact Hs Ovx Ns Ovx Hssupporting

confidence: 90%

Female sex hormones protect against salt-sensitive hypertension but not essential hypertension

Brinson

Rafikova

Sullivan

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Brinson KN, Rafikova O, Sullivan JC. Female sex hormones protect against salt-sensitive hypertension but not essential hypertension. Am J Physiol Regul Integr Comp Physiol 307: R149 -R157, 2014. First published May 14, 2014 doi:10.1152/ajpregu.00061.2014.-Initial studies found that female Dahl salt-sensitive (DS) rats exhibit greater blood pressure (BP) salt sensitivity than female spontaneously hypertensive rats (SHR). On the basis of the central role played by NO in sodium excretion and BP control, we further tested the hypothesis that blunted increases in BP in female SHR will be accompanied by greater increases in renal inner medullary nitric oxide synthase (NOS) activity and expression in response to a high-salt (HS) diet compared with DS rats. Gonad-intact and ovariectomized (OVX) female SHR and DS rats were placed on normal salt (NS; 0.4% salt) or HS (4% salt) diet for 2 wk. OVX did not alter BP in SHR, and HS diet produced a modest increase in BP. OVX significantly increased BP in DS rats on NS; HS further increased BP in all DS rats, although OVX had a greater increase in BP. Renal inner medullary NOS activity, total NOS3 protein, and NOS3 phosphorylated on serine residue 1177 were not altered by salt or OVX in either strain. NOS1 protein expression, however, significantly increased with HS only in SHR, and this corresponded to an increase in urinary nitrate/nitrite excretion. SHR also exhibit greater NOS1 and NOS3 protein expression than DS rats. These data indicate that female sex hormones offer protection against HS-mediated elevations in BP in DS rats but not SHR. We propose that the relative resistance to HS-mediated increases in BP in SHR is related to greater NOS expression and the ability to increase NOS1 protein expression compared with DS rats. nitric oxide; Dahl-salt sensitive rats; ovariectomy; spontaneously hypertensive rats SALT SENSITIVITY OF BLOOD pressure (BP) is associated with an increased risk for the development of hypertension and cardiovascular disease. Among women, the prevalence of salt sensitivity increases following both surgical and natural menopause (14, 38), suggesting that the loss of ovarian hormones renders women prone to salt sensitivity and increases their risk of developing hypertension (38). This is further supported by studies in experimental animals; surgical ovariectomy (OVX) increases the BP response to salt in many rat strains, including Dahl salt-sensitive (DS) and Dahl salt-resistant rats (59), mRen(2).Lewis rats (7), Sprague-Dawley rats treated with aldosterone (57), and spontaneously hypertensive rats (SHR) (10). These data suggest that female sex hormones are critical in influencing sodium handling and BP regulation; however, the mechanisms responsible continue to be investigated.Salt-sensitive hypertension has been linked to the reninangiotensin system, as well as a decrease in NO production and bioavailability (8,19,53). There is ample evidence in the literature supporting a role for increased ANG II and AT 1 receptor activation in female experimental an...

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Section: Intact Ns Intact Hs Ovx Ns Ovx Hssupporting

confidence: 90%

Female sex hormones protect against salt-sensitive hypertension but not essential hypertension

Brinson

Rafikova

Sullivan

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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“…In the present study, we found that ACh induced an endothelium-dependent relaxation of precontracted segments of the perforating branch of the HIMA with pEC 50 values similar to those obtained in previous studies on the arteries of various species, including the main tree of the HIMA [5,7,13,14].…”

Section: Discussionsupporting

confidence: 72%

Muscarinic Receptor Subtypes Mediating Vasorelaxation of the Perforating Branch of the Human Internal Mammary Artery

Pesic

Jovanović²,

Grbović³

2001

Pharmacology

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The effect of acetylcholine (ACh) on the isolated perforating branch of the human internal mammary artery (HIMA) was investigated. ACh induced concentration- and endothelium-dependent relaxation of arterial rings precontracted with phenylephrine (pEC₅₀ = 6.93 ± 0.01). The muscarinic receptor antagonist atropine (no selectivity), pirenzepine (M₁), methoctramine (M₂), and p-fluoro-hexahydro-siladifenidol (M₁/M₃) competitively antagonized the response to ACh. The pA₂ values were 9.81 ± 0.15, 7.74 ± 0.08, 6.27 ± 0.08, and 7.88 ± 0.04, respectively. In conclusion, this study has shown that ACh induced an endothelium-dependent relaxation of the perforating branch of the HIMA by stimulation of muscarinic receptors on the endothelial cells. On the basis of differential antagonist affinity, we suggest that the muscarinic receptors involved in the ACh-induced relaxation of the isolated perforating branch of HIMA are predominantly of M₁ subtype.

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“…1,36,39,48), rabbit carotid artery (46), mouse aorta (13), coronary microvessels from female or male dogs (24), and human vessels, including coronary arteries (11) and from our laboratory small subcutaneous arteries from men (unpublished data). In contrast, others have implied that NO plays a role in the acute dilation to 17␤-E 2 in, for example, isolated female coronary arteries (4,11), aorta and femoral arteries from rat (5, 51), human mammary artery (38), rabbit coronary artery, and uterine arteries from sheep (44,55). The lack of conformity between studies reporting the acute actions of 17␤-E 2 remains unexplained, but in light of our observations it might be attributed to the ERs interplay and relative differences in ER-␣ and ER-␤ expression in the different vascular beds studied.…”

Section: Discussionmentioning

confidence: 83%

Dilatory responses to estrogenic compounds in small femoral arteries of male and female estrogen receptor-β knockout mice

Cruz¹,

Douglas

Gustafsson

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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The objectives of this study were to determine whether acute dilatory responses to estrogen receptor agonists are altered in isolated arteries from estrogen receptor beta-deficient mice (beta-ERKO) and to gain insight into the role of nitric oxide (NO) in these responses. Femoral arteries (approximately 250 microm) from male and female beta-ERKO mice and wild-type (WT) littermates (26 female, 13 in each group; and 24 male, 12 in each group) were mounted on a Multi-Myograph. Concentration-response curves to 17beta-estradiol (17beta-E2) and the selective estrogen receptor-alpha (ER-alpha) agonist propyl-[1H]-pyrazole-1,3,5-triy-trisphenol (PPT) were obtained before and after NO synthase (NOS) inhibition [Nomega-nitro-L-arginine methyl ester (L-NAME), 0.1 mM] in arteries preconstricted with U-46619 (a thromboxane analog). In WT mice, responses to the potent estrogen receptor-beta (ER-beta) agonist 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN) and the contribution of NO were also assessed. Concentration-response curves to 17beta-E2 and PPT were similar in arteries from WT and -ERKO mice of both genders, but NO-mediated relaxation was different, since L-NAME reduced 17-E2 mediated relaxation in arteries from male and female beta-ERKO but not WT mice (P < 0.05). NOS inhibition reduced dilation to PPT in arteries from male and female WT mice, as well as arteries from female beta-ERKO mice (P < 0.05). Responses to DPN in arteries from WT female and male mice did not differ after NOS inhibition. The acute dilatory responses to estrogenic compounds are similar in WT and beta-ERKO mice but differ mechanistically. Because NO appeared to contribute to responses to 17beta-E2 in arteries from beta-ERKO but not WT mice, the presence of ER- apparently inhibits ER--mediated NO relaxation.

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Estrogen Induces Nitric Oxide-Mediated Vasodilation of Human Mammary Arteriesin Vitro

Cited by 21 publications

References 37 publications

Female sex hormones protect against salt-sensitive hypertension but not essential hypertension

Female sex hormones protect against salt-sensitive hypertension but not essential hypertension

Muscarinic Receptor Subtypes Mediating Vasorelaxation of the Perforating Branch of the Human Internal Mammary Artery

Dilatory responses to estrogenic compounds in small femoral arteries of male and female estrogen receptor-β knockout mice

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