Different role of endothelium/nitric oxide in 17β-estradiol- and progesterone-induced relaxation in rat arteries

Chan, Hoi Yun; Yao, Xiaoqiang; Tsang, Suk Ying; Chan, F.H.Y.; Lau, Chi Wai; Huang, Yü

doi:10.1016/s0024-3205(01)01235-8

Cited by 21 publications

(9 citation statements)

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“…In that regard, we observed two increasing phases of uterine blood flow: the first increasing phase (days 0 to 5) was accompanied by increasing concentrations of progesterone and increasing NOS mRNA expression; the second increasing phase (days 11 to estrus) was accompanied by increasing concentrations of estradiol and increasing NOS mRNA expression. Both estrogens and progesterone can cause systemic and uterine vascular relaxation and increased blood flow, which are mediated primarily by NO [16,30,35,36], as reported in sheep [16,19,30,37], pigs [36] and rats [12,35]. Also, we assume that both hormones can cause NO-mediated vasorelaxation in the uterine vascular bed during the estrus cycle in the mare; progesterone seems to stimulate uterine blood flow during early diestrus, and estradiol seems to stimulate it towards estrus.…”

Section: Regulation Of Uterine Blood Flow Cyclic Maressupporting

confidence: 61%

Relationships Between Uterine Blood Flow, Peripheral Sex Steroids, Expression of Endometrial Estrogen Receptors and Nitric Oxide Synthases During the Estrous Cycle in Mares

Honnens¹,

Weisser²,

Welter

et al. 2011

J. Reprod. Dev.

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Abstract. The objective of this study was to investigate the relationships between uterine perfusion and estrogen, progesterone and the uterine nitric oxide synthase (NOS) system in five trotter mares during the estrous cycle. Color Doppler sonography for measurement of uterine blood flow and collection of blood for determination of plasma estrogen and progesterone concentrations were performed on days 0 (= ovulation), 1, 5, 11 and 15 and daily during estrus (days -1 to -4) of one estrous cycle; endometrial biopsy collection for mRNA expression analysis of NOS and estrogen receptors was performed on days 0, 1, 5, 11, 15 and -3. Blood flow in each uterine artery was assessed by calculating the mean time-averaged maximum velocity (TAMV) and the pulsatility index (PI). Plasma concentrations of estrogen and progesterone were determined using specific enzyme immunoassays. The mRNA expressions of endothelial NOS (eNOS), inducible NOS (iNOS) as well as estrogen receptors α (ERα) and β (ERβ) were quantified using reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. The TAMV and PI had a biphasic pattern during the estrous cycle (P<0.05), with maximum and minimum, respectively, values on days 5 and -4. Estrogen receptor mRNA concentrations increased significantly during days 15 (ERα) and -3 (ERβ). Transcript expression of eNOS, but not iNOS, had a biphasic pattern during the cycle (P<0.05) with maximum levels on days 5 and -3 and correlated positively with TAMV (r=0.81, P=0.05). We infer that the uterine NOS system, especially eNOS, plays an important role in the regulation of uterine blood flow during the estrous cycle in mares. Key words: Endometrial messenger RNA expression, Estrous cycle, Nitric oxide synthases, Steroid hormones, Uterine perfusion (J. Reprod. Dev. 57: [43][44][45][46][47][48] 2011) haracteristic uterine blood flow patterns have been reported during the estrous cycle in mares based on color Doppler sonography [1,2]. Uterine perfusion had a wave-shaped profile throughout the cycle, showing maximal blood flow during estrus and the early luteal phase [1][2][3][4]. Variations in uterine blood flow in cycling mares have been attributed to changes in circulating estrogen concentrations. However, due to a weak correlation between the resistance to uterine blood flow and plasma estrogen concentrations, other factors may also regulate uterine blood flow [2].Changes in uterine blood flow during the estrous cycle in many species are mediated mainly by estrogens [5]; although flow was enhanced by high plasma estradiol concentrations [6,7] and decreased during the luteal phase [8,9], the mechanisms involved have not been elucidated. Estrogens appear to act via two pathways: the genomic and non-genomic pathways [10]. Briefly, in the classical genomic pathway, estrogens bind to their nuclear receptors, subsequently regulating the transcription of target genes. For example, administration of estradiol increased estrogen receptors within 48 h in cyclic ewes [11]. Furthermore, a non-genomic pathway wit...

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Section: Regulation Of Uterine Blood Flow Cyclic Maressupporting

confidence: 61%

Relationships Between Uterine Blood Flow, Peripheral Sex Steroids, Expression of Endometrial Estrogen Receptors and Nitric Oxide Synthases During the Estrous Cycle in Mares

Honnens¹,

Weisser²,

Welter

et al. 2011

J. Reprod. Dev.

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“…4), suggesting that the effects of estrogen might result from NO production in vascular smooth muscle cells. While it is often problematic to make direct comparisons of findings obtained from tissues of different species, previous studies have indicated that endothelial cells from bovine and rat aorta share a similar responsiveness to estrogen [24], and that estrogen can relax rat aorta by an endothelium-independent mechanism [25]. Therefore, the present findings are suggestive of a non-endothelial source of NO production in the vascular (aortic) wall.…”

Section: Discussionmentioning

confidence: 45%

Estradiol Relaxes Rat Aorta via Endothelium-Dependent and -Independent Mechanisms

Abou-Mohamed¹,

Elmarakby²,

Carrier³

et al. 2003

Pharmacology

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The effects of estrogen on arterial function are heterogeneous with respect to vessel and/or species. We have investigated 17β-estradiol-induced relaxation in isolated rat aorta with regard to the role of the vascular endothelium and ionic mechanisms. Estrogen induced a concentration-dependent relaxation of 46.5 ± 7.9% and 70.1 ± 12.2% (10^–8 and 10^–7M), which was reduced by endothelial denudation. Furthermore, L-nitroarginine methyl ester completely abrogated this effect; however, estradiol did not relax KCl-contracted rings. Tetraethyl ammonium (1 mmol/l) completely blocked estradiol-induced relaxation. Estradiol increased [cGMP] in isolated aortic rings via NO, but did not significantly affect NOS activity in endothelial cells. Thus, estrogen can relax rat aorta in vitro via both endothelium-dependent and -independent mechanisms involving the NO/cGMP and potassium channel signaling system.

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“…By contrast, Wu et al proposed that formononetin caused opening of iberiotoxin-sensitive Ca 2+ -activated K + channels and glibenclamide-sensitive adenosine triphosphate (ATP)-dependent K + channels in rat aorta [9] . This discordance may lie in the different responses of mesenteric artery and aorta to drugs [39] .…”

Section: Discussionmentioning

confidence: 99%

Vasorelaxant and antihypertensive effects of formononetin through endothelium-dependent and -independent mechanisms

Sun

Cao

2011

Acta Pharmacol Sin

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Aim: To investigate the mechanisms underlying the vasorelaxant effect of formononetin, an O-methylated isoflavone, in isolated arteries, and its antihypertensive activity in vivo. Methods: Arterial rings of superior mesenteric arteries, renal arteries, cerebral basilar arteries, coronary arteries and abdominal aortas were prepared from SD rats. Isometric tension of the arterial rings was recorded using a myograph system. Arterial pressure was measured using tail-cuff method in spontaneously hypertensive rats. Results: Formononetin (1-300 μmol/L) elicited relaxation in arteries of the five regions that were pre-contracted by KCl (60 mmol/L), U46619 (1 μmol/L) or phenylephrine (10 μmol/L). The formononetin-induced relaxation was reduced by removal of endothelium or by pretreatment with L-NAME (100 μmol/L). Under conditions of endothelium denudation, formononetin (10, 30, and 100 μmol/L) inhibited the contraction induced by KCl and that induced by CaCl 2 in Ca 2+ -free depolarized medium. In the absence of extracellular Ca 2+ , formononetin (10, 30, and 100 μmol/L) depressed the constriction caused by phenylephrine (10 μmol/L), but did not inhibit the tonic contraction in response to the addition of CaCl 2 (2 mmol/L). The contraction caused by caffeine (30 mmol/L) was not inhibited by formononetin (100 μmol/L). Formononetin (10 and 100 μmol/L) reduced the change rate of Ca 2+ -fluorescence intensity in response to KCl (50 mmol/L). In spontaneously hypertensive rats, formononetin (5, 10, and 20 mg/kg) slowly lowered the systolic, diastolic and mean arterial pressure. Conclusion: Formononetin causes vasodilatation via two pathways: (1) endothelium-independent pathway, probably due to inhibition of voltage-dependent Ca 2+ channels and intracellular Ca 2+ release; and (2) endothelium-dependent pathway by releasing NO. Both the pathways may contribute to its antihypertensive effect.

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Different role of endothelium/nitric oxide in 17β-estradiol- and progesterone-induced relaxation in rat arteries

Cited by 21 publications

References 0 publications

Relationships Between Uterine Blood Flow, Peripheral Sex Steroids, Expression of Endometrial Estrogen Receptors and Nitric Oxide Synthases During the Estrous Cycle in Mares

Relationships Between Uterine Blood Flow, Peripheral Sex Steroids, Expression of Endometrial Estrogen Receptors and Nitric Oxide Synthases During the Estrous Cycle in Mares

Estradiol Relaxes Rat Aorta via Endothelium-Dependent and -Independent Mechanisms

Vasorelaxant and antihypertensive effects of formononetin through endothelium-dependent and -independent mechanisms

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