Essential role of estrogen in the EDHF-mediated responses of mesenteric arteries from middle-aged female rats: possible contribution of gap junctional protein connexin43

Edhf 2000 ◽  
2003 ◽  
pp. 349-358
Keyword(s):  
Essential Role ◽  
Mesenteric Arteries ◽  
Female Rats ◽  
Middle Aged ◽  
Junctional Protein ◽  
Gap Junctional

scholarly journals The Role of Estrogen in Anxiety-Like Behavior and Memory of Middle-Aged Female Rats

2020 ◽  
Vol 11 ◽  
Author(s):  
Emese Renczés ◽  
Veronika Borbélyová ◽  
Manuel Steinhardt ◽  
Tim Höpfner ◽  
Thomas Stehle ◽  
...  
Keyword(s):  
Female Rats ◽  
Middle Aged

Abstract 509: Essential Role of Vascular Smooth Muscle Bmal1 in Diurnal Variations of Contraction and Blood Pressure

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Wen Su ◽  
Zhongwen Xie ◽  
Zhenheng Guo ◽  
Ming C Gong
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Essential Role ◽  
Smooth Muscle Contraction ◽  
Diurnal Variations ◽  
Mesenteric Arteries ◽  
Isometric Contractions ◽  
Vascular Smooth Muscle Contraction

Bmal1 is an obligatory core clock gene that is ubiquitously expressed but has been demonstrated to have tissue specific functions. However, the vascular smooth muscle specific function of bmal1 is unknown. We generated a smooth muscle specific bmal1 knockout mouse model (SM-bmal1-ko) and investigated the role of bmal1 in vascular smooth muscle contraction and blood pressure regulation. Isometric contractions were measured in isolated right renal artery and 2 nd order branch of mesenteric artery helical strips. Blood pressure was monitored in conscious free-moving mice using radiotelemetry. We demonstrated that bmal1 was selectively deleted in smooth muscle enriched tissues like mesenteric arteries. Moreover, the diurnal variations of bmal1 target genes per1/2 were abolished in mesenteric arteries. The isometric contractions in response to alpha1 agonist phenylephrine and to 5-HT were significantly diminished in vascular helical strips isolated from SM-bmal1-ko mice compared to that from control flox mice. The contractile diurnal variations detected in the renal arteries isolated from control flox mice were significantly diminished in samples isolated from SM-bmal1-ko mice. Moreover, in vivo , the diurnal variations in the instantaneous pressor responses to intravenous phenylephrine injection were significantly diminished in SM-bmal1-ko mice compared to control flox mice. Twenty four hour mean arterial blood pressure was significantly decreased under 12:12 light:dark, constant light or constant dark conditions. Importantly, the amplitude of blood pressure diurnal variations was significantly diminished in SM-bmal1-ko mice. Importantly, neither the level nor the diurnal variations of locomotor activity was affected by bmal1 deletion. This indicates that the central SCN clock function is not affected in the SM-bmal1-ko mice and the blood pressure alterations in SM-bmal1-ko mice is not a consequence of changed locomotor activity. Taken together, our results demonstrate an essential role of bmal1 in the diurnal variations of vascular smooth muscle contraction and blood pressure.

Role of Gap Junctional Protein Connexin40 in the Pathogenesis of Atrial Fibrillation

2000 ◽  
Vol 99 (s43) ◽  
pp. 8P-8P
Author(s):  
P Kanagaratnam ◽  
NJ Severs ◽  
NS Peters
Keyword(s):  
Atrial Fibrillation ◽  
Junctional Protein ◽  
Gap Junctional

scholarly journals Estrogen replacement enhances EDHF-mediated vasodilation of mesenteric and uterine resistance arteries: role of endothelial cell Ca2+

2009 ◽  
Vol 296 (3) ◽  
pp. E503-E512 ◽  
Author(s):  
Natalie Z. Burger ◽  
Olga Y. Kuzina ◽  
George Osol ◽  
Natalia I. Gokina
Keyword(s):  
Endothelial Cell ◽  
Underlying Mechanism ◽  
Mature Female ◽  
Mesenteric Arteries ◽  
Female Rats ◽  
Estrogen Replacement ◽  
Resistance Arteries ◽  
Uterine Arteries ◽  
Small Resistance

Endothelium-derived hyperpolarizing factor (EDHF) plays an important role in the regulation of vascular microcirculatory tone. This study explores the role of estrogen in controlling EDHF-mediated vasodilation of uterine resistance arteries of the rat and also analyzes the contribution of endothelial cell (EC) Ca2+ signaling to this process. A parallel study was also performed with mesenteric arteries to provide comparison with a nonreproductive vasculature. Mature female rats underwent ovariectomy, with one half receiving 17β-estradiol replacement (OVX+E) and the other half serving as estrogen-deficient controls (OVX). Uterine or mesenteric resistance arteries were harvested, cannulated, and pressurized. Nitric oxide and prostacyclin production were inhibited with 200 μM NG-nitro-l-arginine and 10 μM indomethacin, respectively. ACh effectively dilated the arteries preconstricted with phenylephrine but failed to induce dilation of vessels preconstricted with high-K+ solution. ACh EC50 values were decreased by estrogen replacement by five- and twofold in uterine and mesenteric arteries, respectively. As evidenced by fura-2-based measurements of EC cytoplasmic Ca2+ concentration ([Ca2+]i), estrogen replacement was associated with increased basal and ACh-stimulated EC [Ca2+]i rise in uterine, but not mesenteric, vessels. These data demonstrate that EDHF contributes to endothelium-dependent vasodilation of uterine and mesenteric resistance arteries and that estrogen controls EDHF-related mechanism(s) more efficiently in reproductive vs. nonreproductive vessels. Enhanced endothelial Ca2+ signaling may be an important underlying mechanism in estrogenic modulation of EDHF-mediated vasodilation in small resistance uterine arteries.

scholarly journals Essential Role of Ovarian Hormones in Susceptibility to the Consequences of Witnessing Social Defeat in Female Rats

2018 ◽  
Vol 84 (5) ◽  
pp. 372-382 ◽  
Author(s):  
Julie E. Finnell ◽  
Brandon L. Muniz ◽  
Akhila R. Padi ◽  
Calliandra M. Lombard ◽  
Casey M. Moffitt ◽  
...  
Keyword(s):  
Essential Role ◽  
Social Defeat ◽  
Ovarian Hormones ◽  
Female Rats

Gap junctions–guards of excitability

2015 ◽  
Vol 43 (3) ◽  
pp. 508-512 ◽  
Author(s):  
Line Waring Stroemlund ◽  
Christa Funch Jensen ◽  
Klaus Qvortrup ◽  
Mario Delmar ◽  
Morten Schak Nielsen
Keyword(s):  
Sodium Channel ◽  
Crucial Role ◽  
Connexin 43 ◽  
Current Evidence ◽  
Intercalated Disc ◽  
Intercalated Discs ◽  
Cardiac Sodium Channel ◽  
Junctional Protein ◽  
Gap Junctional

Cardiomyocytes are connected by mechanical and electrical junctions located at the intercalated discs (IDs). Although these structures have long been known, it is becoming increasingly clear that their components interact. This review describes the involvement of the ID in electrical disturbances of the heart and focuses on the role of the gap junctional protein connexin 43 (Cx43). Current evidence shows that Cx43 plays a crucial role in organizing microtubules at the intercalated disc and thereby regulating the trafficking of the cardiac sodium channel NaV1.5 to the membrane.

Mutations of connexin 26 at position 75 and dominant deafness: Essential role of arginine for the generation of functional gap-junctional channels

2006 ◽  
Vol 220 (1-2) ◽  
pp. 87-94 ◽  
Author(s):  
Yanqin Deng ◽  
Yongyue Chen ◽  
Luis Reuss ◽  
Guillermo A. Altenberg
Keyword(s):  
Essential Role ◽  
Connexin 26 ◽  
Gap Junctional

Testosterone and β-oestradiol prevent inward remodelling of rat small mesenteric arteries: role of NO and transglutaminase

2013 ◽  
Vol 124 (12) ◽  
pp. 719-728 ◽  
Author(s):  
Lara del Campo ◽  
Bilge Guvenc Tuna ◽  
Mercedes Ferrer ◽  
Ed van Bavel ◽  
Erik N.T.P. Bakker
Keyword(s):  
Sex Hormones ◽  
No Synthase ◽  
Mesenteric Arteries ◽  
Female Rats ◽  
Preventive Effect ◽  
Female Wistar Rats ◽  
Males And Females ◽  
Synthase Inhibitor ◽  
Dose Dependent

Increasing evidence shows that sex hormones exert a protective effect on the vasculature, especially in the regulation of the active vasomotor responses. However, whether sex hormones affect vascular remodelling is currently unclear. In the present study, we tested the hypothesis that testosterone in males and β-oestradiol in females prevent inward remodelling, possibly through inhibition of cross-linking activity induced by enzymes of the TG (transglutaminase) family. Small mesenteric arteries were isolated from male and female Wistar rats. Dose-dependent relaxation to testosterone and β-oestradiol was inhibited by the NO synthase inhibitor L-NAME (NG-nitro-L-arginine methyl ester), confirming that these hormones induce NO release. When arteries were cannulated, pressurized and kept in organ culture with ET-1 (endothelin-1) for 3 days we observed strong vasoconstriction and inward remodelling. Remodelling was significantly inhibited by testosterone in males, and by β-oestradiol in females. This preventive effect of sex hormones was not observed in the presence of L-NAME. Inward remodelling was also reduced by the inhibitor of TG L682.777, both in males and females. In arteries from female rats, ET-1 increased TG activity, and this effect was prevented by β-oestradiol. L-NAME induced a significant increase in TG activity in the presence of sex hormones in arteries from both genders. We conclude that testosterone and β-oestradiol prevent constriction-induced inward remodelling. Inward remodelling, both in males and females, depends on NO and TG activity. In females, inhibition of inward remodelling could be mediated by NO-mediated inhibition of TG activity.

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