Role of female sex hormones in neuronal nitric oxide release and metabolism in rat mesenteric arteries

2002 ◽  
Vol 103 (3) ◽  
pp. 239-247 ◽  
Author(s):  
Nuria MINOVES ◽  
Gloria BALFAGÓN ◽  
Mercedes FERRER
Keyword(s):  
Sex Hormones ◽  
Nerve Impulse ◽  
No Synthase ◽  
Mesenteric Arteries ◽  
Sprague Dawley ◽  
Female Sex ◽  
Female Sex Hormones ◽  
No Synthase Inhibitor ◽  
Ovx Rats ◽  
Synthase Inhibitor

This study examines the effects of female sex hormones on the vasoconstrictor response to electrical field stimulation (EFS), as well as the modulation of this response by neuronal NO. For this purpose, segments of denuded superior mesenteric artery from ovariectomized (OvX) female Sprague–Dawley rats and from control rats (in oestrus phase) were used. EFS induced frequency-dependent contractions, which were greater in segments from OvX rats than in those from control rats. The NO synthase inhibitor NG-nitro-l-arginine methyl ester strengthened EFS-elicited contractions to a greater extent in arteries from OvX rats than in those from control rats. Similar results were observed with the preferential neuronal NO synthase inhibitor 7-nitroindazole. The sensorial neurotoxin capsaicin did not modify EFS-induced contractions in segments from either group. In noradrenaline-precontracted segments, sodium nitroprusside (SNP) induced concentration-dependent relaxation, which was greater in segments from control rats than in those from OvX rats. 8-Bromo-cGMP induced similar concentration-dependent relaxation in noradrenaline-precontracted segments from both OvX and control rats. Diethyldithiocarbamate, a superoxide dismutase (SOD) inhibitor, reduced the relaxation induced by SNP in segments from both groups of rats. SOD, a superoxide anion scavenger, enhanced the relaxation induced by SNP in segments from OvX rats, but did not modify it in segments from control rats. EFS induced NO−2 formation, which was greater in segments from OvX than in those from control rats, and pretreatment with tetrodotoxin, a blocker of nerve impulse propagation, abolished release in both cases. These results suggest that EFS induces greater neuronal NO release in mesenteric segments from OvX rats than in those from control rats and, although NO metabolism is also higher, the contribution of net neuronal NO in the vasomotor response to EFS is greater in segments from OvX rats than in those from control rats.

scholarly journals Erythropoietin Produces a Dual Effect on Carotid Body Chemoreception in Male Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Christian Arias-Reyes ◽  
Sofien Laouafa ◽  
Natalia Zubieta-DeUrioste ◽  
Vincent Joseph ◽  
Aida Bairam ◽  
...  
Keyword(s):  
Carotid Body ◽  
No Synthase ◽  
Male Rats ◽  
High Dose ◽  
No Production ◽  
Sprague Dawley ◽  
En Bloc ◽  
No Synthase Inhibitor ◽  
Sprague Dawley Rats ◽  
Synthase Inhibitor

Erythropoietin (EPO) regulates respiration under conditions of normoxia and hypoxia through interaction with the respiratory centers of the brainstem. Here we investigate the dose-dependent impact of EPO in the CB response to hypoxia and hypercapnia. We show, in isolated “en bloc” carotid body (CB) preparations containing the carotid sinus nerve (CSN) from adult male Sprague Dawley rats, that EPO acts as a stimulator of CSN activity in response to hypoxia at concentrations below 0.5 IU/ml. Under hypercapnic conditions, EPO did not influence the CSN response. EPO concentrations above 0.5 IU/ml decreased the response of the CSN to both hypoxia and hypercapnia, reaching complete inhibition at 2 IU/ml. The inhibitory action of high-dose EPO on the CSN activity might result from an increase in nitric oxide (NO) production. Accordingly, CB preparations were incubated with 2 IU/ml EPO and the unspecific NO synthase inhibitor (L-NAME), or the neuronal-specific NO synthase inhibitor (7NI). Both NO inhibitors fully restored the CSN activity in response to hypoxia and hypercapnia in presence of EPO. Our results show that EPO activates the CB response to hypoxia when its concentration does not exceed the threshold at which NO inhibitors masks EPO’s action.

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.

Female Sex Hormones and Epilepsy

2015 ◽  
Vol 10 (01) ◽  
pp. 65-71
Author(s):  
Chakorn Chansakul
Keyword(s):  
Sex Hormones ◽  
Female Sex ◽  
Female Sex Hormones

scholarly journals The modulation of social behavior and empathy via oral contraceptives and female sex hormones

2021 ◽  
pp. 105250
Author(s):  
Julia Strojny ◽  
Gregor Domes ◽  
Urs Fischbacher ◽  
Bernadette von Dawans
Keyword(s):  
Social Behavior ◽  
Sex Hormones ◽  
Oral Contraceptives ◽  
Female Sex ◽  
Female Sex Hormones

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

2014 ◽  
Vol 307 (2) ◽  
pp. R149-R157 ◽  
Author(s):  
Krystal N. Brinson ◽  
Olga Rafikova ◽  
Jennifer C. Sullivan
Keyword(s):  
Protein Expression ◽  
Sex Hormones ◽  
Serine Residue ◽  
Relative Resistance ◽  
Salt Diet ◽  
Spontaneously Hypertensive ◽  
Female Sex ◽  
Female Sex Hormones ◽  
Oxide Synthase ◽  
Salt Sensitive Hypertension

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.

The influence of female sex hormones on nasal reactivity in seasonal allergic rhinitis

Allergy ◽  
1999 ◽  
Vol 54 (8) ◽  
pp. 865-871 ◽  
Author(s):  
Up Stübner ◽  
Ue Berger ◽  
J Toth ◽  
B Marks ◽  
F Horak ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Sex Hormones ◽  
Seasonal Allergic Rhinitis ◽  
Female Sex ◽  
Female Sex Hormones
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