scholarly journals Sex Differences in the Vasodilation Mediated by G Protein-Coupled Estrogen Receptor (GPER) in Hypertensive Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Nathalie Tristão Banhos Delgado ◽  
Wender do Nascimento Rouver ◽  
Leandro Ceotto Freitas-Lima ◽  
Ildernandes Vieira-Alves ◽  
Virgínia Soares Lemos ◽  
...  
Keyword(s):  
G Protein ◽  
Spontaneously Hypertensive Rats ◽  
Mesenteric Arteries ◽  
Vascular Response ◽  
Hypertensive Rats ◽  
Response Curves ◽  
Spontaneously Hypertensive ◽  
Before And After ◽  
G Protein Coupled ◽  
Relaxing Response

BackgroundThe protective effect of estrogen on the vasculature cannot be explained only by its action through the receptors ERα and ERβ. G protein-coupled estrogen receptors (GPER)—which are widely distributed throughout the cardiovascular system—may also be involved in this response. However, little is known about GPER actions in hypertension. Therefore, in this study we evaluated the vascular response mediated by GPER using a specific agonist, G-1, in spontaneously hypertensive rats (SHR). We hypothesized that G-1 would induce a relaxing response in resistance mesenteric arteries from SHR of both sexes.MethodsG-1 concentration-response curves (1 nM-10 μM) were performed in mesenteric arteries from SHR of both sexes (10–12-weeks-old, weighing 180–250 g). The effects of G-1 were evaluated before and after endothelial removal and incubation for 30 min with the inhibitors L-NAME (300 μM) and indomethacin (10 μM) alone or combined with clotrimazole (0.75 μM) or catalase (1,000 units/mL). GPER immunolocalization was also investigated, and vascular hydrogen peroxide (H2O2) and ROS were evaluated using dichlorofluorescein (DCF) and dihydroethidium (DHE) staining, respectively.ResultsGPER activation promoted a similar relaxing response in resistance mesenteric arteries of female and male hypertensive rats, but with the participation of different endothelial mediators. Males appear to be more dependent on the NO pathway, followed by the H2O2 pathway, and females on the endothelium and H2O2 pathway.ConclusionThese findings show that the GPER agonist G-1 can induce a relaxing response in mesenteric arteries from hypertensive rats of both sexes in a similar way, albeit with differential participation of endothelial mediators. These results contribute to the understanding of GPER activation on resistance mesenteric arteries in essential hypertension.

scholarly journals Lisinopril Alters Contribution of Nitric Oxide and KCa Channels to Vasodilatation in Small Mesenteric Arteries of Spontaneously Hypertensive Rats

2015 ◽  
pp. 39-49 ◽  
Author(s):  
S. ALBARWANI ◽  
S. AL-SIYABI ◽  
I. AL-HUSSEINI ◽  
A. AL-ISMAIL ◽  
I. AL-LAWATI ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Spontaneously Hypertensive Rats ◽  
Mesenteric Arteries ◽  
Bkca Channel ◽  
Hypertensive Rats ◽  
Response Curves ◽  
Spontaneously Hypertensive ◽  
Kca Channels ◽  
Reserve System

To investigate lisinopril effect on the contribution of nitric oxide (NO) and KCa channels to acetylcholine (ACh)-induced relaxation in isolated mesenteric arteries of spontaneously hypertensive rats (SHRs). Third branch mesenteric arteries isolated from lisinopril treated SHR rats (20 mg/kg/day for ten weeks, SHR-T) or untreated (SHR-UT) or normotensive WKY rats were mounted on tension myograph and ACh concentration-response curves were obtained. Westernblotting of eNOS and KCa channels was performed. ACh-induced relaxations were similar in all groups while L-NMMA and indomethacin caused significant rightward shift only in SHR-T group. Apamin and TRAM-34 (SKCa and IKCa channels blockers, respectively) significantly attenuated ACh-induced maximal relaxation by similar magnitude in vessels from all three groups. In the presence of L-NMMA, indomethacin, apamin and TRAM-34 further attenuated ACh-induced relaxation only in SHR-T. Furthermore, lisinopril treatment increased expression of eNOS, SKCa and BKCa proteins. Lisinopril treatment increased expression of eNOS, SKCa, BKCa channel proteins and increased the contribution of NO to ACh-mediated relaxation. This increased role of NO was apparent only when EDHF component was blocked by inhibiting SKCa and IKCa channels. Such may suggest that in mesenteric arteries, non-EDHF component functions act as a reserve system to provide compensatory vasodilatation if (and when) hyperpolarization that is mediated by SKCa and IKCa channels is reduced.

scholarly journals Greater fractalkine expression in mesenteric arteries of female spontaneously hypertensive rats compared with males

2009 ◽  
Vol 296 (4) ◽  
pp. H1080-H1088 ◽  
Author(s):  
Jennifer C. Sullivan ◽  
Jennifer L. Pardieck ◽  
Derek Doran ◽  
Yan Zhang ◽  
Jin-Xiong She ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Transforming Growth Factor ◽  
Mesenteric Arteries ◽  
Hypertensive Rats ◽  
Response Curves ◽  
Male And Female ◽  
Monocyte Chemoattractant Protein 1 ◽  
Spontaneously Hypertensive ◽  
Markers Of Inflammation ◽  
Tnf Α

A mircoarray analysis was performed to identify novel inflammatory genes that are differentially expressed in the mesenteric arteries of male and female spontaneously hypertensive rats (SHRs). Fractalkine was found to be the inflammatory gene with the greatest differential expression in mesenteric arteries, with the expression being greater in female SHRs compared with males. Greater inflammatory mediators in female SHRs were verified by measuring urinary monocyte chemoattractant protein-1, transforming growth factor-β, and tumor necrosis factor-α (TNF-α) excretion, all of which were greater in female SHRs compared with males. Real-time PCR, Western blot analysis, and ELISA verified greater soluble fractalkine in mesenteric arteries of female SHRs. Consistent with increased fractalkine expression, TNF-α-converting enzyme and TNF-α levels in mesenteric arteries were also greater in female SHRs. We next tested the hypothesis that mesenteric arteries from female SHRs will have greater fractalkine-induced dysfunction. Acetylcholine, sodium nitroprusside, phenylephrine, and KCl concentration-response curves were performed in third-order mesenteric arteries from male and female SHRs pretreated with either vehicle or fractalkine (1 μg/ml). Fractalkine decreased sensitivity to 1) acetylcholine in arteries from male SHRs, 2) phenylephrine in arteries from both sexes, and 3) KCl in arteries from female SHRs. In conclusion, urinary and vascular markers of inflammation are greater in female SHRs compared with males, although blood pressure and cardiovascular risk are less in females.

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