scholarly journals KV7 Channel Expression and Function Within Rat Mesenteric Endothelial Cells

2020 ◽  
Vol 11 ◽  
Author(s):  
Samuel N. Baldwin ◽  
Shaun L. Sandow ◽  
Gema Mondéjar-Parreño ◽  
Jennifer B. Stott ◽  
Iain A. Greenwood
Keyword(s):  
Endothelial Cells ◽  
Protein Expression ◽  
Mesenteric Artery ◽  
Vascular Reactivity ◽  
Vascular Control ◽  
Arterial Diameter ◽  
No Donor ◽  
Rat Mesenteric Artery ◽  
Channel Expression ◽  
And Function

Background and Purpose: Arterial diameter is dictated by the contractile state of the vascular smooth muscle cells (VSMCs), which is modulated by direct and indirect inputs from endothelial cells (ECs). Modulators of KCNQ-encoded kV7 channels have considerable impact on arterial diameter and these channels are known to be expressed in VSMCs but not yet defined in ECs. However, expression of kV7 channels in ECs would add an extra level of vascular control. This study aims to characterize the expression and function of KV7 channels within rat mesenteric artery ECs.Experimental Approach: In rat mesenteric artery, KCNQ transcript and KV7 channel protein expression were determined via RT-qPCR, immunocytochemistry, immunohistochemistry and immunoelectron microscopy. Wire myography was used to determine vascular reactivity.Key Results: KCNQ transcript was identified in isolated ECs and VSMCs. KV7.1, KV7.4 and KV7.5 protein expression was determined in both isolated EC and VSMC and in whole vessels. Removal of ECs attenuated vasorelaxation to two structurally different KV7.2-5 activators S-1 and ML213. KIR2 blockers ML133, and BaCl2 also attenuated S-1 or ML213-mediated vasorelaxation in an endothelium-dependent process. KV7 inhibition attenuated receptor-dependent nitric oxide (NO)-mediated vasorelaxation to carbachol, but had no impact on relaxation to the NO donor, SNP.Conclusion and Implications: In rat mesenteric artery ECs, KV7.4 and KV7.5 channels are expressed, functionally interact with endothelial KIR2.x channels and contribute to endogenous eNOS-mediated relaxation. This study identifies KV7 channels as novel functional channels within rat mesenteric ECs and suggests that these channels are involved in NO release from the endothelium of these vessels.

Effect of prostaglandin E2 on vascular reactivity to norepinephrine in isolated rat mesenteric artery, hind limb and splenic artery

1979 ◽  
Vol 2 (1) ◽  
pp. 67-75 ◽  
Author(s):  
K. Kondo ◽  
J. Misumi ◽  
T. Okuno ◽  
R. Nakamura ◽  
T. Saruta ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Mesenteric Artery ◽  
Hind Limb ◽  
Splenic Artery ◽  
Vascular Reactivity ◽  
Rat Mesenteric Artery ◽  
Isolated Rat

scholarly journals Levobupivacaine induces vasodilatation, but not vasoconstriction, in rat mesenteric artery

2016 ◽  
Vol 45 (5) ◽  
pp. 258-264 ◽  
Author(s):  
Liciane dos Santos MENEZES ◽  
Liane Maciel de Almeida SOUZA ◽  
Márcio Roberto Viana dos SANTOS ◽  
Patrícia Santos Cunha MENDONÇA ◽  
Ítalo José Alves MOREIRA ◽  
...  
Keyword(s):  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Vascular Reactivity ◽  
Force Transducer ◽  
K Channel ◽  
Independent Manner ◽  
Vasodilator Effect ◽  
Rat Mesenteric Artery ◽  
Male Wistar Rats ◽  
Cotton Threads

Abstract Introduction Levobupivacaine (LEVO) can replace analgesia because it exhibits low toxicity and causes minor vasoconstriction, enabling its use in patients in whom vasoconstrictors are contraindicated. Objective We aimed to evaluate the effects of LEVO in isolated rat superior mesenteric artery by using the vascular reactivity technique and compare its effect to that of lidocaine. Material and method Arterial rings were obtained from the mesenteric artery of male Wistar rats and kept in organ baths. For recording isometric contractions, each ring was suspended by cotton threads from a force transducer, which was connected to a data acquisition system. Result Both lidocaine and LEVO did not show a vasoconstrictor effect on the basal tone of the arterial rings with functional endothelium. However, when the rings were pre-contracted with phenylephrine, both drugs were able to induce concentration-dependent vasodilatation. The vasodilator effect induced by LEVO did not change after removal of the endothelium, or with the addition of tetraethylammonium (1 mM), a non-selective K+ channel blocker. In the rings without functional endothelium, which were pre-contracted with depolarizing Tyrode’s solution (KCl 80 mM), LEVO-induced vasodilatation was not significantly different from that observed in the rings pre-contracted with phenylephrine. Moreover, it did not show a significant additional vasodilator effect compared to the maximal vasodilator effect of nifedipine. Conclusion This study demonstrated that LEVO produces a vasodilator effect in the rat superior mesenteric artery in an endothelium-independent manner. This effect seems to be mediated via Ca2+ channel blockade in the vascular smooth muscle cells.

scholarly journals Vasomotor action of androgens in the mesenteric artery of hypertensive rats. Role of perivascular innervation

PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0246254
Author(s):  
Lucía Isidoro-García ◽  
Diva M. Villalpando ◽  
Mercedes Ferrer
Keyword(s):  
Mesenteric Artery ◽  
Electrical Field Stimulation ◽  
Mesenteric Arteries ◽  
Hypertensive Rats ◽  
No Donor ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Vasomotor Function ◽  
Wistar Kyoto ◽  
And Function

Androgens may exert cardiovascular protective actions by regulating the release and function of different vascular factors. In addition, testosterone (TES) and its 5-reduced metabolites, 5α- and 5β-dihydrotestosterone (5α- and 5β-DHT) induce vasorelaxant and hypotensive effects. Furthermore, hypertension has been reported to alter the release and function of the neurotransmitters nitric oxide (NO), calcitonin gene-related peptide (CGRP) and noradrenaline (NA). Since the mesenteric arteries possess a dense perivascular innervation and significantly regulate total peripheral vascular resistance, the objective of this study was to analyze the effect of TES, 5α- and 5β-DHT on the neurogenic release and vasomotor function of NO, CGRP and NA. For this purpose, the superior mesenteric artery from male spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto (WKY) rats was used to analyze: (i) the effect of androgens (10 nM, incubated for 30 min) on the neurogenic release of NO, CGRP and NA and (ii) the vasoconstrictor-response to NA and the vasodilator responses to the NO donor, sodium nitroprusside (SNP) and exogenous CGRP. The results showed that TES, 5α- or 5β-DHT did not modify the release of NO, CGRP or NA induced by electrical field stimulation (EFS) in the arteries of SHR; however, in the arteries of WKY rats androgens only caused an increase in EFS-induced NO release. Moreover, TES, and especially 5β-DHT, increased the vasodilator response induced by SNP and CGRP in the arteries of SHR. These findings could be contributing to the hypotensive/antihypertensive efficacy of 5β-DHT previously described in conscious SHR and WKY rats, pointing to 5β- DHT as a potential drug for the treatment of hypertension.

scholarly journals NFAT regulation of cystathionine γ-lyase expression in endothelial cells is impaired in rats exposed to intermittent hypoxia

2017 ◽  
Vol 312 (4) ◽  
pp. H791-H799 ◽  
Author(s):  
Laura V. Gonzalez Bosc ◽  
Jessica M. Osmond ◽  
Wieslawa K. Giermakowska ◽  
Carolyn E. Pace ◽  
Jennifer L. Riggs ◽  
...  
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
Sleep Apnea ◽  
Mesenteric Artery ◽  
Intermittent Hypoxia ◽  
Mesenteric Arteries ◽  
Male Rats ◽  
Nuclear Factor ◽  
Activated T Cells ◽  
Rat Mesenteric Artery

Sleep apnea is a risk factor for cardiovascular disease, and intermittent hypoxia (IH, 20 episodes/h of 5% O2-5% CO2 for 7 h/day) to mimic sleep apnea increases blood pressure and impairs hydrogen sulfide (H2S)-induced vasodilation in rats. The enzyme that produces H2S, cystathionine γ-lyase (CSE), is decreased in rat mesenteric artery endothelial cells (EC) following in vivo IH exposure. In silico analysis identified putative nuclear factor of activated T cell (NFAT) binding sites in the CSE promoter. Therefore, we hypothesized that IH exposure reduces Ca2+ concentration ([Ca2+]) activation of calcineurin/NFAT to lower CSE expression and impair vasodilation. In cultured rat aortic EC, inhibiting calcineurin with cyclosporine A reduced CSE mRNA, CSE protein, and luciferase activity driven by a full-length but not a truncated CSE promoter. In male rats exposed to sham or IH conditions for 2 wk, [Ca2+] in EC in small mesenteric arteries from IH rats was lower than in EC from sham rat arteries (Δfura 2 ratio of fluorescence at 340 to 380 nm from Ca2+ free: IH = 0.05 ± 0.02, sham = 0.17 ± 0.03, P < 0.05), and fewer EC were NFATc3 nuclear positive in IH rat arteries than in sham rat arteries (IH = 13 ± 3, sham = 59 ± 11%, P < 0.05). H2S production was also lower in mesenteric tissue from IH rats vs. sham rats. Endothelium-dependent vasodilation to acetylcholine (ACh) was lower in mesenteric arteries from IH rats than in arteries from sham rats, and inhibiting CSE with β-cyanoalanine diminished ACh-induced vasodilation in arteries from sham but not IH rats but did not affect dilation to the H2S donor NaHS. Thus, IH lowers EC [Ca2+], NFAT activity, CSE expression and activity, and H2S production while inhibiting NFAT activation lowers CSE expression. The observations that IH exposure decreases NFATc3 activation and CSE-dependent vasodilation support a role for NFAT in regulating endothelial H2S production. NEW & NOTEWORTHY This study identifies the calcium-regulated transcription factor nuclear factor of activated T cells as a novel regulator of cystathionine γ-lyase (CSE). This pathway is basally active in mesenteric artery endothelial cells, but, after exposure to intermittent hypoxia to mimic sleep apnea, nuclear factor of activated T cells c3 nuclear translocation and CSE expression are decreased, concomitant with decreased CSE-dependent vasodilation.

scholarly journals The expression and function of Ca2+ -sensing receptors in rat mesenteric artery; comparative studies using a model of type II diabetes

2008 ◽  
Vol 154 (3) ◽  
pp. 652-662 ◽  
Author(s):  
A H Weston ◽  
M Absi ◽  
E Harno ◽  
A R Geraghty ◽  
D T Ward ◽  
...  
Keyword(s):  
Comparative Studies ◽  
Type Ii Diabetes ◽  
Mesenteric Artery ◽  
Type Ii ◽  
Rat Mesenteric Artery ◽  
And Function

scholarly journals Limits of isolation and culture: intact vascular endothelium and BKCa

2009 ◽  
Vol 297 (1) ◽  
pp. H1-H7 ◽  
Author(s):  
Shaun L. Sandow ◽  
T. Hilton Grayson
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Physiological Role ◽  
Vascular Endothelial ◽  
Experimental Conditions ◽  
Disease States ◽  
Vasoactive Substances ◽  
Channel Expression ◽  
Calcium Activated Potassium Channels ◽  
And Function

The potential physiological role of plasmalemmal large-conductance calcium-activated potassium channels (BKCa) in vascular endothelial cells is controversial. Studies of freshly isolated and cultured vascular endothelial cells provide disparate results, both supporting and refuting a role for BKCa in endothelial function. Most studies using freshly isolated, intact, healthy arteries provide little support for a physiological role for BKCa in the endothelium, although recent work suggests that this may not be the case in diseased vessels. In isolated and cultured vascular endothelial cells, the autocrine action of growth factors, hormones, and vasoactive substances results in phenotypic drift. Such an induced heterogeneity is likely a primary factor accounting for the apparent differences, and often enhanced BKCa expression and function, in isolated and cultured vascular endothelial cells. In a similar manner, heterogeneity in endothelial BKCa expression and function in intact arteries may be representative of normal and disease states, BKCa being absent in normal intact artery endothelium and upregulated in disease where dysfunction induces signals that alter channel expression and function. Indeed, in some intact vessels, there is evidence for the presence of BKCa, such as mRNA and/or specific BK subunits, an observation that is consistent with the potential for rapid upregulation, as may occur in disease. This perspective proposes that the disparity in the results obtained for BKCa expression and function from freshly isolated and cultured vascular endothelial cells is largely due to variability in experimental conditions and, furthermore, that the expression of BKCa in intact artery endothelium is primarily associated with disease. Although answers to physiologically relevant questions may only be available in atypical physiological conditions, such as those of isolation and culture, the limitations of these methods require open and objective recognition.

Effects of potassium and ouabain on the vascular reactivity to norepinephrine in the rat mesenteric artery

1979 ◽  
Vol 57 (8) ◽  
pp. 908-912 ◽  
Author(s):  
Kazuoki Kondo ◽  
Tetsuji Okuno ◽  
Konosuke Konishi ◽  
Takao Saruta ◽  
Eiichi Kato
Keyword(s):  
Prostaglandin E2 ◽  
Mesenteric Artery ◽  
Vascular Reactivity ◽  
Potassium Concentration ◽  
Vascular Wall ◽  
Vascular Response ◽  
Vascular Bed ◽  
Rat Mesenteric Artery ◽  
Low Potassium ◽  
Mesenteric Vascular Bed

In the perfused rat mesenteric vascular bed, the effects of potassium and ouabain on the vascular response to norepinephrine were studied. Neither changing the concentration of potassium (1.9 to 7.9 mM) nor adding ouabain (8.6 × 10−7 to 2.2 × 10−4 M) to the perfusate changed the basal pressure. A slight increase in the potassium concentration in the perfusate attenuated the vascular response to norepinephrine, and a slight decrease in the potassium concentration potentiated this response. Ouabain in the perfusate potentiated the vascular response to norepinephrine in a dose-related manner. The effect of potassium on the vascular response was inhibited in the presence of ouabain. In preparations in which vascular reactivity had been abolished by indomethacin and then restored by prostaglandin E2, the effects of potassium and ouabain on the vascular reactivity to norepinephrine were similar to those found in the untreated preparations. These results indicate that a slight change in potassium concentration in the perfusate can affect the vascular response to norepinephrine by changing the activity of a Na+–K+-dependent ATPase. It is also suggested that the potentiating effect of low potassium concentration on the norepinephrine response is, at least in the rat mesenteric vascular bed, not mediated by the synthesis of prostaglandin E2 in the vascular wall.

Nitric oxide and vascular reactivity in developing zebrafish,Danio rerio

2000 ◽  
Vol 279 (6) ◽  
pp. R2200-R2207 ◽  
Author(s):  
Regina Fritsche ◽  
Thorsten Schwerte ◽  
Bernd Pelster
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Methyl Ester ◽  
Vascular Reactivity ◽  
Vascular System ◽  
Vascular Endothelial Cells ◽  
Vessel Diameter ◽  
No Donor ◽  
Dorsal Vein ◽  
Vasoactive Substances

We used a newly developed digital motion analysis video technique to study the effects of nitric oxide (NO) and epinephrine on the early larval arterial and venous vasculature of zebrafish. Application of the NO donor sodium nitroprusside resulted in a significant increase in both the venous and arterial vessel diameters, whereas N G-nitro-l-arginine methyl ester caused a significant decrease in the same diameters. Thus our results show that both the venous and arterial vasculature of the 5- and 6-day-old zebrafish larvae are influenced by endogenously produced NO. By use of immunohistochemistry, NO synthase immunoreactivity was demonstrated in endothelial cells of the dorsal vein. Local application of epinephrine onto the dorsal artery had no effect on vessel diameter. However, if the embryos were preincubated with N ω-nitro-l-arginine methyl ester, addition of epinephrine resulted in a significant reduction in both arterial and venous vessel diameters. Thus this study provides increasing evidence that before a functional autonomic innervation of the peripheral vascular system, vascular tone in larval tissue is regulated by a complex interaction of vasoactive substances that are produced locally by vascular endothelial cells.

The vascular dilatation induced by Hydroxysafflor yellow A (HSYA) on rat mesenteric artery through TRPV4-dependent calcium influx in endothelial cells

2020 ◽  
Vol 256 ◽  
pp. 112790
Author(s):  
Jianfeng Yang ◽  
Rui Wang ◽  
Xiaohan Cheng ◽  
HuiChong Qu ◽  
Jing Qi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Mesenteric Artery ◽  
Calcium Influx ◽  
Hydroxysafflor Yellow A ◽  
Rat Mesenteric Artery ◽  
Vascular Dilatation
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