Effects of cooling on histamine-induced contractions of human
umbilical artery: The role of ion channels

Ke, Atalik; Kilic, Murat; Zu, Nurullahoglu; Doğan, Necdet

doi:10.1358/mf.2007.29.9.1116315

Cited by 4 publications

(5 citation statements)

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“…Our findings demonstrate that sevoflurane produced vasodilation, at least in part, via an effect on the sarcolemmal voltage-operated calcium channel (VOCC). Prior incubation with the VOCC channel blocker verapamil, at concentrations similar to that previously reported [ 17 , 18 ], significantly inhibited sevoflurane-mediated vasodilation of the pre-constricted chorionic plate arterial rings. These findings demonstrate that sevoflurane-mediated vasodilation in this circulation is dependent in part on a blocking effect at the VOCC channel.…”

Section: Discussionsupporting

confidence: 81%

“…Series 3 examined the role of the sarcolemmal voltage-operated Ca ++ channel (VOCC). Following U46619 pre-constriction, verapamil 1 × 10 -6 M, which specifically blocks the VOCC channel [ 9 , 17 , 18 ] or vehicle was added, and the rings exposed to sevoflurane or perfusing gas alone as described for series 1A. Series 4 examined the role of the sarcolemmal voltage-independent Ca ++ channels (VICC) [ 9 , 10 ].…”

Section: Methodsmentioning

confidence: 99%

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Role of potassium and calcium channels in sevoflurane-mediated vasodilation in the foeto-placental circulation

et al. 2009

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BackgroundSevoflurane has been demonstrated to vasodilate the foeto-placental vasculature. We aimed to determine the contribution of modulation of potassium and calcium channel function to the vasodilatory effect of sevoflurane in isolated human chorionic plate arterial rings.MethodsQuadruplicate ex vivo human chorionic plate arterial rings were used in all studies. Series 1 and 2 examined the role of the K+ channel in sevoflurane-mediated vasodilation. Separate experiments examined whether tetraethylammonium, which blocks large conductance calcium activated K+ (KCa++) channels (Series 1A+B) or glibenclamide, which blocks the ATP sensitive K+ (KATP) channel (Series 2), modulated sevoflurane-mediated vasodilation. Series 3 – 5 examined the role of the Ca++ channel in sevoflurane induced vasodilation. Separate experiments examined whether verapamil, which blocks the sarcolemmal voltage-operated Ca++ channel (Series 3), SK&F 96365 an inhibitor of sarcolemmal voltage-independent Ca++ channels (Series 4A+B), or ryanodine an inhibitor of the sarcoplasmic reticulum Ca++ channel (Series 5A+B), modulated sevoflurane-mediated vasodilation.ResultsSevoflurane produced dose dependent vasodilatation of chorionic plate arterial rings in all studies. Prior blockade of the KCa++ and KATP channels augmented the vasodilator effects of sevoflurane. Furthermore, exposure of rings to sevoflurane in advance of TEA occluded the effects of TEA. Taken together, these findings suggest that sevoflurane blocks K+ channels. Blockade of the voltage-operated Ca++channels inhibited the vasodilator effects of sevoflurane. In contrast, blockade of the voltage-independent and sarcoplasmic reticulum Ca++channels did not alter sevoflurane vasodilation.ConclusionSevoflurane appears to block chorionic arterial KCa++ and KATP channels. Sevoflurane also blocks voltage-operated calcium channels, and exerts a net vasodilatory effect in the in vitro foeto-placental circulation.

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Section: Discussionsupporting

confidence: 81%

Section: Methodsmentioning

confidence: 99%

Role of potassium and calcium channels in sevoflurane-mediated vasodilation in the foeto-placental circulation

et al. 2009

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“…This was supported by Atalik et al. who also concluded that the endothelium had no role in temperature‐induced responses in the rabbit aorta, calf coronary artery and human umbilical artery. However, in contrast to these observations, it has been shown that cooling decreased sensitivity of the rabbit ear artery to stimulation by histamine and endothelin‐1 by increasing the release of NO.…”

Section: Discussionmentioning

confidence: 69%

“…In their studies, Mustafa and Thulesius 15,18 concluded that coolinginduced relaxation of the rat pulmonary artery and rabbit carotid artery was independent of the vascular endothelium as cooling induced relaxation in artery segments with and without endothelium. This was supported by Atalik et al 35,36 who also concluded that the endothelium had no role in temperature-induced responses in the rabbit aorta, calf coronary artery and human umbilical artery. However, in contrast to these observations, it has been shown that cooling decreased sensitivity of the rabbit ear artery to stimulation by histamine 14 and endothelin-1 37 by increasing the release of NO.…”

Section: Effect Of Pvat On the Anticontractile Effect Of Coolingmentioning

confidence: 70%

Attenuation of the anti‐contractile effect of cooling in the rat aorta by perivascular adipose tissue

Rafique

Al‐Bader

Oriowo

2017

Auton Autocoid Pharmacol

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In addition to providing mechanical support for blood vessels, the perivascular adipose tissue (PVAT) secretes a number of vasoactive substances and exerts an anticontractile effect. The main objective of this study was to find out whether the anticontractile effect of cooling in the rat aorta is affected by PVAT. Our hypothesis was that PVAT would enhance the anticontractile effect of cooling in the rat aorta. Aorta segments, with or without PVAT, were used in this investigation. Cumulative concentration-response curves were established for phenylephrine at 37°C or 24°C. Phenylephrine (10 M - 10 M) induced concentration-dependent contractions of aorta segments with or without PVAT at 37°C. The maximum response, but not pD value, was reduced in aorta segments with PVAT. Cooling the tissues to 24 °C resulted in a significant reduction in the maximum response in aorta segments without PVAT with no change in pD values. However, the anticontractile effect of cooling was attenuated in the presence of PVAT with no significant (p > 0.05) change in either the maximum response or pD value. L-NAME potentiated PE-induced contractions and this was greater in aorta segments without PVAT at both temperatures. The expression of eNOS protein and basal tissue level of nitric oxide (NO) were greater in aorta segments with PVAT at both temperatures. However, PE significantly increased tissue levels of NO only in aorta segments without PVAT. We concluded that PVAT-induced loss of anticontractile effect of cooling against PE-induced contractions could be due to impaired generation of NO in aorta segments with PVAT.

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“…Notably, umbilical vessels play a vital role in feto-placental circulation [ 9 ]. Due to lack of autonomic innervation, vessel tone of human umbilical vessels is mainly regulated by vasoactive substances released locally or carried by the blood stream, such as histamine [ 10 , 11 ].…”

Section: Introductionmentioning

confidence: 99%

In vitro fertilization with frozen embryo transfer increased histamine-mediated contractile sensitivity via PKCβ in human umbilical vein

Tang

et al. 2023

Reprod Biol Endocrinol

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Objective In vitro fertilization-embryo transfer (IVF-ET) technologies (especially frozen ET) have been widely used, which might affect maternal and fetal health. Information regarding influence of IVF-ET on the vasoconstriction of human umbilical vein (HUV) is limited. This study determined effects of frozen ET on histamine-mediated vascular responses in HUV and related mechanisms. Methods and results HUVs were collected from frozen ET conceived pregnancy and spontaneously conceived pregnancy (control). Histamine concentration in umbilical plasma was higher in frozen ET group than the control. Histamine-mediated contractile response curve was left-shifted in the frozen ET group when comparing with the control. In isolated HUV rings, H1R showed a critical role in regulating vascular constriction, while H2R played little roles in regulating vessel tone. Iberiotoxin and 4-aminopyridine didn’t significantly change histamine-mediated constriction in HUVs. Histamine-induced vasoconstrictions were significantly decreased by nifedipine, KN93, or GF109203X, while the inhibitory effects were significantly greater in the frozen ET group in comparison to the control. The constrictions by Bay K8644, phenylephrine, or PDBu were stronger in frozen ET, respectively. There was a decrease in the protein expressions of H1R and H2R, an increase in protein expressions of BKCaα and PKCβ. Conclusions Histamine-induced constriction in HUV was mainly via H1R. The increased sensitivity to histamine in HUV following frozen ET cycles were linked to the enhanced PKCβ protein expression and function. The new data and findings in this study provide important insight into influences of frozen ET on fetal vessel development and potential influence in long-term.

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Effects of cooling on histamine-induced contractions of human umbilical artery: The role of ion channels

Cited by 4 publications

References 0 publications

Role of potassium and calcium channels in sevoflurane-mediated vasodilation in the foeto-placental circulation

Role of potassium and calcium channels in sevoflurane-mediated vasodilation in the foeto-placental circulation

Attenuation of the anti‐contractile effect of cooling in the rat aorta by perivascular adipose tissue

In vitro fertilization with frozen embryo transfer increased histamine-mediated contractile sensitivity via PKCβ in human umbilical vein

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