Histamine-induced vasodilatation in the perfused mesenteric arterial bed of diabetic rats

Yousif, Mariam H. M.; Oriowo, Mabayoje A.; Cherian, A. George; Adeagbo, Ayotunde S.O.

doi:10.1016/s1537-1891(03)00004-1

Cited by 14 publications

(18 citation statements)

References 33 publications

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“…The endothelium regulates vascular tone via synthesis and release of vasodilatory substances including nitric oxide (NO) and prostacyclin (PGI 2 ) following the stimulation by various chemical substances or physical factors (12)(13)(14)(15). Well-described agonists of endothelial relaxing factors are acetylcholine (12,14), histamine in rat mesenteric arteries (16) or bradykinin in guinea pig aorta (17). Following stimulation of the receptors, endothelial NO synthase (NOS) converts L-arginine into NO (18)(19)(20); NO may produce relaxation by decreasing Ca 2+ levels in smooth muscle cells through a cGMP-dependent pathway or through hyperpolarization due to increased conductance of K + channels (21).…”

Section: Introductionmentioning

confidence: 99%

Anaphylaxis of small arteries: putative role of nitric oxide and prostanoids

Laukevičienė¹,

Uginčius²,

Korotkich³

et al. 2010

Medicina

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Section: Introductionmentioning

confidence: 99%

Anaphylaxis of small arteries: putative role of nitric oxide and prostanoids

Laukevičienė¹,

Uginčius²,

Korotkich³

et al. 2010

Medicina

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“…However, the histamine-induced vasomotor activity in retinal arterioles that control blood flow and its distribution has not been characterized. Although EDHF has been suggested to play a considerable role in mesenteric vasodilation to histamine, 26 the importance of this dilation in retinal arterioles remains undetermined. Herein, we examined the contribution of EDHF to retinal arteriolar dilation to histamine and investigated the signaling mechanisms involved in this vasomotor activity.…”

mentioning

confidence: 99%

Histamine-Induced Dilation of Isolated Porcine Retinal Arterioles: Role of Endothelium-Derived Hyperpolarizing Factor

Otani

Nagaoka

Omae

et al. 2016

Invest. Ophthalmol. Vis. Sci.

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Citation: Otani S, Nagaoka T, Omae T, et al. Histamine-induced dilation of isolated porcine retinal arterioles: role of endothelium-derived hyperpolarizing factor. Invest Ophthalmol Vis Sci. 2016;57:4791-4798. DOI:10.1167/iovs.15-19038 PURPOSE. Although endothelium-dependent nitric oxide (NO)-mediated dilation of retinal arterioles has been well described, the role of endothelium-derived hyperpolarizing factor (EDHF) in the retinal arteriolar response remains unclear. In the current study, we examined the contribution of EDHF to the retinal arteriolar dilation to the inflammatory agent histamine and investigated the signaling mechanisms underlying this vasomotor activity.METHODS. Porcine retinal arterioles were isolated, cannulated, and pressurized without flow for functional study by using video microscopic techniques. The immunohistochemical staining was performed to determine histamine receptor subtypes.RESULTS. Histamine (0.1-30 lM) produced concentration-dependent dilation of retinal arterioles in a manner sensitive to H1-and H2-receptor antagonists chlorpheniramine and famotidine, respectively. Histamine-induced vasodilation was almost abolished after endothelial removal. In the intact vessels, vasodilation to histamine was partially inhibited by the inhibitors of cyclooxygenase (indomethacin), NO synthase (N G -nitro-L-arginine methyl ester, L-NAME), or Ca 2þ -activated K þ (K Ca ) channels (apamin plus charybdotoxin). Combination of the above inhibitors abolished histamine-induced vasodilation. Residual vasodilation in the presence of indomethacin and L-NAME was further reduced by the cytochrome P450 enzyme inhibitor sulfaphenazole but not by the gap junction inhibitor carbenoxolone or the hydrogen peroxide scavenger catalase. Immunohistochemical signals for H1-and H2-receptor expression were found only in the endothelium. CONCLUSIONS.The endothelium plays an essential role in the dilation of porcine retinal arterioles to histamine via H1-and H2-receptor activation. The EDHF derived from cytochrome P450 contributed in part to this vasodilation via K Ca channel activation, in addition to the endothelial release of NO and prostanoids.

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“…The involvement of hyperpolarizing mechanisms in histamine-induced relaxation also has been observed in pulmonary (Hasunuma et al, 1991), mesenteric (Yousif et al, 2003) and renal (Yousif, 2005) arterial bed, pulmonary artery Suzuki, 1989a, 1989b;Torok, 2000) and rat thoracic aorta (Chen and Suzuki, 1989b) and human mesenteric arteries (Tottrup and Kraglund, 2004). These authors suggest the involvement of an endothelium-derived hyperpolarizing factor (EDHF).…”

Section: Discussionmentioning

confidence: 84%

“…Furthermore, the absence of relaxation observed in preparations set in depolarizing nutritive solution corroborates the involvement of hyperpolarizing mechanisms in the histamine actions upon the rat portal vein. In fact, it has been proposed that hyperpolarizing mechanisms are suppressed in the presence of a high K + concentration (Zygmunt et al, 1994;Gerber et al, 1998;Yousif et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…The involvement of NO has been proposed in the histamine-induced relaxation in mesenteric arterial bed (Jin et al, 2006), mesenteric artery (Adeagbo and Triggle, 1993;Yousif et al, 2003) and pulmonary arteries (Hasunuma et al, 1991) of the rat and coronary arterial bed of the guinea pig (Pierpaoli et al, 2003). In parallel, both NO and prostanoids are involved in the histamine-induced relaxation of bovine retinal arteries (Benedito et al, 1991).…”

Section: Discussionmentioning

confidence: 99%

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The possible involvement of hyperpolarizing mechanisms in histamine-induced relaxation of the rat portal vein

Rossignoli

Rodrigues

Tinti

et al. 2008

J. Smooth Muscle Res.

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The present study evaluated the effects of histamine 10 -2 M on longitudinal preparations of rat portal vein. It was observed that histamine 10 -2 M induced relaxation of rat portal vein preparations pre-contracted with phenylephrine 10 -4 M. On the other hand, no pharmacological effects were observed in preparations not pre-contracted. The observed histamine-induced relaxing effect was absent in preparations pre-contracted with KCl (120 mM) or in the presence of depolarizing nutritive solution. However, the histamine-induced relaxation was still present in the endothelium-removed preparations. The histamine-induced relaxation also was not prevented by astemizole ( M or L-NAME 10 -4 M plus indomethacin 10 -5 M also did not prevent the histamineinduced relaxation observed in rat portal vein. Thus, the histamine-induced relaxation observed in rat portal vein appears to involve a non-endothelial hyperpolarizing mechanism independent of H1, H2 and H3 receptors.

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Histamine-induced vasodilatation in the perfused mesenteric arterial bed of diabetic rats

Cited by 14 publications

References 33 publications

Anaphylaxis of small arteries: putative role of nitric oxide and prostanoids

Anaphylaxis of small arteries: putative role of nitric oxide and prostanoids

Histamine-Induced Dilation of Isolated Porcine Retinal Arterioles: Role of Endothelium-Derived Hyperpolarizing Factor

The possible involvement of hyperpolarizing mechanisms in histamine-induced relaxation of the rat portal vein

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