Enhanced Y1-receptor-mediated vasoconstrictive action of neuropeptide Y (NPY) in superior mesenteric arteries in portal hypertension

Wiest, Reiner; Jurzik, Lars; Moleda, Lukas; Froh, Matthias; Schnabl, Bernd; Hörsten, Stephan von; Schölmerich, J.; Straub, Rainer H.

doi:10.1016/j.jhep.2005.08.023

Cited by 16 publications

(18 citation statements)

References 38 publications

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“…Nonetheless, systemic concentrations only reflect the ''spill-over'' of neurotransmitters from the synaptic cleft in multiple compartments into the circulation, representing remaining NPY after degradation/metabolism at various sites [4]. Here portal hypertensive rats not only presented well-known vascular hyporeactivity [1][2][3][4]15,16], but an accelerated decrease in pressure response to repetitive PNS. This desensitization process seems to be physiological, being present also in healthy rats, but the extent is exaggerated in portal hypertension.…”

Section: Discussionmentioning

confidence: 93%

“…induzierte α 1 -adrenerge mesenteriale arterielle Vasokonstriktion in zirrhotischen Ratten in signifikant höherem Maße steigert als bei gesunden Tieren [15,16].…”

Section: Dysbalance In Sympathetic Neurotransmitter Release and Actiounclassified

“…A prehepatic portal hypertensive animal model extensively studied in our laboratory was used [15,16]. Briefly, after a midline abdominal incision, the portal vein was freed from the surrounding tissue.…”

Section: Induction Of Portal Hypertension: Portal Vein Ligation (Pvl)mentioning

confidence: 99%

“…It mediates this effect via sensitizing vascular smooth muscle to NA, although the exact pathway is unknown [14]. We previously found that NPY augments a 1 -adrenergic mesenteric vasoconstriction induced by exogenous NA in cirrhotic rats to a greater extent than in healthy animals [15,16].…”

Section: Introductionmentioning

confidence: 99%

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Dysbalance in sympathetic neurotransmitter release and action in cirrhotic rats: Impact of exogenous neuropeptide Y

Dietrich¹,

Moleda²,

Kees

et al. 2013

Journal of Hepatology

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Section: Discussionmentioning

confidence: 93%

“…induzierte α 1 -adrenerge mesenteriale arterielle Vasokonstriktion in zirrhotischen Ratten in signifikant höherem Maße steigert als bei gesunden Tieren [15,16].…”

Section: Dysbalance In Sympathetic Neurotransmitter Release and Actiounclassified

Section: Induction Of Portal Hypertension: Portal Vein Ligation (Pvl)mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Dysbalance in sympathetic neurotransmitter release and action in cirrhotic rats: Impact of exogenous neuropeptide Y

Dietrich¹,

Moleda²,

Kees

et al. 2013

Journal of Hepatology

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“…Concentrationdependent vasorelaxation to the endothelium-independent vasodilator (SNP: 0.1 nmol/L-10 μmol/L) was tested. Only experiments on vessels with SNP-induced relaxation being more than 95% were accounted as valid [28] .…”

Section: Myograph Experimentsmentioning

confidence: 99%

Vasorelaxant and antihypertensive effects of formononetin through endothelium-dependent and -independent mechanisms

Sun

Cao

2011

Acta Pharmacol Sin

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Aim: To investigate the mechanisms underlying the vasorelaxant effect of formononetin, an O-methylated isoflavone, in isolated arteries, and its antihypertensive activity in vivo. Methods: Arterial rings of superior mesenteric arteries, renal arteries, cerebral basilar arteries, coronary arteries and abdominal aortas were prepared from SD rats. Isometric tension of the arterial rings was recorded using a myograph system. Arterial pressure was measured using tail-cuff method in spontaneously hypertensive rats. Results: Formononetin (1-300 μmol/L) elicited relaxation in arteries of the five regions that were pre-contracted by KCl (60 mmol/L), U46619 (1 μmol/L) or phenylephrine (10 μmol/L). The formononetin-induced relaxation was reduced by removal of endothelium or by pretreatment with L-NAME (100 μmol/L). Under conditions of endothelium denudation, formononetin (10, 30, and 100 μmol/L) inhibited the contraction induced by KCl and that induced by CaCl 2 in Ca 2+ -free depolarized medium. In the absence of extracellular Ca 2+ , formononetin (10, 30, and 100 μmol/L) depressed the constriction caused by phenylephrine (10 μmol/L), but did not inhibit the tonic contraction in response to the addition of CaCl 2 (2 mmol/L). The contraction caused by caffeine (30 mmol/L) was not inhibited by formononetin (100 μmol/L). Formononetin (10 and 100 μmol/L) reduced the change rate of Ca 2+ -fluorescence intensity in response to KCl (50 mmol/L). In spontaneously hypertensive rats, formononetin (5, 10, and 20 mg/kg) slowly lowered the systolic, diastolic and mean arterial pressure. Conclusion: Formononetin causes vasodilatation via two pathways: (1) endothelium-independent pathway, probably due to inhibition of voltage-dependent Ca 2+ channels and intracellular Ca 2+ release; and (2) endothelium-dependent pathway by releasing NO. Both the pathways may contribute to its antihypertensive effect.

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Hemodynamic Changes in Splanchnic Blood Vessels in Portal Hypertension

Colle

Geerts

Steenkiste

et al. 2008

The Anatomical Record

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Portal hypertension (PHT) is associated with a hyperdynamic state characterized by a high cardiac output, increased total blood volume, and a decreased splanchnic vascular resistance. This splanchnic vasodilation is a result of an important increase in local and systemic vasodilators (nitric oxide, carbon monoxide, prostacyclin, endocannabinoids, and so on), the presence of a splanchnic vascular hyporesponsiveness toward vasoconstrictors, and the development of mesenteric angiogenesis. All these mechanisms will be discussed in this review. To decompress the portal circulation in PHT, portosystemic collaterals will develop. The presence of these portosystemic shunts are responsible for major complications of PHT, namely bleeding from gastrointestinal varices, encephalopathy, and sepsis. Until recently, it was accepted that the formation of collaterals was due to opening of preexisting vascular channels, however, recent data suggest also the role of vascular remodeling and angiogenesis. These points are also discussed in detail.

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Enhanced Y1-receptor-mediated vasoconstrictive action of neuropeptide Y (NPY) in superior mesenteric arteries in portal hypertension

Cited by 16 publications

References 38 publications

Dysbalance in sympathetic neurotransmitter release and action in cirrhotic rats: Impact of exogenous neuropeptide Y

Dysbalance in sympathetic neurotransmitter release and action in cirrhotic rats: Impact of exogenous neuropeptide Y

Vasorelaxant and antihypertensive effects of formononetin through endothelium-dependent and -independent mechanisms

Hemodynamic Changes in Splanchnic Blood Vessels in Portal Hypertension

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