Endothelium‐dependent contraction in intrapulmonary arteries: mediation by endothelial NK1 receptors and TXA2

@article{Shirahase1995EndotheliumdependentCI,
  title={Endothelium‐dependent contraction in intrapulmonary arteries: mediation by endothelial NK1 receptors and TXA2},
  author={Hiroaki Shirahase and Mamoru Kanda and Kazuyoshi Kurahashi and S. Nakamura and Hachiro Usui and Yoshiharu Shimizu},
  journal={British Journal of Pharmacology},
  year={1995},
  volume={115}
}
1 We have examined whether three natural tachykinins, substance P (SP), neurokinin A (NKA) and neurokinin B (NKB) induce an endothelium‐dependent contraction (EDC) in the rabbit isolated intrapulmonary artery. 2 Removal of the endothelium almost abolished the contraction induced by SP (10−8 m) while it did not attenuate the contraction induced by SP (10−7 m), NKA (10−9‐10−7 m) or NKB (10−9‐10−7 m). 3 The EDC induced by SP (10−8 m) was abolished by NK1 antagonists (FK‐888, CP‐96345, CP‐99994 and… 
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Endothelium‐dependent relaxation followed by contraction mediated by NK1 receptors in precontracted rabbit intrapulmonary arteries
TLDR
It is concluded that NK1 agonists caused a biphasic endothelium‐dependent response (EDR and EDC) in submaximally precontracted intrapulmonary arteries and the EDC and EDR mediated by NK1 receptors may play physiological and/or pathophysiological roles in modulation of vascular tone.
NK1 receptor-mediated endothelium-dependent relaxation and contraction with different sensitivity to post-receptor signaling in pulmonary arteries.
Endothelium-dependent contraction induced by substance P in canine cerebral arteries: involvement of NK1 receptors and thromboxane A2.
The mechanism of bradykinin‐induced endothelium‐dependent contraction and relaxation in the porcine interlobar renal artery
TLDR
Bradykinin caused the endothelium‐dependent triphasic regulation of vascular tone in the porcine renal artery and was involved in the bradykinIn‐induced contraction.
Thapsigargin‐induced endothelium‐dependent triphasic regulation of vascular tone in the porcine renal artery
TLDR
Thapsigargin‐induced Ca2+ entry in endothelial cells led to triphasic changes in the tone of the porcine renal artery and Nitric oxide and hyperpolarizing factor are both involved in the initial relaxation.
The mechanisms for tachykinin‐induced contractions of the rabbit corpus cavernosum
TLDR
Tachykinin‐induced contractions were mainly mediated through the activation of NK1 receptor expressed in the rabbit corpus cavernosum smooth muscle, and affected by the endopeptidase activity, suggesting that tachykinins may play a role in controlling the corpus cavernsum tone.
Neurokinins Induce Relaxation of Human Pulmonary Vessels Through Stimulation of Endothelial NK1 Receptors
TLDR
Human pulmonary arteries and veins express endothelial NK1 receptors that mediate relaxation through a combination of cyclooxygenase and nitric oxide activities and are subjected to rapid tachyphylaxis.
Evidence that the substance P‐induced enhancement of pacemaking in lymphatics of the guinea‐pig mesentery occurs through endothelial release of thromboxane A2
TLDR
The hypothesis that the substance P‐induced increase in pumping rate is mediated via the endothelium through NK1 receptors coupled by a PTx sensitive G‐protein to phospholipase A2 and resulting in generation of the arachidonic acid metabolite, thromboxane A2, this serving as the diffusible activator is supported.
Regional heterogeneity of substance P-induced endothelium-dependent contraction, relaxation, and -independent contraction in rabbit pulmonary arteries.
A vasoconstrictor role for cyclooxygenase-1-mediated prostacyclin synthesis in mouse renal arteries.
TLDR
In mouse renal arteries, high expression of TP receptors together with little functional involvement from the vasodilator P GI2 receptors results in a potent vasoconstrictor effect evoked by PGI2, which implies that endogenous COX-1-mediated PGI 2 synthesis leads to vasoconStrictor activity and this could be an integral part of endothelium-derived mechanisms in regulating local renal vascular function.
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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