Coronary vasoconstriction by endothelin-1 in anesthetized goats: role of endothelin receptors, nitric oxide and prostanoids

Abstract Horses (n = 20) were divided into 2 groups: oligofructose (OF)-induced equine laminitis group (group OF; n = 11) which received 10 g/kg b.w. of OF dissolved in 4 L water via nasogastric intubation, and control group (NS; n = 9) which received 4 L of saline. Blood was collected at 4 h intervals over 72 h study period and analysed by ELISA, kinetic limulus amoebocyte lysate assay, and glucose-oxidase methods. The level of insulin changed significantly in horses which received OF (P < 0.01); there was a significant negative correlation between the level of adiponectin and insulin over time. The results suggested that insulin may play an important role in the development of OF-induced equine laminitis by altering the level of endothelin-1 and nitric oxide.

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Role of nitric oxide and endothelin-1 in monocrotaline-induced pulmonary hypertension in rats

Cardiovascular Research ◽

10.1016/0008-6363(95)00108-5 ◽

1995 ◽

Vol 30 (5) ◽

pp. 739-746 ◽

Cited By ~ 25

Author(s):

R Mathew

Keyword(s):

Nitric Oxide ◽

Pulmonary Hypertension ◽

Endothelin 1

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Nitric oxide attenuates endothelin-1-induced vasoconstriction in canine stomach

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1996.271.1.g27 ◽

1996 ◽

Vol 271 (1) ◽

pp. G27-G35

Author(s):

J. G. Wood ◽

Q. Zhang ◽

Z. Y. Yan ◽

L. Y. Cheung

Keyword(s):

Nitric Oxide ◽

Methyl Ester ◽

Ischemia Reperfusion ◽

Nitric Oxide Donor ◽

Question Mark ◽

Endothelin 1 ◽

Vasoconstrictor Response ◽

Anesthetized Dogs ◽

Spermine Nonoate

We previously observed that endothelin-1 (ET-1)-induced gastric vasoconstriction is enhanced after ischemia-reperfusion. The purpose of our present study was to examine the role of nitric oxide in regulating ET-1-induced vasoconstriction under normal conditions and after ischemia-reperfusion. Using a mechanically perfused stomach segment from chloralose-anesthetized dogs, we examined 1) responses to NG-nitro-L-arginine methyl ester (L-NAME) alone and in combination with L-arginine, 2) whether L-NAME affects ET-1-induced vasoconstriction under normal conditions and after ischemia-reperfusion, and 3) if spermine NONOate inverted question mark1,3-propanediamine-N-[4-1-(3-aminopropyl)-2-hydroxy-2-nitrosohydrazi no] butyl; a nitric oxide donor inverted question mark attenuates the augmented response to ET-1 after ischemia-reperfusion. Our results show that 1) L-NAME significantly increased baseline vascular resistance and this response was reduced by L-arginine, 2) ET-1-induced vasoconstriction was enhanced by L-NAME, and 3) administration of spermine NONOate during reperfusion largely attenuated the vasoconstrictor response to ET-1 after ischemia-reperfusion. Our findings are consistent with the hypothesis that nitric oxide modulates responses to ET-1 under normal conditions, and loss of this vasodilator after ischemia-reperfusion results in an augmented response to ET-1.

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