Effects of arachidonate deficiency on endothelium-dependent vascular reactions

R. E. Loiacono, K. Kudo, G. J. Dusting, A. J. Sinclair

Research output: Contribution to journalArticleResearchpeer-review

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Abstract

1. The release of endothelium‐derived relaxing factor (EDRF), which appears to be impaired in vessels chronically exposed to hypertension, may involve mobilization of arachidonate from phospholipids. In this study the effects of arachidonate deficiency on endothelium‐dependent responses were examined in rat isolated aorta. 2. Weanling rats were fed an essential fatty acid‐deficient (EFAD) diet for 8 weeks which reduced plasma and aortic phospholipid arachidonate content from 17 to 1.8% and from 21 to 8%, respectively. After this time the rats were killed and the reactivity of aortic rings was studied in organ baths. 3. In aortic rings from control rats the concentration‐response curves for the contractile action of phenylephrine were shifted to the left 3.5‐fold by removal of the endothelium, and the maximum was not altered. 4. In contrast, in EFAD rings with endothelium, the maximal vasoconstriction to phenylephrine was less than in control rings, and removal of the endothelium increased the maximum (from 1.9±0.2 to 3.2±0.1 g, P < 0.05) and reduced the EC50 7‐fold. 5. In EFAD rings precontracted with phenylephrine (0.3 μml/l) the relaxations produced by the endothelium‐dependent dilator acetylcholine were not significantly different from those produced in control rings. The dilator actions of sodium nitroprusside were also similar in EFAD and control rings. 6. Thus, endothelium‐dependent dilatation in the aorta is not impaired by partial depletion of phospholipid arachidonate. However, contractile responses to α‐adrenoceptor agonists are depressed by spontaneously released EDRF in rat aorta, so that the results suggest that depletion of phospholipid arachidonate either augments spontaneous release of EDRF, or impairs EDRF inactivating mechanisms.

Original languageEnglish
Pages (from-to)149-154
Number of pages6
JournalClinical and Experimental Pharmacology and Physiology
Volume14
Issue number3
DOIs
Publication statusPublished - 1 Jan 1987
Externally publishedYes

Keywords

  • acetylcholine
  • arachidonate
  • endothelium‐derived relaxing factor
  • essential fatty acid deficiency
  • nitroprusside
  • phenylephrine
  • phospholipids
  • rat aorta
  • vasoconstriction
  • vasodilatation

Cite this

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title = "Effects of arachidonate deficiency on endothelium-dependent vascular reactions",
abstract = "1. The release of endothelium‐derived relaxing factor (EDRF), which appears to be impaired in vessels chronically exposed to hypertension, may involve mobilization of arachidonate from phospholipids. In this study the effects of arachidonate deficiency on endothelium‐dependent responses were examined in rat isolated aorta. 2. Weanling rats were fed an essential fatty acid‐deficient (EFAD) diet for 8 weeks which reduced plasma and aortic phospholipid arachidonate content from 17 to 1.8{\%} and from 21 to 8{\%}, respectively. After this time the rats were killed and the reactivity of aortic rings was studied in organ baths. 3. In aortic rings from control rats the concentration‐response curves for the contractile action of phenylephrine were shifted to the left 3.5‐fold by removal of the endothelium, and the maximum was not altered. 4. In contrast, in EFAD rings with endothelium, the maximal vasoconstriction to phenylephrine was less than in control rings, and removal of the endothelium increased the maximum (from 1.9±0.2 to 3.2±0.1 g, P < 0.05) and reduced the EC50 7‐fold. 5. In EFAD rings precontracted with phenylephrine (0.3 μml/l) the relaxations produced by the endothelium‐dependent dilator acetylcholine were not significantly different from those produced in control rings. The dilator actions of sodium nitroprusside were also similar in EFAD and control rings. 6. Thus, endothelium‐dependent dilatation in the aorta is not impaired by partial depletion of phospholipid arachidonate. However, contractile responses to α‐adrenoceptor agonists are depressed by spontaneously released EDRF in rat aorta, so that the results suggest that depletion of phospholipid arachidonate either augments spontaneous release of EDRF, or impairs EDRF inactivating mechanisms.",
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Effects of arachidonate deficiency on endothelium-dependent vascular reactions. / Loiacono, R. E.; Kudo, K.; Dusting, G. J.; Sinclair, A. J.

In: Clinical and Experimental Pharmacology and Physiology, Vol. 14, No. 3, 01.01.1987, p. 149-154.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Effects of arachidonate deficiency on endothelium-dependent vascular reactions

AU - Loiacono, R. E.

AU - Kudo, K.

AU - Dusting, G. J.

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N2 - 1. The release of endothelium‐derived relaxing factor (EDRF), which appears to be impaired in vessels chronically exposed to hypertension, may involve mobilization of arachidonate from phospholipids. In this study the effects of arachidonate deficiency on endothelium‐dependent responses were examined in rat isolated aorta. 2. Weanling rats were fed an essential fatty acid‐deficient (EFAD) diet for 8 weeks which reduced plasma and aortic phospholipid arachidonate content from 17 to 1.8% and from 21 to 8%, respectively. After this time the rats were killed and the reactivity of aortic rings was studied in organ baths. 3. In aortic rings from control rats the concentration‐response curves for the contractile action of phenylephrine were shifted to the left 3.5‐fold by removal of the endothelium, and the maximum was not altered. 4. In contrast, in EFAD rings with endothelium, the maximal vasoconstriction to phenylephrine was less than in control rings, and removal of the endothelium increased the maximum (from 1.9±0.2 to 3.2±0.1 g, P < 0.05) and reduced the EC50 7‐fold. 5. In EFAD rings precontracted with phenylephrine (0.3 μml/l) the relaxations produced by the endothelium‐dependent dilator acetylcholine were not significantly different from those produced in control rings. The dilator actions of sodium nitroprusside were also similar in EFAD and control rings. 6. Thus, endothelium‐dependent dilatation in the aorta is not impaired by partial depletion of phospholipid arachidonate. However, contractile responses to α‐adrenoceptor agonists are depressed by spontaneously released EDRF in rat aorta, so that the results suggest that depletion of phospholipid arachidonate either augments spontaneous release of EDRF, or impairs EDRF inactivating mechanisms.

AB - 1. The release of endothelium‐derived relaxing factor (EDRF), which appears to be impaired in vessels chronically exposed to hypertension, may involve mobilization of arachidonate from phospholipids. In this study the effects of arachidonate deficiency on endothelium‐dependent responses were examined in rat isolated aorta. 2. Weanling rats were fed an essential fatty acid‐deficient (EFAD) diet for 8 weeks which reduced plasma and aortic phospholipid arachidonate content from 17 to 1.8% and from 21 to 8%, respectively. After this time the rats were killed and the reactivity of aortic rings was studied in organ baths. 3. In aortic rings from control rats the concentration‐response curves for the contractile action of phenylephrine were shifted to the left 3.5‐fold by removal of the endothelium, and the maximum was not altered. 4. In contrast, in EFAD rings with endothelium, the maximal vasoconstriction to phenylephrine was less than in control rings, and removal of the endothelium increased the maximum (from 1.9±0.2 to 3.2±0.1 g, P < 0.05) and reduced the EC50 7‐fold. 5. In EFAD rings precontracted with phenylephrine (0.3 μml/l) the relaxations produced by the endothelium‐dependent dilator acetylcholine were not significantly different from those produced in control rings. The dilator actions of sodium nitroprusside were also similar in EFAD and control rings. 6. Thus, endothelium‐dependent dilatation in the aorta is not impaired by partial depletion of phospholipid arachidonate. However, contractile responses to α‐adrenoceptor agonists are depressed by spontaneously released EDRF in rat aorta, so that the results suggest that depletion of phospholipid arachidonate either augments spontaneous release of EDRF, or impairs EDRF inactivating mechanisms.

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KW - arachidonate

KW - endothelium‐derived relaxing factor

KW - essential fatty acid deficiency

KW - nitroprusside

KW - phenylephrine

KW - phospholipids

KW - rat aorta

KW - vasoconstriction

KW - vasodilatation

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SP - 149

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JO - Clinical and Experimental Pharmacology and Physiology

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SN - 0305-1870

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