Effects of diabetes and evening primrose oil treatment on responses of aorta, corpus cavernosum and mesenteric vasculature in rats

Alison Margaret Jack, A. Keegan, Mary Anne Cotter, Norman E Cameron

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

Diabetes causes endothelial dysfunction, with deleterious effects on nitric oxide (NO) mediated vasodilatation. However, in many vessels other local vasodilators such as endothelium-derived hyperpolarizing factor (EDHF), prostacyclin, epoxides or endocannabinoids are also important. Several of these factors may be derived from omega-6 essential fatty acids via arachidonate metabolism. Diabetes inhibits this pathway, a defect that may be bypassed by diets enriched with w-6 gamma-linolenic acid-containing oils such as evening primrose oil (EPO). The aim was to examine the effects of preventive EPO treatment on endothelium-dependent and neurally mediated vasorelaxation. Diabetes was induced by streptozotocin in rats; duration was 8 weeks. Vascular responses were examined in vitro on thoracic aorta, corpus cavernosum and perfused mesenteric bed preparations. Diabetes caused 25% and 35% deficits, respectively, in aorta and corpus cavernosum NO-mediated endothelium-dependent relaxation to acetylcholine that were largely unaffected by EPO treatment. Moreover, a 44% reduction in maximum corpus cavernosum vasorelaxation to nitrergic nerve stimulation was not prevented by EPO. However, for the mesenteric vascular bed, a 29% diminution of responses to acetylcholine, mediated by both NO and EDHF, was 84% attenuated by EPO treatment. When the EDHF component was isolated during NO synthase inhibition, a 76% diabetic deficit was noted. This was completely prevented by EPO treatment, which also caused supernormal EDHF responses in nondiabetic rats. EPO treatment prevented the development of deficits in endothelium-dependent relaxation in diabetic rats. Effects were particularly marked on the resistance vessel EDHF system, which may have potential therapeutic relevance for diabetic microvascular complications. (C) 2002 Elsevier Science Inc. All rights reserved.

Original languageEnglish
Pages (from-to)1863-1877
Number of pages14
JournalLife Sciences
Volume71
Issue number16
DOIs
Publication statusPublished - 2002

Keywords

  • diabetes
  • endothelial function
  • lipid metabolism
  • nitric oxide
  • EDHF
  • corpus cavernosum
  • GAMMA-LINOLENIC ACID
  • ALPHA-LIPOIC ACID
  • ENDOTHELIUM-DEPENDENT HYPERPOLARIZATION
  • ALDOSE REDUCTASE INHIBITION
  • PORCINE CORONARY-ARTERIES
  • NITRIC-OXIDE PRODUCTION
  • ESSENTIAL FATTY-ACIDS
  • DIETARY SUPPLEMENTATION
  • ARACHIDONIC-ACID
  • POLYOL PATHWAY

Cite this

Effects of diabetes and evening primrose oil treatment on responses of aorta, corpus cavernosum and mesenteric vasculature in rats. / Jack, Alison Margaret; Keegan, A.; Cotter, Mary Anne; Cameron, Norman E.

In: Life Sciences, Vol. 71, No. 16, 2002, p. 1863-1877.

Research output: Contribution to journalArticle

Jack, Alison Margaret ; Keegan, A. ; Cotter, Mary Anne ; Cameron, Norman E. / Effects of diabetes and evening primrose oil treatment on responses of aorta, corpus cavernosum and mesenteric vasculature in rats. In: Life Sciences. 2002 ; Vol. 71, No. 16. pp. 1863-1877.
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T1 - Effects of diabetes and evening primrose oil treatment on responses of aorta, corpus cavernosum and mesenteric vasculature in rats

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AU - Keegan, A.

AU - Cotter, Mary Anne

AU - Cameron, Norman E

PY - 2002

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AB - Diabetes causes endothelial dysfunction, with deleterious effects on nitric oxide (NO) mediated vasodilatation. However, in many vessels other local vasodilators such as endothelium-derived hyperpolarizing factor (EDHF), prostacyclin, epoxides or endocannabinoids are also important. Several of these factors may be derived from omega-6 essential fatty acids via arachidonate metabolism. Diabetes inhibits this pathway, a defect that may be bypassed by diets enriched with w-6 gamma-linolenic acid-containing oils such as evening primrose oil (EPO). The aim was to examine the effects of preventive EPO treatment on endothelium-dependent and neurally mediated vasorelaxation. Diabetes was induced by streptozotocin in rats; duration was 8 weeks. Vascular responses were examined in vitro on thoracic aorta, corpus cavernosum and perfused mesenteric bed preparations. Diabetes caused 25% and 35% deficits, respectively, in aorta and corpus cavernosum NO-mediated endothelium-dependent relaxation to acetylcholine that were largely unaffected by EPO treatment. Moreover, a 44% reduction in maximum corpus cavernosum vasorelaxation to nitrergic nerve stimulation was not prevented by EPO. However, for the mesenteric vascular bed, a 29% diminution of responses to acetylcholine, mediated by both NO and EDHF, was 84% attenuated by EPO treatment. When the EDHF component was isolated during NO synthase inhibition, a 76% diabetic deficit was noted. This was completely prevented by EPO treatment, which also caused supernormal EDHF responses in nondiabetic rats. EPO treatment prevented the development of deficits in endothelium-dependent relaxation in diabetic rats. Effects were particularly marked on the resistance vessel EDHF system, which may have potential therapeutic relevance for diabetic microvascular complications. (C) 2002 Elsevier Science Inc. All rights reserved.

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KW - endothelial function

KW - lipid metabolism

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KW - EDHF

KW - corpus cavernosum

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KW - ALPHA-LIPOIC ACID

KW - ENDOTHELIUM-DEPENDENT HYPERPOLARIZATION

KW - ALDOSE REDUCTASE INHIBITION

KW - PORCINE CORONARY-ARTERIES

KW - NITRIC-OXIDE PRODUCTION

KW - ESSENTIAL FATTY-ACIDS

KW - DIETARY SUPPLEMENTATION

KW - ARACHIDONIC-ACID

KW - POLYOL PATHWAY

U2 - 10.1016/S0024-3205(02)01912-4

DO - 10.1016/S0024-3205(02)01912-4

M3 - Article

VL - 71

SP - 1863

EP - 1877

JO - Life Sciences

JF - Life Sciences

SN - 0024-3205

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ER -