Elsevier

Life Sciences

Volume 49, Issue 13, 1991, Pages PL85-PL90
Life Sciences

Pharmacology letters Accelerated communication
Influence of diabetes on norepinephrine-induced inositol 1,4,5-trisphosphate levels in rat aorta

https://doi.org/10.1016/0024-3205(91)90084-OGet rights and content

Abstract

The effects of norepinephrine on total tissue levels of inositol 1,4,5-triphosphate were measured by protein binding assay in aortas from rats with chronic streptozotocin-induced diabetes and from age-matched control rats. In both control and diabetic aortas, norepinephrine induced a rapid, transient and concentration-dependent elevation of inositol 1,4,5-trisphosphate content during contraction. Maximum production of inositol 1,4,5-trisphosphate in response to norepinephrine was greater in diabetic than in control aortas. However, the sensitivities of control and diabetic aortas to norepinephrine for inositol 1,4,5-trisphosphate production were not significantly different. Enhanced norepinephrine-induced production of inositol 1,4,5-trisphosphate in diabetic aortas may contribute to the increased maximum contractile responsiveness of these arteries to the agonist. However, since enhanced contractile responses of diabetic aortas to norepinephrine were also detected at times when inositol 1,4,5-trisphosphate levels were not significantly increased, other factors also appear to be involved in mediating enhanced contractions of diabetic arteries to norepinephrine.

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Cited by (18)

  • The diabetic vasculature: Physiological mechanisms of dysfunction and influence of aerobic exercise training in animal models

    2014, Life Sciences
    Citation Excerpt :

    A plethora of studies have reported enhanced responses to α-adrenergic agonist, such as norepinephrine and phenylephrine, in different T1DM vessels (McLeod and McNeil, 1985; Agrawal and McNeill, 1987; Kamata et al., 1988; Abebe and MacLeod, 1991a, 1991b; Taylor et al., 1994) and T2DM vessels (Khazaei et al., 2008; Brondum et al., 2008). Most of these studies related this alteration to increased inositol 1,4,5-trisphosphate (IP3) and DAG production and consequently enhanced contractile response (Abebe and MacLeod, 1991b). Moreover, the abnormal release of vasoconstrictors has been demonstrated.

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Present address: Allergic Disease Center, School of Medicine, Creighton University, Omaha, NE 68178

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