Insulin blunts sympathetic vasoconstriction through the α2-adrenergic pathway in humans

Giuseppe Lembo, Guido Iaccarino, Virgilio Rendina, Massimo Volpe, Bruno Trimarco

Research output: Contribution to journalArticle

Abstract

We investigated the mechanisms underlying the insulin-induced attenuation of sympathetic forearm vasoconstriction in healthy humans. In 5 subjects, we applied 20 mm Hg lower body negative pressure for 30 minutes in control conditions and during a 60-minute infusion of insulin (0.05 mU/kg per minute) in the brachial artery and measured forearm norepinephrine kinetics and hemodynamics. In 11 subjects, we applied graded lower body negative pressure at 5, 10, 15, and 20 mm Hg for 5 minutes each in control conditions and during the simultaneous intrabrachial administration of insulin (0.05 mU/kg per minute) (5 subjects) or insulin plus ouabain (3.5 μg/min per liter) (6 subjects) to investigate whether insulin acts through a potentiation of the vascular smooth muscle Na+,K+-ATPase. To assess a possible effect of insulin on a specific adrenergic receptor pathway, in a further study group we evaluated (1) the forearm vascular response to intrabrachial infusion of the α1-adrenergic receptor agonist phenylephrine (0.5, 1, and 2 μg/kg per minute; n=7) and of the α2-adrenergic receptor agonist BHT-933 (0.5, 1, 2, and 4 μg/kg per minute; n=9), and (2) the effects of intra-arterial infusion of prazosin (0.5 μg/100 mL per minute) alone or combined with insulin on the forearm vascular response to graded lower body negative pressure (7 subjects). Insulin blunted the peak increase in forearm vascular resistance (from 13±2 to 6±2 U, P2-adrenergic vasoconstrictive pathway.

Original languageEnglish
Pages (from-to)429-438
Number of pages10
JournalHypertension
Volume24
Issue number4
Publication statusPublished - Oct 1994

Keywords

  • lower body negative pressure
  • Na,K-transporting ATPase
  • norepinephrine
  • ouabain
  • vascular resistance

ASJC Scopus subject areas

  • Internal Medicine

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