Insulin-mediated increases in renal plasma flow are impaired in insulin-resistant normal subjects

JC ter Maaten*, SJL Bakker, EH Serne, HJ Moshage, ROB Gans

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

13 Citations (Scopus)

Abstract

Background Impaired vasodilatation in skeletal muscle is a possible mechanism linking insulin resistance to blood pressure regulation. Increased renal vascular resistance has been demonstrated in the offspring of essential hypertensives. We assessed whether insulin-mediated renal vasodilatation is impaired in insulin-resistant normal subjects.

Design In two groups of 10 insulin-resistant and 10 insulin-sensitive normal subjects, we compared the effects of sequential physiological and supraphysiological insulin dosages (50 and 150 mU kg(-1) h(-1)) on renal plasma flow (RPF) and leg blood flow using the euglycaemic clamp technique, I-131-labelled Hippuran clearances and venous occlusion plethysmography. Time-control experiments were performed in the same subjects.

Results Whole-body glucose uptake amounted to 4.9 +/- 2.1 and 11.0 +/- 2.4 mg kg (-1)min(-1) in the insulin-resistant and to 12.7 +/- 2.3 and 17.4 +/- 2.6 mg kg (-1)min(-1) in the insulin-sensitive subjects during physiological and supraphysiological hyperinsulinaemia, respectively. RPF increased more in insulin-sensitive compared to insulin-resistant subjects during physiological hyperinsulinaemia (13.7 vs. 6.8%, P <0.05). RPF increased to comparable levels during supraphysiological hyperinsulinaemia. Insulin-mediated changes in leg blood flow did not differ between groups. In the combined group, we found a positive correlation between insulin-mediated glucose uptake and changes in RPF during physiological hyperinsulinaemia (r = 0.57, P = 0.009), whereas insulin-mediated glucose uptake correlated with changes in leg blood flow during supraphysiological hyperinsulinaemia (r = 0.54. P = 0.017).

Conclusions Our results suggest that the sensitivities of the skeletal muscle and renal vascular bed differ for insulin's vasodilatory action. Insulin-mediated increases in RPF are impaired in insulin-resistant but otherwise normal subjects during physiological hyperinsulinaemia.

Original languageEnglish
Pages (from-to)1090-1098
Number of pages9
JournalEuropean Journal of Clinical Investigation
Volume30
Issue number12
Publication statusPublished - Dec-2000

Keywords

  • blood pressure
  • glucose
  • insulin
  • insulin resistance
  • leg blood flow
  • renal plasma flow
  • MUSCLE BLOOD-FLOW
  • HYPERINSULINEMIA-INDUCED HYPERTENSION
  • GLOMERULAR-FILTRATION RATE
  • SKELETAL-MUSCLE
  • HEALTHY-VOLUNTEERS
  • ANGIOTENSIN-II
  • NORMOTENSIVE SUBJECTS
  • EXOGENOUS INSULIN
  • SODIUM RETENTION
  • FAMILY HISTORY

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