• diabetes mellitus;
  • hyperglycaemia;
  • renin–angiotensin system;
  • systemic blood pressure;
  • type 1

Abstract. Jacobsen P, Rossing K, Hansen BV, Bie P, Vaag A, Parving H-H (Steno Diabetes Center, Gentofte; University of Aarhus, Aarhus; and University of Southern Denmark, Odense, Denmark). Effect of short-term hyperglycaemia on haemodynamics in type 1 diabetic patients. J Intern Med 2003; 254: 464–471.

Objectives. Mechanisms underlying glucose-mediated development and progression of diabetic complications are incompletely understood. We tested the impact of short-term hyperglycaemia on systemic blood pressure and regulatory hormones in type 1 diabetic patients.

Design and methods. We included 18 patients [13 men, mean (SEM) diabetes duration 10 (1) years] without signs of autonomic neuropathy or renal complications in a randomized single-blinded cross-over trial using insulin–glucose clamp technique. Patients were clamped for 90 min to blood glucose of 5 mmol L−1 (euglycaemia) and 15 mmol L−1 (hyperglycaemia) in random order. Blood pressure was measured noninvasively every 5 min (Takeda TM2421 device). Regulatory hormones were determined at the end of each clamp period.

Results. Systolic blood pressure increased [mean (95% CI)] 3 (1, 5) mmHg during hyperglycaemia from 123 (SEM 2) during euglycaemia, P = 0.01. Diastolic blood pressure remained unchanged at 78 (2) mmHg. Hyperglycaemia reduced plasma concentrations of: renin [14 (4, 23)%, P = 0.02], angiotensin II [17 (8, 25)%, P < 0.01] and adrenaline [20 (10, 29)%, P < 0.01]. Plasma concentration of atrial natriuretic peptide increased by 11 (6, 17) pg mL−1 (P < 0.01) from 43 (2) pg mL−1. We calculated a median (range) increase in extracellular volume and plasma volume (PV) of 2.6 (0.7–5.3)% and 5.0 (−4.7 to 8.6)%, respectively.

Conclusions. In type 1 diabetic patients without signs of autonomic neuropathy short-term hyperglycaemia induced a modest increase in systolic blood pressure and suppression of the renin–angiotensin system, possibly caused by PV expansion because of fluid shift from intra- to extracellular compartment.