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Department of Physiology and Biophysics, Keck School of Medicine of the University of Southern California, Los Angeles, California 90089
We set out to
examine whether angiotensin-driven hypertension can alter insulin
action and whether these changes are reflected as changes in
interstitial insulin (the signal to which insulin-sensitive cells
respond to increase glucose uptake). To this end, we measured hemodynamic parameters, glucose turnover, and insulin dynamics in both
plasma and interstitial fluid (lymph) during hyperinsulinemic euglycemic clamps in anesthetized dogs, with or without simultaneous infusions of angiotensin II (ANG II). Hyperinsulinemia per se failed to
alter mean arterial pressure, heart rate, or femoral blood flow. ANG II
infusion resulted in increased mean arterial pressure (68 ± 16 to 94 ± 14 mmHg, P < 0.001) with a
compensatory decrease in heart rate (110 ± 7 vs. 86 ± 4 mmHg,
P < 0.05). Peripheral resistance was
significantly increased by ANG II from 0.434 to 0.507 mmHg · ml
1 · min
(P < 0.05). ANG II infusion increased femoral
artery blood flow (176 ± 4 to 187 ± 5 ml/min,
P < 0.05) and resulted in additional increases in both plasma and lymph insulin (93 ± 20 to 122 ± 13 µU/ml and 30 ± 4 to 45 ± 8 µU/ml,
P < 0.05). However, glucose uptake
was not significantly altered and actually had a tendency to be lower
(5.9 ± 1.2 vs. 5.4 ± 0.7 mg · kg1 · min1,
P > 0.10). Mimicking of the ANG
II-induced hyperinsulinemia resulted in an additional increase in
glucose uptake. These data imply that ANG II induces insulin resistance
by an effect independent of a reduction in interstitial insulin.
lymph insulin; euglycemic hyperinsulinemia; endogenous glucose production; blood flow
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