We assessed the effect of the vasodilating calcium channel blocker nit
rendipine on glucose tolerance in young spontaneously hypertensive rat
s (SHR) (n = 15). The nitrendipine group received 1 g/kg chow for 3 we
eks. Untreated SHR (n = 14) served as controls. At 3 weeks body weight
was comparable, whereas systolic blood pressure was 157+/-9 mm Hg in
nitrendipine-treated rats versus 191+/-10 mm Hg in controls (mean+/-SD
, P<.00001). Fasting glucose was 6.8+/-2.7 mmol/L in nitrendipine-trea
ted versus 8.9+/-1.5 mmol/L in control rats (P<.03). An intravenous gl
ucose tolerance test (300 mg/kg) showed plasma glucose levels at 2, 5,
15, and 30 minutes to be significantly lower in the nitrendipine-trea
ted group versus controls (two-way ANOVA, P<.03). Glucose utilization
was estimated by the uptake of [H-3]deoxyglucose after its intravenous
administration (2 mu Ci/100 g body wt) to instrumented awake animals.
Heart and striated muscle uptake was, respectively, 7983+/-5812 and 9
51+/-731 cpm . mu L/ g min in the nitrendipine-treated group versus 35
32+/-2316 and 424+/-201 cpm . mu L/g min in controls (P<.02 and P<.04,
respectively). [H-3]Deoxyglucose plasma half-life and fasting and pos
t-glucose load insulin levels were comparable in the two groups. The r
esults show that nitrendipine improves glucose tolerance by increasing
muscle glucose uptake. We suggest that glucose tolerance in SHR is in
fluenced by muscle blood flow and can be improved by vasodilation.