Glucose homeostasis was studied in the spontaneously hypertensive rat (SHR). The fasting plasma glucose levels were similar in the SHR and normotensive Wistar-Kyoto (WKY) rat (102.7 ± 2.4 vs. 107.4 ± 4.2 mg/dl, P > 0.01). One hour after glucose challenge, the plasma glucose level was slightly but insignificantly increased in both SHR and WKY rat (117 ± 2.5 vs. 114.3 ± 3.2 mg/dl, P > 0.01). After N(G)-nitro-L-arginine methyl ester (L-NAME) 20 mg/kg per day was administered intraperitoneally (i.p.) for 4 days, the plasma glucose level was significantly increased in the rats (SHR 167.3 ± 4.9; WKY rat 136.0 ± 4.8 mg/dl); the increase was significantly more pronounced in the SHR. The fasting insulin levels were similar in the SHR and WKY rats (2.3 ± 0.4 vs. 2.0 ± 0.3 ng/ml, P > 0.01). One hour after glucose challenge the insulin level was significantly increased in the WKY rat (4.8 ± 0.7 ng/ml) but not in the SHR (2.2 ± 0.4 ng/ml). With L-NAME treatment, plasma insulin increase was noted in the WKY rat but not SHR (4.6 ± 0.6 vs. 2.6 ± 0.4 ng/ml, n = 8, P < 0.01). One hour after insulin 1 IU/kg was injected intramuscularly (i.m.) the plasma glucose level was significantly decreased in both the SHR (from 115.0 ± 6.5 to 48.6 ± 3.6 mg/dl, n = 8) and WKY rat (from 108.3 ± 3.8 to 52.6 ± 4.2 mg/dl, n = 8). No significant difference was noted between the decrease of the two groups (P > 0.01). The present findings suggested that NO plays a role in the glucose homeostasis of rats. NO-synthase blockade resulted in an increase of plasma glucose level. The SHR maintains normal glucose level and tolerance in spite of a defective insulin release response. This is probably due the compensatory effect of a more prominent NO-dependent glucose homeostatic function.
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