We used the perturbation-facilitated optical–optical double resonance technique to access the ungerade ion-pair states of I2 using the (1 + 1) photo-excitation sequence through the B3Π(0u+)–c1g parity mixing states. By analyzing the second step of the double resonance to the F0u+(3P0), γ1u(3P2), and H1u(3P1) states, the g–u coupling schemes were elucidated in the intermediate B3Π(0u+)–c1g state. We were also able to populate the δ2u(3P2) state through the g–u mixing state, and to improve its molecular constants. The interference effect between the parallel γ1u(3P2)–c1g and perpendicular δ2u(3P2)–c1g transitions was used to derive the ratio of their electronic transition moments, (μ||e/μ⊥e) ∼ 5.5.

ABSTRACT-We investigated whether angiotensin II was involved with diabetic nephropathy in the mouse model. Twelve days after streptozotocin (STZ) injection, the urinary albumin excretion (UAE) level was increased by 118% of the baseline value. On days 21, 28, 35 and 42 after STZ injection, the UAE levels were significantly increased compared with the level at day 12. A marked elevation of creatinine clearance and diabetic-induced renal hypertrophy were also observed on day 49 after STZ injection. The 35-day treat ments of captopril and Dup 753 (angiotensin II type 1 receptor antagonist) significantly attenuated the in crement of UAE levels (26.4% on dayl4 and 34.6% on day 28). PD123177 (angiotensin II type 2 receptor antagonist) also attenuated the increment of UAE (24.7% on dayl4) at the dose of 150 mg/kg. Furthermore, Dup 753 partially prevented diabetic-induced renal hypertrophy. These results suggest that angiotensin II type 2 receptor as well as type 1 receptor may be involved in the development of diabetic nephropathy in the STZ-induced diabetic mice, and these mice are beneficial models of early diabetic nephropathy.

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