Fig. 1.
Treatment with prazosin (0.15 mg/kg) reversed 6-hydroxydopamine (6-OHDA)-induced acute hypertension and increased survival time. (A) Representative nucleus tractus solitarii (NTS) position of 6-OHDA lesions (arrows). (B) Rats with bilateral 6-OHDA lesions of NTS died suddenly within 7 h with severe pulmonary hemorrhagic edema complications developing before death (n = 8). (C) Rats with bilateral 6-OHDA lesions of NTS survived for at least 14 h with no pulmonary edema at 14 h when treated with prazosin (n = 8). (D) Rats with 6-OHDA lesions had a significantly high acute increase in their mean blood pressure. The acute increase in mean blood pressure was acutely reversed to below baseline levels when prazosin was administered 10 min after the 6-OHDA lesions were induced (n = 8). (E) Heart rate increased significantly after 6 h in the group of rats treated with prazosin (n = 8). (F) An acute and excessive increase in the epinephrine serum level was induced within 3 h and remained high until 6 h post-6-OHDA NTS lesion. The change in the epinephrine serum level was similar in the intervention with the prazosin treatment and remained high until 12 h (n = 8 per group). (G) An acute and excessive increase in the norepinephrine serum level was induced within 3 h and remained high until 6 h post-6-OHDA NTS lesions. The change in the norepinephrine serum level was similar within 6 h in the intervention with the prazosin treatment and higher at 12 h (n = 8 per group). The data represent the means ± SD. *P < 0.05 and **P < 0.001 versus the respective group at 0 h. †P < 0.05 versus the respective group at 3 h. ‡P< 0.001 versus the respective group at 6 h. §P < 0.05 and §§P < 0.001 6-OHDA versus 6-OHDA plus prazosin.

Treatment with prazosin (0.15 mg/kg) reversed 6-hydroxydopamine (6-OHDA)-induced acute hypertension and increased survival time. (A) Representative nucleus tractus solitarii (NTS) position of 6-OHDA lesions (arrows). (B) Rats with bilateral 6-OHDA lesions of NTS died suddenly within 7 h with severe pulmonary hemorrhagic edema complications developing before death (n = 8). (C) Rats with bilateral 6-OHDA lesions of NTS survived for at least 14 h with no pulmonary edema at 14 h when treated with prazosin (n = 8). (D) Rats with 6-OHDA lesions had a significantly high acute increase in their mean blood pressure. The acute increase in mean blood pressure was acutely reversed to below baseline levels when prazosin was administered 10 min after the 6-OHDA lesions were induced (n = 8). (E) Heart rate increased significantly after 6 h in the group of rats treated with prazosin (n = 8). (F) An acute and excessive increase in the epinephrine serum level was induced within 3 h and remained high until 6 h post-6-OHDA NTS lesion. The change in the epinephrine serum level was similar in the intervention with the prazosin treatment and remained high until 12 h (n = 8 per group). (G) An acute and excessive increase in the norepinephrine serum level was induced within 3 h and remained high until 6 h post-6-OHDA NTS lesions. The change in the norepinephrine serum level was similar within 6 h in the intervention with the prazosin treatment and higher at 12 h (n = 8 per group). The data represent the means ± SD. *P < 0.05 and **P < 0.001 versus the respective group at 0 h. †P < 0.05 versus the respective group at 3 h. ‡P< 0.001 versus the respective group at 6 h. §P < 0.05 and §§P < 0.001 6-OHDA versus 6-OHDA plus prazosin.

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