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  • Title: Normotension in conscious rats after placement of bilateral electrolytic lesions in the rostral ventrolateral medulla.
    Author: Cochrane KL, Nathan MA.
    Journal: J Auton Nerv Syst; 1989 Apr; 26(3):199-211. PubMed ID: 2666490.
    Abstract:
    The effects of bilateral electrolytic lesions of the rostral ventrolateral medulla (RVLM) on mean arterial pressure (MAP) and heart rate (HR) were examined in 8 rats at one and 5 days after placement of the lesions. The MAP (111 +/- 2 mm Hg) and HR (393 +/- 17 bpm) of the lesion group were similar to the values recorded in the control group (117 +/- 3 mm Hg, 405 +/- 11 bpm; n = 18). Blockade of the synthesis of angiotensin II with captopril in the lesion group significantly decreased MAP to 93 +/- 2 mm Hg on the first postlesion day. In contrast, the MAP of the control group after captopril fell slightly to 111 +/- 4 mm Hg. Captopril did not alter MAP or HR on postlesion day 5 in either group. Administration of chlorisondamine, an autonomic ganglionic blocking agent, reduced MAP in the lesion and control groups to similar values of 59 +/- 2 mm Hg and 64 +/- 2 mm Hg, respectively. Baroreflex-mediated tachycardia to a decrease in MAP was abolished in the lesion group at one day postlesion and attenuated at 5 days postlesion. In contrast, the baroreflex-mediated bradycardia to an increase in MAP was unaffected by the lesions. Plasma renin activity (PRA) in the lesion group was elevated by nearly 50% as compared to the control group on the first postlesion day (7.3 +/- 0.8 and 4.9 +/- 0.5 ng AI/ml/h, respectively). A 90% elevation in plasma norepinephrine (NE) concentration was also observed in the lesion group as compared to the control group (437 +/- 80 pg/ml and 228 +/- 22 pg/ml, respectively) on postlesion day one. By postlesion day 5, the PRA of the lesion and control groups were nearly identical (4.4 +/- 0.7 and 4.0 +/- 1.0 ng AI/ml/h, respectively), and the plasma NE concentrations were also very similar (201 +/- 41 pg/ml and 175 +/- 22 pg/ml, respectively). We conclude that bilateral destruction of the RVLM does not cause hypotension or bradycardia in conscious rats. Therefore, areas other than the RVLM are capable of maintaining MAP and HR. Sympathetic vasomotor and cardiomotor tone appears unaffected by the lesions. However, increased activity of the renin-angiotensin system may contribute transiently to the maintenance of vasomotor tone and, consequently, MAP after lesion of the RVLM. The RVLM may be important in mediating baroreflex increase in HR.
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