Abstract 447: Intracerebroventricular Administration of Autologous Bone Marrow-derived Cells Attenuates Sympathetic Hyperactivity in Deoxycorticosterone Acetate-salt Hypertensive Rats

Abstract

Objectives: Administration of deoxycorticosterone acetate (DOCA) in combination with salt loading and surgical removal of one kidney induces hypertension. Central mechanism is involved in this hypertension. Bone marrow-derived cells (BMCs) include mesenchymal stem cells play critical role in repairing damaged tissue and anti-inflammation. We hypothesized that increase in number of BMCs in the brain would attenuate the DOCA-salt hypertension. Methods: Sprague-Dawley rats underwent unilateral nephrectomy were divided into following 4 groups: rats received sham treatment with intracerebroventricular (icv) administration of medium (S/M group, n=5); rats received sham treatment with icv administration of BMCs (S/B group, n=5); rats received DOCA-salt treatment with icv administration of medium (D/M group, n=4); rats received DOCA-salt treatment with icv administration of BMCs (D/B group, n=7). Three weeks following the initiation of DOCA-salt treatment, rats had surgery to implant arterial and venous catheters. Resting mean arterial pressure (MAP) of rats was recorded in conscious unrestrained state and resting sympathetic tone was evaluated with a peak depressor response produced by hexamethonium (C6) injection. Results: Resting MAPs of S/M, S/B, D/M and D/B group were 116±4, 120±5, 194±4, 172±9 mmHg, respectively. DOCA-salt treatment significantly increased MAP in both D/M and D/B group. D/B group tended to have lower MAP than D/M group, however, post hoc analysis did not reach significant. The peak depressor responses to C6 injection in S/M, S/B, D/M and D/B group were 41±2, 46±5, 97±10, 69±5 mmHg, respectively. DOCA-salt treatment significantly increased the peak depressor response to C6 and icv administration of BMCs attenuated the increase in peak depressor response. Conclusion: BMCs in the brain may have protective role against sympathetic hyperactivity caused by DOCA-salt treatment.