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Brain‐derived neurotrophic factor overexpression in the paraventricular nucleus increases blood pressure via angiotensin type‐1 receptor‐mediated mechanisms (686.3)

BDNF expression increases in the PVN during hypertensive stimuli including stress and hyperosmolarity, and we have shown previously that overexpression of BDNF in the PVN leads to significant increases in mean arterial blood pressure (MAP). Here, we tested the hypothesis that BDNF‐induced pressor responses are mediated by angiotensin signaling in the central nervous system. MAP was recorded in male Sprague‐Dawley rats using telemetry. At 11wks of age, adeno‐associated viral vectors (AAV2‐GFP or AAV2‐BDNF) were injected bilaterally into the PVN, and losartan (Los; 15µg/ 0.5µL/ hour) or saline was infused icv for 4 wks using osmotic pumps. During the 4 wks after vector injections, MAP remained unchanged in the GFP+saline (dMAP=2.5±0.4 mmHg) and GFP+Los (dMAP=2.6±1.2 mmHg) groups. MAP increased markedly in both BDNF groups, but the increase was significantly reduced in BDNF+Los (dMAP=15.0±3.2 mmHg) compared with BDNF+saline (dMAP=28.7±2.2 mmHg, p<0.05). RT‐PCR from PVN tissue samples of AAV2‐GFP and AAV2‐BDNF‐injected rats indicated that BDNF significantly upregulated AT1R mRNA (2‐ddCt was 1.1±0.2 in GFP and 2.0±0.4 in BDNF rats using 18s as internal control, p<0.05). In contrast, mRNA levels of angiotensinogen, angiotensin converting enzyme (ACE), ACE2 and AT2R were unaffected by BDNF. We conclude that the BDNF‐induced MAP increase is partially mediated by AT1R, which is upregulated by BDNF within the PVN.