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Brain targeted (Pro)renin receptor over‐expression induces the development of hypertension via modulation of baroreflex sensitivity and renal sympathetic nerve activity in renin transgenic mice
Author(s) -
Li Wencheng,
Shan Zhiying,
Raizada Mohan K.,
Sigmund Curt D.,
Feng Yumei
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1078.10
Subject(s) - endocrinology , medicine , renin–angiotensin system , baroreflex , plasma renin activity , receptor , blood pressure , transgene , kidney , genetically modified mouse , chemistry , heart rate , gene , biochemistry
(Pro)renin receptor ((P)RR) is a new member of the brain renin angiotensin system. To investigate the role of central (P)RR in the blood pressure (BP) regulation, adeno‐associated virus (AAV‐PRR) coding human (P)RR was intercerebroventricular (ICV) administrated to non‐transgenic (NT) and renin transgenic (R+) mice (n=4) for (P)RR over‐expression. MAP and HR were recorded by radio telemeters for three weeks. Although baseline MAP, HR and spontaneous baroreflex sensitivity (SBRS) were similar between NT and R+ mice, (P)RR over‐expression significantly increased BP (mmHg) in R+ (136 ± 9.0) compared to NT (105 ± 0.8; P<0.05) mice, while SBRS (msec/mmHg) was decreased (R+, 1.31 ± 0.03, NT, 1.87 ± 0.06). Furthermore basal renal sympathetic nerve activity (percentage of baseline VS. maximum) was comparable between NT (23.6±2.6%) and R+ (30.7±1.3%) mice. Interestingly, (P)RR over‐expression significantly increased RSNA in both NT (45.7±1.4%) and R+ (51.5±5.0%) mice compared to their baseline respectively (P<0.05). Moreover, the RSNA tended to be higher in R+ compared to NT mice following (P)RR over‐expression. All together, these data suggested that central (P)RR over‐expression increased BP through modulation of SBRS and RSNA in renin transgenic mice indicating a regulatory role of (P)RR in the central regulation of blood pressure.(NIH1P30HL101285)