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Relaxin in the subfornical organ (SFO) increases arterial pressure and lumbar sympathetic nerve activity in female rats: Role of Angiotensin II
Author(s) -
Brown Randall J,
Phaup J. Glenn,
Hasser Eileen M.,
Heesch Cheryl M.
Publication year - 2012
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.26.1_supplement.891.19
Subject(s) - subfornical organ , angiotensin ii , medicine , endocrinology , microinjection , mean arterial pressure , efferent nerve , relaxin , rostral ventrolateral medulla , efferent , blood pressure , heart rate , hormone , afferent
Relaxin (RLN), an ovarian hormone secreted in pregnancy, activates the SFO, a circumventricular organ, and regions within the brain parenchyma associated with control of blood volume and sympathetic nerve activity. Previously we demonstrated that intracarotid artery (ica) infusion of RLN (0.154 μM/hr) resulted in activation (increased Fos expression) of both vasopressinergic and spinally projecting neurons in the hypothalamic paraventricular nucleus (PVN). Current experiments in 6 inactin‐anesthetized and sinoaortic‐denervated female rats evaluated effects of acute microinjection of RLN into the SFO on mean arterial pressure (MAP) and efferent lumbar sympathetic nerve activity (LSNA), and a potential interaction with angiotensin II (Ang II). The SFO was functionally identified by pressor (+ 18 ± 3mmHg) and sympathoexcitatory (+ 12 ± 2%) responses to microinjected Ang II (20μM, 50nl). Thirty min. after SFO Ang II, when MAP and LSNA had returned to baseline values, RLN in the SFO (15.4 μM, 50 nl) produced prolonged increases in MAP (+ 27 ± 5mmHg) and LSNA (+ 14 ± 3%). In the presence of RLN‐related pressor effects, ica administration of the AT 1 receptor antagonist L158,809 (40 μg/Kg) restored MAP to baseline levels. These data further support a role for CNS actions of RLN in regulating efferent sympathetic nerve activity during pregnancy, likely through Ang II and an SFO‐PVN pathway. NIH RO1 HL091164 (CMH)