Premium
AT 1 receptors in the paraventricular nucleus (PVN) are required for sympathoexcitation due to angiotensin II in the subfornical organ of nonpregnant and pregnant rats.
Author(s) -
Kvochina Lyudmyla I,
Phaup Jeffery G.,
Hasser Eileen M.,
Heesch Cheryl M.
Publication year - 2009
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.23.1_supplement.792.2
Subject(s) - subfornical organ , microinjection , endocrinology , medicine , mean arterial pressure , receptor , angiotensin ii , chemistry , agonist , muscimol , angiotensin receptor , blood pressure , rostral ventrolateral medulla , heart rate
Activation of AT 1 receptors in the subfornical organ (SFO) by circulating angiotensin A II (A II) increases mean arterial pressure (MAP) through a pathway which includes the PVN. A II levels are increased and CNS actions of A II may support sympathetic nerve activity in pregnancy. The role of the PVN, and AT 1 receptors in the PVN, in responses to microinjection of A II into the SFO was tested in nonpregnant (NP) and term pregnant (P) rats. In 7 NP and 8 P sinoaortic denervated (SAD) inactin anesthetized rats, baseline mean arterial pressure (MAP) was lower (P= 96 ±5; NP= 120 ±8 mmHg) and heart rate was higher (P =374 ±11; NP =330 ±10 bpm) in P rats. The increase in MAP in response to A II (20 µM, 50 nl) in the SFO was greater in P compared to NP rats (ΔMAP: P = +22 ±3; NP = +14 ±2 mmHg). Bilateral microinjection of the GABA A receptor agonist, muscimol (1.5 mM, 100 nl), into the PVN decreased MAP (ΔMAP: P= ‐43±7 mmHg; NP= ‐46±4 mmHg) and LSNA (ΔLSNA: P= ‐34±13%; NP= ‐37±3%) and eliminated responses to activation of the SFO in both groups. In 3P and 2NP rats AT 1 receptor blockade (L158, 809, 20 mM, 100 nl) in the PVN also eliminated responses to activation of the SFO with A II. Thus, AT 1 receptors in the PVN are required for sympathoexcitation mediated by SFO A II in both NP and P rats. (NIH HL 36245).