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Pronounced fall in renal sympathetic activity after blockade of endogenous angiotensin‐(1‐7) in the paraventricular nucleus during hyperosmolar conditions
Author(s) -
Silva Ana Quenia Gomes,
Santos Robson A.S.,
Fontes Marco Antonio Peliky
Publication year - 2008
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.22.1_supplement.1236.1
Subject(s) - losartan , microinjections , medicine , endocrinology , saline , hypertonic saline , sympathetic nervous system , chemistry , renin–angiotensin system , anesthesia , central nervous system , blood pressure
Angiotensin‐(1‐7) participates in the maintenance of sympathetic outflow exerted by hypothalamic paraventricular nucleus (PVN) neurons. Plasma levels of Ang‐(1‐7) are increased in plasma hyperosmolar conditions, which may alter PVN neuronal activity. We investigated if endogenous Ang‐(1‐7) in the PVN contributes to the maintenance of sympathetic output during plasma hyperosmolality. Male Wistar rats (~300g) were anesthetized (Urethane; 1.2g/Kg) and prepared for MAP, HR and RSNA recording. After 30 minutes of hypertonic saline (HTS; 2.5M) intravenous infusion, A‐779 (1nmol; n=6), Losartan (1nmol; n=6) or vehicle (NaCl 0.9%, 100nl; n=5) were microinjected into the PVN. In all groups, HTS infusion evoked a large increase in MAP (in mmHg, A779: 16±4; Los: 26±0; vehicle: 20±6; P<0.01) and a decrease in RSNA (A779: −18±3%; Los: −12±7%; vehicle: −22±5%; P <0.01) compared with isotonic saline group (ITS; 0.15M; n=4; −7±3mmHg; +13±11%). Microinjections of A‐779 after HTS infusion caused a greater fall in MAP (in mmHg, A779: −40±9 vs Los: −16±7; vehicle: −7±3; P <0.01) and RSNA (A779: −26±6% vs Los: −12±5%; vehicle: −2±3%; P <0.01) compared to both Losartan and vehicle groups; HR was not affected. These results suggest that during plasma hyperosmolality, Ang‐(1‐7) exerts a pronounced excitatory effect on PVN neurons, particularly over the sympathetic vasomotor output. Financial Support: CNPq, Pronex and Fapemig.