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Neural control of the kidney in a thyroxine induced model of heart hypertrophy (HH): impact of Nitric Oxide Synthase (NOS) blockade
Author(s) -
Buckley Maria M,
Johns Edward J
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.967.5
Subject(s) - endocrinology , medicine , nitric oxide synthase , nitric oxide , chemistry , reflex , stimulation , blood pressure
This study investigated the how the cardiopulmonary mediated reflex inhibition of renal sympathetic nerve activity (RSNA) in normal rats and those with HH induced by thyroxine administration might be modulated by nitric oxide (NO). Male Wistar rats were anaesthetized with chloralose/urethane and HH was induced by thyroxine administration (1 mg/kg/day, sc) for 1 week. All animals were subjected to 2 periods of volume expansion (VE) at 0.25% body weight/min for 30 min in the absence then presence of the NOS inhibitor L‐NAME (10µg/min/kg). Data, means ± SEM, were subjected to ANOVA and significance taken at P<0.05. Blood pressure (BP) was 93±6mmHg and 89±5mmHg in normal and HH groups, respectively. VE in normal rats decreased RSNA by 30% (P<0.05) in the absence and 60% in the presence of L‐NAME. In the HH group, RSNA did not change during the first VE while in the presence of L‐NAME it decreased by 40% (P<0.005). These findings demonstrate that the inhibition of RSNA in response to VE is tonically suppressed by NO at some stage along the reflex arc. Moreover, in the thyroxine induced HH model, it appears that the influence of NO is enhanced suppressing the renal sympatho‐inhibition to VE.