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Cardiac sympathetic nerves do not contribute to AngII‐salt hypertension
Author(s) -
Hirsch Dalay Marie,
Osborn John
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.640.8
We have previously investigated the contribution of splanchnic, renal and lumbar sympathetic nerve activity (SNA) to AngII‐salt hypertension and found that the primary neural target in this model is the splanchnic vascular bed. The present study investigated the role of cardiac SNA in AngII‐salt rats. Male Sprague Dawley rats consuming a high salt diet were instrumented with telemeters to measure mean arterial pressure (MAP) and heart rate (HR). In Protocol 1, rats were also subjected to cardiac denervation by stellate ganglionectomy (SGx) or a sham (SHAM) surgery. In Protocol 2, rats were treated with the beta blocker atenolol (ATEN) or vehicle (VEH) for the entire protocol. MAP was monitored for 3 days, then AngII was administered (150 ng/kg/min, sc) for 14 days. Protocol 1 results: baseline MAP was similar in SGX (102.96 ± 3.37 mmHg) and SHAM (105.45± 3.06) rats in contrast to HR which was lower in SGX (340.59 ± 2.77 bpm) compared to SHAM (415.13 ± 6.23). However, the hypertensive response to AngII was identical in both groups. Protocol 2 results: although baseline MAP and HR were lower in ATEN rats (88.68 ± 2.73 mmHg and 351.60 ± 7.13 bpm) compared to VEH rats (103.17 ± 1.72 mmHg and 419.24 ± 11.90 bpm), MAP increased to the same level by end of the AngII periods. We conclude that cardiac SNA does not contribute to AngII‐salt hypertension in the rat. Supported by R01 HL076312