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Serotonin‐induced hypotension is not due to a reduction in preganglionic splanchnic sympathetic nerve activity in the Sprague Dawley rat
Author(s) -
Davis Robert Patrick,
Orer Hakan S.,
Barman Susan M.,
Watts Stephanie W.
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.645.3
Chronic serotonin (5‐hydroxytryptamine; 5‐HT) infusion (7 days) results in a sustained fall in blood pressure (BP) in the normotensive (Sprague Dawley; SD) and hypertensive (deoxycorticosterone acetate (DOCA)‐salt and spontaneously hypertensive) rats. The exact mechanism(s) underlying this response are not yet fully understood. Therefore, we sought to investigate whether 5‐HT infusion altered sympathetic nerve activity (SNA) in the normotensive rat. We hypothesized that 5‐HT infusion (iv) would reduce SNA while concomitantly lowering BP in the SD rat. BP and left splanchnic preganglionic SNA (SNA; 30 – 3K Hz bandpass) were recorded in 4 urethane‐anesthetized, paralyzed (gallamine triethiodide), and artificially respired SD rats before and during 1‐hr 5‐HT infusion (25 μg/kg/hr, iv). SNA was rectified and integrated with a 1‐volt reset. The integrated signal of SNA was quantified in 10‐min data blocks at baseline and during 5‐HT infusion. Mean BP was significantly ( p = 0.0011) reduced from 101 ± 4 to 63 ± 3 mmHg during 5‐HT infusion. In contrast, splanchnic SNA was unaffected during 5‐HT infusion. SNA was 102 ± 5% of the control at BP nadir. After 5‐HT infusion was stopped there was a tendency for SNA to increase (151 ± 26% of control; not significant). This study demonstrates that 5‐HT is not acting through a preganglionic sympathoinhibitory mechanism to mediate a sustained reduction in BP in the normotensive rat.