Central Administration of Hydrogen Sulfide Alleviates Rodent Angiotensin II Hypertension

IntroductionActivation of autonomic neural pathways plays a significant role in pathogenesis of hypertension (HTN). Hydrogen sulfide (H2S) is an endogenous neuro‐ and immunomodulatory molecule that is reportedly reduced in both rodent and human HTN. However, central role of H2S in HTN is not well understood. We hypothesized that chronic intracerebroventricular (ICV) infusion of sodium hydrosulfide (NaHS), an H2S donor, will alleviate rodent angiotensin II (Ang II) HTN.MethodsAdult male Sprague Dawley rats were implanted with radiotelemetry transmitters (DSI) in the descending aorta. Following baseline BP measurements, rats were randomly divided into three groups: (i) ICV NaHS; (ii) HTN; and (iii) ICV NaHS‐treated HTN rats. HTN was induced by chronic infusion of Ang II (200 ng/kg/min s.c.) for four weeks using mini‐osmotic pumps. ICV NaHS (30 nmol/h) or ICV saline was administered simultaneously with s.c. Ang II or saline infusion. At endpoint, H2S levels were measured in plasma samples of all rats.ResultsAt week four, mean arterial pressure (MAP) was significantly reduced in the ICV NaHS‐treated HTN group when compared with HTN group (104±7 vs. 166±5 mmHg, respectively; P< 0.01). This was associated with a lower MAP at night in the ICV NaHS‐treated HTN vs. HTN group (Delta MAP from day to night: 15.29±4 vs. 31.37±17 mmHg, respectively), suggesting reduced sympathetic drive following treatment with NaHS. Interestingly, this also reflected in significantly higher plasma H2S levels in the ICV NaHS‐treated HTN vs. HTN group (0.070±0.000 AU vs. 0.067±0.000 AU, respectively; P<0.05).ConclusionThese results support our hypothesis that alterations in central H2S signaling are associated with HTN, as centrally administered NaHS alleviated rodent Ang II HTN via reduction of sympathetic tone at night.Support or Funding InformationTUBITAK 2214‐A and UF CVM.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.