AI Article Synopsis
- Evidence suggests a link between high blood pressure (hypertension) and chronic inflammation, observed in both human studies and rat models, particularly in spontaneously hypertensive rats (SHR).
- The inflammatory response involves leukotriene B (LTB), whose role in hypertension is not fully understood but shows increased T cells and macrophages in the brainstem of SHRs.
- Blocking the LTB receptor (BLT1) with a specific drug reduced arterial pressure in SHRs, indicating that targeting the LTB pathway could be a potential new treatment for neurogenic hypertension.
Article Abstract
Key Points: Evidence indicates an association between hypertension and chronic systemic inflammation in both human hypertension and experimental animal models. Previous studies in the spontaneously hypertensive rat (SHR) support a role for leukotriene B (LTB ), a potent chemoattractant involved in the inflammatory response, but its mode of action is poorly understood. In the SHR, we observed an increase in T cells and macrophages in the brainstem; in addition, gene expression profiling data showed that LTB production, degradation and downstream signalling in the brainstem of the SHR are dynamically regulated during hypertension. When LTB receptor 1 (BLT1) receptors were blocked with CP-105,696, arterial pressure was reduced in the SHR compared to the normotensive control and this reduction was associated with a significant decrease in systolic blood pressure (BP) indicators. These data provide new evidence for the role of LTB as an important neuro-immune pathway in the development of hypertension and therefore may serve as a novel therapeutic target for the treatment of neurogenic hypertension.
Abstract: Accumulating evidence indicates an association between hypertension and chronic systemic inflammation in both human hypertension and experimental animal models. Previous studies in the spontaneously hypertensive rat (SHR) support a role for leukotriene B (LTB ), a potent chemoattractant involved in the inflammatory response. However, the mechanism for LTB -mediated inflammation in hypertension is poorly understood. Here we report in the SHR, increased brainstem infiltration of T cells and macrophages plus gene expression profiling data showing that LTB production, degradation and downstream signalling in the brainstem of the SHR are dynamically regulated during hypertension. Chronic blockade of the LTB receptor 1 (BLT1) receptor with CP-105,696, reduced arterial pressure in the SHR compared to the normotensive control and this reduction was associated with a significant decrease in low and high frequency spectra of systolic blood pressure, and an increase in spontaneous baroreceptor reflex gain (sBRG). These data provide new evidence for the role of LTB as an important neuro-immune pathway in the development of hypertension and therefore may serve as a novel therapeutic target for the treatment of neurogenic hypertension.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5063948 | PMC |
| http://dx.doi.org/10.1113/JP272065 | DOI Listing |
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