Abstract P072: Prostaglandin I 2 (PGI 2 ) Signaling Attenuates Hypertension And Associated Vascular Inflammation
| Autor: | Allison E Norlander, Jian Zhang, Masako Abney, Stokes Peebles |
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| Rok vydání: | 2022 |
| Předmět: | |
| Zdroj: | Hypertension. 79 |
| ISSN: | 1524-4563 0194-911X |
| DOI: | 10.1161/hyp.79.suppl_1.p072 |
| Popis: | In recent years, inflammation was determined to play a causal role in hypertension. Interestingly, evidence suggests that long-lasting use of cyclooxygenase inhibitors, which prevent metabolism of arachidonic acid (AA) to prostaglandins and thromboxane, increases blood pressure. Prostaglandin I 2 (PGI 2 ) is an AA metabolite that has immunomodulatory effects. Our group has demonstrated that PGI 2 acts to directly inhibit the functionality of pro-inflammatory DCs and CD4+ Th1 and Th2 cells, while promoting the function of tolerogenic DCs and T regulatory cells (Treg). Further, mice deficient in the receptor for PGI 2 , IP, develop elevated blood pressure in response to high salt diet, suggesting that PGI 2 signaling is important for controlling blood pressure elevation in response to stimuli. These studies led us to hypothesize that PGI 2 signaling attenuates hypertension and associated vascular inflammation. We found that infusion of the PGI 2 analog, treprostinil (TPL), into mice resulted in blunted blood pressure following 4 weeks of angiotensin II (Ang II) infusion (490ng/kg/min) compared to mice that received Ang II and TPL vehicle (42.8 mmHg reduction, p3 compared to 2.04x10 3 cells/aorta, p3 compared to 1.95x10 3 cells/aorta, p3 compared to 1.36x10 3 cells/aorta p2 augments the immune response associated with hypertension may shed new insight into potential therapeutics. |
| Databáze: | OpenAIRE |
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