LAUSR

Menopause and rheumatoid arthritis (RA) are both known to cause elevation of blood Pressure in women, and it is known that RA is more prevalent in women around menopausal age. However, the mechanism of elevated blood pressure in postmenopausal RA women is not known. Thus, the aim of this study was to identify the underlying mechanisms of increased blood pressure in postmenopausal RA women by using ovariectomised RA rat models. Ratswere randomly divided into six groups: sham, ovariectomised (Ovx), RA induced ovariectomised (Ovx+RA), and RA induced ovariectomised plus 17 β-oestradiol, baricitinib orlosartan. Blood pressure was measured through carotid artery cannulation. Haematoxylin andEosin (H&E) and Picro Sirius Red staining was performed on the aorta and heart tissues toevaluate histological alterations and collagen deposition. Immunohistochemistry, immunofluorescence and qPCR methods were used to evaluate the oxidative, inflammatory, growth and fibrosis, and apoptosis markers in the aorta and heart tissues. Mean arterial pressure(MAP) was significantly raised in the Ovx rats compared to sham rats and slightly raised without significant difference in the Ovx+RA rats compared to Ovx rats. MAP in the RA induced ovariectomised rats were significantly reduced with 17 β-oestradiol and losartantreatment. H&E and Picro Sirius staining revealed enhanced collagen deposition in the aortaand heart tissues and increased fibrosis in the heart tissue of the Ovx+RA rats. The collagen deposition and fibrosis were reduced with 17 β-oestradiol treatment. Immunohistochemistry, immunofluorescence and qPCR studies revealed that Ovx+RA rats had elevated expression of oxidative markers such as endothelial nitric oxide synthase (eNOS), inducible nitric oxidesynthase (iNOS), NADPH oxidase 2 (Nox2) and NADPH oxidase 4 (Nox4), inflammatory markers such as toll-like receptor 4 (TLR4) and nuclear factor kappa-light-chain-enhancer ofactivated B cells (NF-ĸB), growth and fibrosis marker such as vascular endothelial growth factor (VEGF), and apoptosis marker such as caspase-3 in the aorta and heart tissues. The expressions of these markers were reduced with 17 β-oestradiol treatment. In conclusion, hypertension in postmenopausal RA women occurs due to enhanced oxidative stress, inflammation, fibrosis, and apoptosis; oestrogen treatment reduces the blood pressure inpostmenopausal RA women by inhibiting these mechanisms. The research work is supported by Fundamental research grant scheme 2020, Ministry of Higher education, Malaysia. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.