HIV, immune activation and salt-sensitive hypertension (HISH): a research proposal

Sepiso K Masenga, Benson M Hamooya, Selestine Nzala, Geoffrey Kwenda, Douglas C Heimburger, Wilbroad Mutale, John R Koethe, Annet Kirabo, Sody M Munsaka, Sepiso K Masenga, Benson M Hamooya, Selestine Nzala, Geoffrey Kwenda, Douglas C Heimburger, Wilbroad Mutale, John R Koethe, Annet Kirabo, Sody M Munsaka

Abstract

Objective: The objective of this study is to quantify and compare the effect of excess dietary salt on immune cell activation and blood pressure in HIV versus HIV negative individuals.

Results: Salt-sensitivity is associated with increased immune cell activation in animal studies. This concept has not been tested in people living with HIV. This study will therefore add more information in elucidating the interaction between HIV infection and/or anti-retroviral therapy (ART), immune-activation/inflammation and hypertension.

Keywords: HIV; Hypertension; Immune activation; Salt-sensitivity.

Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
In the salt deprivation phase, Participants will be recruited on day 0, urine sample collected and requested to avoid adding salt to their food or consume processed foods that contain salt for the next 7 days. In the low salt phase, participants will be provided with 2.3 g of sodium everyday apportioned in three parts to add to their meals. In the high salt phase participants will be provided with 9 g of dietary salt and split as previously described above. Blood pressure (BP) will be measured everyday (day 0 to 21) between 17:00 and 19:00 h or between 06:00 and 08:00 h. Ambulatory blood pressure (AMBP) will be measured on days 7, 14 and 21. A 24-h urine will be collected on days 14 and 21 for urinalysis
Fig. 2
Fig. 2
HIV and Salt-sensitive hypertension working Hypothesis. We hypothesize that HIV infection and treatment can lead to increased accumulation of sodium in tissues. This can activate the immune system leading to hypertension. Sodium enters antigen presenting cells and is exchanged for calcium through the sodium hydrogen exchanger 1. Calcium activates protein kinase C (PKC), which then activates NADPH oxidase by phosphorylating its subunit p47phox. This leads to increased production of superoxide with subsequent formation of immunogenic isolevuglandin (IsoLG)-protein adducts. IsoLGs activate DCs which in turn promote T cell proliferation and production of cytokines that contribute to salt-sensitive hypertension [4]

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Source: PubMed

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