Hot Off The Press: Noriko Daneshtalab
Immune system regulation of hypertension evident in the homeostatic role of cyclooxygenase-2-derived PGE2 in response to increased dietary salt.
Hypertension on its own is a complex trait traditionally determined by both genetic and environmental factors with a high prevalence (~30% worldwide) and a major risk factor for other cardiovascular diseases.
Interestingly, it is also a disease which patients with autoimmune diseases such as psoriasis and arthritis are more prone to having at a higher prevalence than the normal population. These patients also have a significantly higher cardiovascular morbidity and mortality (e.g. arrhythmia and stroke) compared to non-arthritic populations.
The use of nonsteroidal anti-inflammatory drugs (NSAIDS) by the autoimmune patients have been traditionally implicated in the increase in hypertension; the inhibition of cyclooxygenase (COX) 1 and 2 isozymes reduce renal blood flow, glomerular filtration rate, and cause sodium retention by reducing urinary sodium excretion particularly when sodium-loaded. In salt-sensitive subjects, this retention of sodium will cause blood pressure to rise (2) and may affect the BP-lowering effect of some antihypertensive medications.
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