The Relationship Between Hypertension and Inflammation (R01)

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-Purpose. This Funding Opportunity Announcement (FOA) solicits grant applications that propose the study of the sequence of events in which the vascular inflammatory state contributes to the development and maintenance of hypertension. Ample evidence suggests that inflammation may play a role in the pathogenesis of hypertension or that it may characterize a functional state of the vessel wall as a consequence of high blood pressure. Angiotensin II (Ang II), a widely recognized vasoconstrictor and anti-natriuretic involved in blood pressure regulation, also acts as a pro-inflammatory factor in the cardiovascular system. Ang II stimulates the expression of several inflammatory cytokines, which in turn affect blood pressure. A potential linkage between Ang II and immuno-cytokines is their shared ability to induce the level of reactive oxygen species (ROS), which serve as second messengers for many intracellular signaling pathways. The production of ROS not only decreases bioavailability of nitric oxide (NO), a vasodilator, but also initiates the functional and morphological alterations, such as remodeling, in the vascular wall that accompany the hypertensive state over time. This FOA would provide an opportunity to bring focus on the potential causal relationship between hypertension and inflammation in a cohesive, integrated manner. A new understanding of hypertension and inflammation would provide novel opportunities to prevent and treat the disease. -Mechanism of Support. This FOA will utilize the NIH Research Project Grant (R01) award mechanism. -Funds Available and Anticipated Number of Awards. Because the nature and scope of the proposed research will vary from application to application, it is anticipated that the size and duration of each award will also vary. The total amount awarded and the number of awards will depend upon the numbers, quality, duration, and costs of the applications received.

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