Opportunity Information: Apply for PA 07 138
Apply for PA 07 138
- The National Institutes of Health in the health sector is offering a public funding opportunity titled "The Relationship Between Hypertension and Inflammation (R01)" and is now available to receive applicants.
- Interested and eligible applicants and submit their applications by referencing the CFDA number(s): 93.837 Cardiovascular Diseases Research.
- This funding opportunity was created on Dec 5, 2008 and posted on Dec 12, 2006.
- Applicants must submit their applications by Multiple Receipt Dates See Link to Full Announcement for details.. (Agency may still review applications by suitable applicants for the remaining/unused allocated funding in 2026.)
- Eligible applicants include: For profit organizations other than small businesses Independent school districts Native American tribal governments (Federally recognized) Others (see text field entitled Additional Information on Eligibility for clarification) County governments Native American tribal organizations (other than Federally recognized tribal governments) State governments Small businesses Private institutions of higher education Special district governments Nonprofits that do not have a 501(c)(3) status with the IRS, other than institutions of higher education Nonprofits having a 501(c)(3) status with the IRS, other than institutions of higher education Public and State controlled institutions of higher education Public housing authorities/Indian housing authorities City or township governments.
- Foreign institutions are not eligible to apply. Eligible agencies of the Federal Government can apply. Faith based or community based organizations can apply.
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Opportunity Summary:
The NIH funding opportunity "The Relationship Between Hypertension and Inflammation (R01)" (Funding Opportunity Number PA-07-138) supports research aimed at clarifying how vascular inflammation and high blood pressure are connected, and more importantly, in what order key events occur as hypertension develops and persists. The central idea behind the announcement is that inflammation may not just be a byproduct of hypertension, but could be a driving force that helps cause or sustain it. At the same time, the FOA recognizes the alternative possibility that inflammation may reflect a dysfunctional vessel-wall state that emerges after blood pressure has already become elevated. Applications are expected to tackle this question directly by mapping the sequence of biological changes linking inflammatory signaling in the vasculature to the onset, progression, or maintenance of hypertension.
A major scientific theme highlighted in the announcement is the role of angiotensin II (Ang II). While Ang II is well known for its classic blood pressure effects as a vasoconstrictor and anti-natriuretic hormone, the FOA emphasizes that it also behaves as a pro-inflammatory factor within the cardiovascular system. Ang II can stimulate the expression of inflammatory cytokines, and those cytokines can then influence vascular function and blood pressure regulation. The announcement also points to a mechanistic bridge between Ang II signaling and immune/cytokine pathways: both can increase reactive oxygen species (ROS). ROS are described not merely as damaging byproducts, but as second messengers that alter intracellular signaling cascades relevant to vascular tone and structure. In practical terms, elevated ROS can reduce nitric oxide (NO) bioavailability, undermining a key vasodilatory pathway, and can also contribute to longer-term structural changes in vessels. Those changes include functional and morphological alterations such as vascular remodeling, which is commonly seen as hypertension becomes chronic.
From NIH's perspective, this FOA is meant to concentrate the field on the potential causal relationship between inflammation and hypertension in a cohesive and integrated way, rather than treating inflammation as a secondary observation. The rationale is that a clearer understanding of how inflammatory processes influence blood pressure control, endothelial function, oxidative stress, and vascular remodeling could open new doors for prevention and treatment. The announcement signals interest in work that can connect molecular and cellular inflammatory events to physiological outcomes, helping explain how inflammatory states translate into sustained increases in blood pressure over time.
The mechanism of support is the NIH Research Project Grant (R01), meaning applicants are expected to propose substantial, hypothesis-driven research projects with clear aims, rigorous methodology, and meaningful impact on understanding the hypertension-inflammation relationship. Because research approaches can vary widely (for example, basic mechanistic studies, translational investigations, or integrative vascular biology projects), NIH notes that award size and project duration will vary accordingly. There is no fixed number of awards or set-aside budget described; instead, total funding and the number of grants depend on the volume of submissions and their scientific quality, duration, and costs.
In terms of administrative details, this is a discretionary grant opportunity under the health category, with CFDA number 93.837 (Cardiovascular Diseases Research). Cost sharing or matching is not required. The opportunity historically used multiple receipt dates (applicants would follow NIH standard due dates referenced in the full announcement). The posting information listed includes a posted date of December 12, 2006, and the opportunity was later archived (archive date April 5, 2009), which indicates it is no longer active, though it remains useful as a reference for the types of projects NIH sought at the time.
Eligibility is broad across many U.S.-based organizational types. Eligible applicants include public and state-controlled institutions of higher education, private institutions of higher education, nonprofits (including 501(c)(3) and certain non-501(c)(3) entities other than institutions of higher education), for-profit organizations (including small businesses), and a wide range of governmental entities (state, county, city/township, special district governments, and eligible federal agencies). Tribal governments and tribal organizations are also included. Faith-based and community-based organizations may apply as well. A key restriction is that foreign institutions are not eligible to apply, though eligible U.S. federal agencies may submit applications. The full announcement was hosted by NIH at the provided link, and NIH’s Office of Extramural Research (OER) webmaster contacts were listed for access or technical issues.
FAQs: NIH PA-07-138 - The Relationship Between Hypertension and Inflammation (R01)
What is the funding opportunity title and number?
The funding opportunity is titled "The Relationship Between Hypertension and Inflammation (R01)" and carries Funding Opportunity Number PA-07-138.
Which agency is offering this opportunity?
This opportunity is offered by the National Institutes of Health (NIH).
What type of grant mechanism is used?
The mechanism of support is the NIH Research Project Grant (R01).
What is the main scientific purpose of this FOA?
The FOA supports research aimed at clarifying how vascular inflammation and high blood pressure are connected, with particular emphasis on determining the sequence of key events as hypertension develops and persists.
What central question are applications expected to address?
Applications are expected to directly test whether inflammation is a driving force that helps cause or sustain hypertension, or whether inflammation primarily reflects vascular dysfunction that arises after blood pressure has already become elevated.
Why does the FOA emphasize the “order of events” in hypertension and inflammation?
NIH highlights event timing because determining whether inflammatory signaling precedes hypertension (and contributes to its onset) versus follows hypertension (as a consequence of elevated pressure and vessel-wall dysfunction) changes how the field interprets causality and identifies prevention and treatment targets.
What kinds of biological connections does the FOA want applicants to map?
The FOA seeks studies that map the sequence of biological changes linking inflammatory signaling in the vasculature to the onset, progression, or maintenance of hypertension.
What role does angiotensin II (Ang II) play in the scientific theme of the FOA?
The FOA highlights angiotensin II as more than a classic blood pressure regulator (vasoconstrictor and anti-natriuretic hormone). It emphasizes Ang II as a pro-inflammatory factor in the cardiovascular system that can stimulate inflammatory cytokine expression, which in turn can influence vascular function and blood pressure regulation.
How does the FOA connect Ang II signaling to inflammatory and immune pathways?
The FOA points to reactive oxygen species (ROS) as a mechanistic bridge, noting that both Ang II signaling and immune/cytokine pathways can increase ROS.
How are reactive oxygen species (ROS) described in this opportunity?
ROS are described not only as damaging byproducts but also as second messengers that can alter intracellular signaling cascades relevant to vascular tone and vascular structure.
What vascular effects of elevated ROS are highlighted?
The FOA notes that elevated ROS can reduce nitric oxide (NO) bioavailability, undermining a key vasodilatory pathway, and can contribute to longer-term structural changes in vessels.
What is nitric oxide (NO) and why is it mentioned?
Within the context of this FOA, nitric oxide (NO) is highlighted as an important vasodilatory pathway. The FOA notes that increased ROS can reduce NO bioavailability, which can negatively affect vascular function and blood pressure regulation.
Does the FOA discuss vascular remodeling?
Yes. The FOA notes that oxidative and inflammatory processes can contribute to functional and morphological vessel changes, including vascular remodeling, which is commonly seen as hypertension becomes chronic.
What broader outcomes is NIH interested in connecting to inflammation?
NIH signals interest in work that links molecular and cellular inflammatory events to physiological outcomes, including blood pressure control, endothelial function, oxidative stress, and vascular remodeling.
Is the FOA focused on inflammation as a secondary observation or a causal factor?
The FOA is intended to focus the field on inflammation as a potential causal contributor to hypertension in a cohesive and integrated way, rather than treating inflammation primarily as a secondary observation.
What types of research approaches are consistent with this FOA?
The FOA indicates that approaches can vary widely, including basic mechanistic studies, translational investigations, or integrative vascular biology projects, as long as they address the core hypertension-inflammation relationship and sequence of events.
What does the R01 mechanism imply about the project scope?
Because this is an R01, applicants are expected to propose substantial, hypothesis-driven research with clear aims, rigorous methodology, and meaningful impact on understanding the relationship between hypertension and inflammation.
Is there a set budget or a fixed number of awards?
No. The FOA does not describe a fixed number of awards or a set-aside budget. Total funding and the number of grants depend on the volume of submissions and their scientific quality, project duration, and costs.
Will award size and project duration be the same for all projects?
No. NIH notes that award size and project duration will vary depending on the proposed research approach and associated needs.
Is cost sharing or matching required?
No. Cost sharing or matching is not required for this opportunity.
What is the CFDA number and program area?
The CFDA number is 93.837, under Cardiovascular Diseases Research.
What is the assistance listing or category for this opportunity?
The opportunity is described as a discretionary grant opportunity under the health category.
Who is eligible to apply?
Eligibility is broad across many U.S.-based organization types, including public and state-controlled institutions of higher education, private institutions of higher education, nonprofits (including 501(c)(3) and certain non-501(c)(3) entities other than institutions of higher education), for-profit organizations (including small businesses), and many governmental entities.
Which governmental entities are included as eligible applicants?
Eligible governmental applicants include state governments, county governments, city/township governments, special district governments, and eligible federal agencies.
Are tribal governments and tribal organizations eligible?
Yes. Tribal governments and tribal organizations are included among eligible applicants.
Can faith-based or community-based organizations apply?
Yes. The FOA states that faith-based and community-based organizations may apply.
Are foreign institutions eligible to apply?
No. A key restriction is that foreign institutions are not eligible to apply.
Can U.S. federal agencies submit applications?
Yes. The FOA indicates that eligible U.S. federal agencies may submit applications.
Were there specific application deadlines?
The opportunity historically used multiple receipt dates, with applicants following NIH standard due dates referenced in the full announcement.
When was this FOA posted?
The posted date listed for this FOA is December 12, 2006.
Is this funding opportunity still active?
No. The opportunity was later archived (archive date April 5, 2009), indicating it is no longer active, though it may remain useful as a reference for the types of projects NIH sought at the time.
Where was the full announcement hosted and who was listed for technical help?
The full announcement was hosted by NIH at the provided link in the original posting, and NIH Office of Extramural Research (OER) webmaster contacts were listed for access or technical issues.
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