Area:
Neuroscience Biology, Animal Physiology Biology, Medicine and Surgery
We are testing a new system for linking grants to scientists.
The funding information displayed below comes from the
NIH Research Portfolio Online Reporting Tools and the
NSF Award Database.
The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
You can help! If you notice any innacuracies, please
sign in and mark grants as correct or incorrect matches.
Sign in to see low-probability grants and correct any errors in linkage between grants and researchers.
High-probability grants
According to our matching algorithm, Mark E. Dunlap is the likely recipient of the following grants.
| Years |
Recipients |
Code |
Title / Keywords |
Matching
score |
| 1995 — 1997 |
Dunlap, Mark E |
R01Activity Code Description:
To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Pre and Postganglionic Vagal Mechanisms in Heart Failure @ Case Western Reserve University
DESCRIPTION: (Adapted from Applicant's Abstract) The studies outlined in the current proposal will determine the contribution of pre- and post-ganglionic mechanisms to abnormal vagal control in heart failure. Patients and animals with heart failure show attenuated vagal control of heart rate, which could be due to changes in nerve activity, ganglionic transmission, synthesis or release of acetylcholine, acetylcholinesterase activity, or muscarinic receptor density or function. Preliminary data suggest that despite reduced vagal control of heart rate, post-synaptic mechanisms are augmented in heart failure (likely due to a form of denervation hypersensitivity). The project will determine the sites and mechanisms of altered vagal control in heart failure. Studies will include experiments in intact animals, in isolated spontaneously beating right atria, on atrial strips to measure release of acetylcholine, and on tissue samples. Specific hypotheses to be tested are: 1. Cholinergic mechanisms become abnormal very early in developing cardiac dysfunction. 2. This reduction in vagal control leads to changes in muscarinic receptor density and function during early stages of cardiac dysfunction and contributes to preserved baroreflex control of RR interval. 3. As left ventricular dysfunction becomes more severe, the abnormalities of vagal control become so profound that even upregulation of muscarinic receptors cannot compensate, resulting in grossly abnormal vagal mechanisms in heart failure. 4. Attenuated efferent vagal control in heart failure is likely due to pre-synaptic mechanisms. These studies will lead to a detailed understanding of abnormal cholinergic mechanisms that are present in heart failure. Since low vagal tone portends increased mortality, understanding these mechanisms may lead to efforts to restore vagal control and blunt the sympathetic excitatory state that is present in heart failure.
|
1 |