Polymorphisms in the AT1 gene have been associated with various parameters related to the pathogenesis of cardiovascular diseases and to myocardial infarction.
This study demonstrates the first well-suited electrophysiological recording of cardiomyocytes on multielectrode arrays as a benefit for functional biomonitoring for the detection of AT1 receptor/ligand interactions and other marker proteins in sera directed to cardiovascular diseases.
This review addresses several of the unanswered questions with regard to tissue angiotensin II generation, focussing in particular on the heart and vascular wall: (1) what is the origin of the renin that is required to generate angiotensin II locally, (2) where does tissue angiotensin generation occur (intra- versus extracellular), (3) what is the importance of alternative (non-renin, non-ACE) angiotensin-generating enzymes, (4) do ACE inhibitors and AT(1) receptor antagonists exert local effects that are renin-angiotensin system independent (thereby incorrectly leading to the conclusion that they interfere with the local generation or effects of angiotensin II), and (5) to what degree do differences in tissue angiotensin generation underlie the association between cardiovascular diseases and renin-angiotensin system gene polymorphisms?
The finding of polymorphic sites in the functional promoter of the human AT1 locus will be beneficial to the study of the role of the AT1 receptor gene in hypertension and other cardiovascular diseases.
While the AT1-receptor polymorphism may not cause cardiovascular disorders directly, it can perhaps contribute to a process that is started by other factors, such as increased activity or uptake by tissues of plasma renin, which leads to local activation of the renin-angiotensin system.