Vasopressor meets vasodepressor
Since more than 8 months, the history of a paradigm shift in GPCR pharmacology is number 1 in its scientific domain.
More than a decade ago, our scientific findings initiated a paradigm shift in G-protein-coupled receptor (GPCR) pharmacology. In the year 2000, we found that the AT1 receptor (AT1R) for the vasopressor angiotensin II and the B2 receptor (B2R) for the vasodepressor bradykinin can form a functional heteromeric complex in vivo, which shows enhanced AT1R-stimulated signaling relative to the receptor monomer. Those data challenged the prevailing concept of GPCR function, which stated that GPCRs such as AT1R and B2R exist predominantly as monomers.
In a subsequent study in the year 2001, we provided the first evidence for a pathophysiological role of GPCR heteromerization. We found that increased AT1R-B2R heterodimerization contributes to the enhanced angiotensin II-stimulated vasopressor response of pregnant women with preeclampsia, a life-threatening pregnancy-associated form of hypertension.
After more than a decade of scientific discussions, the concept of AT1R-B2R heterodimerization was finally accepted. The exciting history of AT1R--B2R heteromer discovery and its pathophysiological role are of great interest for the scientific community.
On January 26 (2016) our publication titled "Vasopressor meets Vasodepressor" was again recognized the number 1 publication in its scientific domain according to BioMedLib (Virginia, USA). external pageRead morecall_made