Myoendothelial communication in the renal vasculature and the impact of drugs used clinically to treat hypertension
Publikation: Bidrag til tidsskrift › Review
The renal vasculature has many peculiarities including highly irregular branching. Renal blood flow must sustain adequate perfusion and maintain a high glomerular filtration. Renal autoregulation helps control renal blood flow. The local autoregulatory mechanism, tubuloglomerular feedback, elicits a vasoconstriction that can be found not only in neighboring nephrons but over large areas of the kidney indicating that the renal vasculature supports strong conduction of vascular responses. The basis for conduction is intercellular communication through gap junctions. The endothelium is strongly coupled and serves as a vascular conduction highway leading the signal to the vascular smooth muscle cells through myoendothelial coupling. Extensive intercellular coupling is also found in renin secreting cells where gap junctions seem to tie the cells together to improve control of renin secretion. Lack of coupling leads to dysregulation of renin secretion and hypertension. However, the activity of the renin-angiotensin system also controls gap junction expression in the kidney. Treatment reducing angiotensin II activity, as used in hypertension treatment, can affect expression of renal and vascular gap junction.
|Tidsskrift||Current Opinion in Pharmacology|
|Status||Udgivet - 2019|
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