The kidney regulates salt and water excretion and therefore kidney function is crucial in the regulation of blood pressure.
In the western world hypertension is a major health problem which has fatal consequences such as myocardial infarction, stroke and renal failure. The mechanisms behind the development and maintenance of hypertension are largely unknown despite intense research.
We suggest that changes in kidney function are involved in development of hypertension. This is supported by the fact that transplantation of kidneys from hypertensive patiens to normotensive patiens makes recipients hypertensive and vice versa.
We investigate the mechanisms regulating the excretory function of the kidney. This includes control of renal blood flow (RBF), glomerular filtration rate (GFR) and the renin-angiotensin system. We focus on intercellular communication via gap junctions, vascular regulation via K+ and Ca2+ channels, the sympathetic nervous system and changes in renal autoregulation
Intercellular communication in the kidney
Gap junctions between vascular smooth muscle cells and endothelial cells allow signals to travel between cells. Stimulation in one part of an arteriole leads to a response at a distant site. We have shown that this signal conduction participates in renal autoregulation. Also, the control of the renin-angiotensin system depends on functional gap junctions. This implicates gap junctions as a major contributor in the control of renal hemodynamics.
Ion channels in the renal vasculature
Ion channels in the renal resistance vessels affect the cell membrane potential. This leads to changed permeability of voltage sensitive Ca2+ channels and vascular tone. We have shown that in diet induced and genetically induced hypertension the expression and function of vascular K+ channels is changed. This implicates K+ channels as a major contributor in the control of renal hemodynamics.
Renal effects of GLP-1
The gut hormone GLP-1 also has renal effects. It increases renal blood flow, glomerular filtration rate and sodium excretion. We have shown that GLP-1 receptors are expressed in renal vascular smooth muscle cells but expression seems to be reduced in hypertensive animals. We also show that GLP-1 attenuates renal autoregulation. This implicates GLP-1 as a major contributor in the control of renal hemodynamics.
Part of the research theme
Charlotte Mehlin Sørensen