Ion channels in the renal vasculature
K+ channels in renal vasculature
We have found that inhibition of single types of K+ channels has only minor effects on renal hemodynamics whereas inhibition of several types of K+ channels causes massive renal vasoconstriction. We suggest that inhibition of K+ channels mediate the action of vasoconstrictors e.g. angiotensin II. We investigate whether PKC mediated inhibition of K+ channels has a role in this mechanism.
K+ channels in hypertension
The function and expression of K+ channels in the renal vasculature is changed during hypertension. This may contribute to the increased renal vascular resistance. We have shown that vascular K+ channel expression is altered during diet-induce hypertension. We investigate if function is also changes in rats with genetic and diet induced hypertension.
Agonist stimulation and TRP channels in renal vasculature
Only 50% of the norepinephrine induced Ca2+ entry is mediated via voltage sensitive L-type channels in renal preglomerular resistance vessels. We hypothesize that agonist induced Ca2+ entry is partially mediated by non-selective cation channels of the TRP-type. We also hypothesize that the voltage sensitive Ca2+ channels are activated by Na+ and/or Ca2+ currents mediated via TRP channels.
Ca2+ channels in renal vasculature
Renal autoregulation depends on Ca2+ entry through voltage gated Ca2+ channels in the preglomerular arterioles. However, the mechanism behind constriction of the efferent arteriole is different. In genetically modified mice lacking expression of either L-type or T-type Ca2+ channels in the vasculature, we investigate the effect of increases in renal perfusion pressure on the afferent and efferent diameter. Experiments are performed in absence or presence of drugs known to affect renal autoregulation.