Nitric oxide donor sodium nitroprusside dilates rat small arteries by activation of inward rectifier potassium channels.

The role of vascular smooth muscle inward rectifier K+ (K(IR)) channels in the mechanisms underlying vasodilation is still unclear. The hypothesis that K(IR) channels are involved in sodium nitroprusside (SNP)-induced dilation of rat-tail small arteries was tested. SNP relaxed tail small arteries with an EC50 of 2.

Rho kinase inhibition partly weakens myogenic reactivity in rat small arteries by changing calcium sensitivity.

The hypothesis that Rho kinase is involved in myogenic reactivity was investigated in pressurized rat tail small arteries using videomicroscopic diameter determination and calcium fluorimetry. The potent Rho kinase inhibitor Y-27632 reversibly increased vessel diameter at 80 mmHg without changing the intracellular calcium concentration ([Ca](i)) shifting the relationship between diameter change and [Ca](i) to higher calcium levels. Neither endothelium removal nor inhibition of neural transmission affected the Y-27632-induced effect.

Protons inhibit the BK(Ca) channel of rat small artery smooth muscle cells.

The regulation of the activity of calcium-activated potassium (BK(Ca)) channels by intracellular proton ions (pH(i)) was investigated using the patch-clamp technique in smooth muscle cells freshly isolated from rat tail small arteries. Single-channel conductance and voltage dependence of activation were not different at pH(i) 7.0, 7.

4-aminopyridine affects rat arterial smooth muscle BK(Ca) currents by changing intracellular pH.

The hypothesis whether or not 4-AP can affect vascular smooth muscle BK(Ca) currents was tested using the patch-clamp technique, pH- and calcium-fluorimetry, and freshly isolated rat arterial smooth muscle cells. Application of 4-AP reversibly inhibited BK(Ca) currents at an intracellular calcium ([Ca](i)) of 250 nM with a half-block of 2. 5 mM at +50 mV.