Mechanism of Hypoxia-induced Contraction of Porcine Renal Arteries

The mechanism of hypoxia-induced vessel contraction was studied in isolated porcine renal arteries （diameter： 1.5～2.0 mm）. The intact arteries exposed to Krebs solution aerated with hypoxic gas （95% N_2 and 5% CO_2; PO_2＝15.0±1.7mmHg） exhibited contraction followed by relaxation （a transient contraction）. Removal of endothelium attenuated the transient contraction. Removal of both endothelium and adventitia completely inhibited contraction induced by hypoxia. Phentolamine, 10^<-6>M, or α, β-methylene adenosine 5'-triphosphate （ATP）, 3×10＾<-6>M, did not significantly affect the hypoxia-induced contraction, indicating that norepinephrine and ATP in sympathetic nerve terminals may not be involved in hypoxia-induced contraction. Aspirin, 10＾<-6>M, or indomethacin, 10＾<-5>M, greatly attenuated the transient contraction. These findings suggest that cyclooxygenase related products derived from adventitia and/or endothelium may contribute to a transient contraction. Treatment with 10＾<-6>M nicardipine or Ca＾<2+>-free solution also attenuated the transient contractions, but the contraction of the arteries in response to hypoxia for 20～30 min was significantly potentiated by both treatments. These findings suggest that adventitia as well as endothelium modify the renal vascular response to hypoxia. It seems that renal arteries exhibit extracellular Ca＾<2+>-sensitive and-insensitive responses to hypoxia