Mechanism of action of angiotensin II in human isolated subcutaneous resistance arteries

摘要: 1. Human isolated subcutaneous arteries were mounted in a myograph and isometric tension measured. In some experiments, intracellular calcium [Ca(2+)]i was also measured using fura-2. 2. Angiotensin II (100 pM - 1 microM) increased tone concentration-dependent manner. The effects of angiotensin nM) inhibited by an AT1-receptor antagonist, candesartan pM). 3. Ryanodine (10 microM), had no effect on II-induced responses, but removal extracellular Ca(2+) abolished rise tone. Inhibition entry Ni(2+) (2 mM), responses. dihydropyridine, L-type channel amlodipine only partially attenuated 4. protein kinase C (PKC) chelerythrine (1 or overnight exposure to phorbol ester (PDBu; 500 contraction. 5. Genistein tyrosine inhibitor, contraction, did not inhibit the [Ca(2+)]i, suggesting that at this concentration it affected sensitivity contractile apparatus. affect responses norepinephrine (NE) high potassium (KPSS). 6. A selective MEK PD98059 (30 both contraction NE KPSS. 7. AT1 activation causes influx via channels dihydropyridine-insensitive route, does release from sites. Activation kinase(s) ERK 1/2 pathway, classical novel PKC, play role human resistance arteries.