Vasoconstrictors may act through inhibition
of K+ channels leading to depolarization.
Endothelin, vasopressin and angiotensin II
may act, in part through inhibition of KATP
channels via PKC activity (both direct and
indirect) through inhibition of PKA.
KATP channels may be activated in several
pathologic states:
(1) Coronary, cerebral and skeletal muscle
arteries dilate in response to hypoxia probably
through alteration in ATP levels.
(2) Ischemia/reperfusion: Reactive hyperemia
may cause increased adenosine
(3) Acidosis activates KATP
(4) Endotoxins and septic shock can activate
KATP