Minoxidil's mechanism of action on blood pressure as a potassium channel opening molecule

Research
1

Precise pharmacology to my knowledge. Always check against a potential error though:

Minoxidil (Oral route) → SULT1A1 → Minoxidil Sulfate → Opening of potassium channels → Closure of Voltage Gated Calcium Channels → Hyperpolarization of cell membranes → Reduction of intracellular calcium (ca2+) → Decrease in formation of calcium calmoludin protein-ligand complex → Reduced activation of myosin light chain kinase → Reduced phosphorylation of the myosin light chains → (this is where minoxidil differentiates, blood pressure vs hair growth medicine) Failure to contract vascular smooth muscles → Relaxation of arterioles → Significant drop in blood pressure (typically at high dose only though, eg. well above 5mg). → Induction of reflex tachycardia for the compensation of decrease in blood pressure, possible downstream effects (eg. fluid retention, pericardial effusion etc.)

2

I’m having trouble parsing this but I think the sequence is inverted (KATP opening causes K efflux and hyperpolarization first, which reduces VGCC opening)

and minoxidil is better described as an indirect KATP opener than a direct calcium channel blocker. There’s some nuance there because as a prodrug it’s different than its active sulfated metabolite.

and SULT1A1 (with possible contribution from other SULT isoforms like SULT1A3) is the more standard sulfotransferase named in minoxidil activation, especially in hair follicles