Blood Vessels 2 Flashcards
why is NPY preferentially release by high freq stim: Ca influx via ___ is ___?
Ca influx via N type Ca channels is localized; buffereing prevents diffusion in cytoplasm
NA release vs NPY release: Ca levels needed?
NA vesicles need high Ca for release, NPY vesicles sensitive to small increases in Ca
why is NPY preferentially release by high freq stim: location of vesicles?
high freq stimulation Ca influx overcomes buffering capacity of cytoplasm and reaches NPN vesicles that tend to be away from release sites. (NA closer)
kidney: renal nerves contain what NT? effect?
DA: renal vasodilation, increases glomerular filtration rate, sodium excretion
parasympathetic vasodilation in cerebral/cephalic arteries: what two NTs?
ACh and VIP.
cerebral vessel constriction via?
5HT innervation of cerebral vessels; powerful vasoconstrictor
cardiovacular response to IV adrenaline? due to what?
systolic + diastolic BP increase: due to alpha vasoconstrictor effect + B1 stimulation of heart
cardiovascular response as adrenaline falls? due to?
characteristic late fall in diastolic + mean BP: beta 2 effect on blood vessels
IV adrenaline: skeletal muscle? due to?
lots of b2 receptors = blood flow increases (B2 = relaxation aka vasodilation)
cellular mech. of a1 adrenergic effect: transduction mech?
a1 adrenergics: PLC = IP3 and DAG. IP3 causes increase in calcium, activates calmodulin, then MLCK (myosin light chain kinase)
once MLCK is activate what happens?
myosin light chain kinase + ATP = myosin is phosphorylated. now can interact with actin = contraction
cellular mech of b2 adrenergic effects (transduction pathway)?
B2 adrenergic = increased cAMP = PKA. PKA inhibits MLCK. end result is vasodilation
cAMP effect on vascular smooth muscle
RELAXATION (B2 adrenergicsL cAMP inhibits MLCK)
receptors for ACh on blood vessels? but? so dependent on?
receptors for ACh present on endothelial cells of blood vessels, but no parasympathetic cholinergic innervation = endothelium dependent relaxation of blood vessels
mAChR and blood vessels: mechanism?
activation of NOS, release of NO, interacts with guanylyl cyclase = vascular smooth muscle relxation