Calcium Sensitization in Vascular Myocytes

Calcium Sensitization in Vascular Myocytes
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Calcium sensitization In Vascular Myocytes
1. Vascular smooth muscle agonists can raise the cytosolic free Ca2 through
a. inositol trisphosphate (IP3) mediated release of an intracellular Ca2 store.
b. action potentials mediated by sarcolemmal voltage-sensitive sodium channels.
c. diacylglycerol (DAG)-mediated activation of receptor-operated cation channels.
d. the activation of calmodulin.
e. Beta2-adrenergic receptor stimulation.
Calcium Sensitization In Vascular Myocytes
2. Large artery contraction is mediated by different pathways to resistance
vessel contraction, because
a. resistance vessels usually express very few voltage-sensitive Ca2 channels.
b. resistance vessels commonly show depolarization-dependent contraction.
c. large arteries often exhibit depolarization-independent contraction.
d. sympathetic stimulation inhibits contraction in small arterial vessels.
3. Calcium sensitization in vascular myocytes
a. is achieved by maintaining a high level of free Ca2 ions in the cytosol.
b. often contributes to the maintenance of vascular tone over long periods.
c. is mediated by the activation of myosin light chain phosphatase.
d. is brought about by receptor-induced activation of rhoA kinase.a. the α1-,α2-adrenoceptor blocker phentolamine reduces vascular tone.
b. Alpha1-adrenoceptors bind adrenaline more avidly than noradrenaline.
c. the activation of α1-adrenoceptors inhibits the phospholipase C pathway.
d. Alpha2-adrenoceptors activate the cAMP pathway.
e. Beta1-adrenoceptors are more common than β2 in most blood vessels.
f. Beta2-adrenoceptors bind adrenaline more avidly than noradrenaline.
5. Action potentials in vasomotor sympathetic fibers can trigger
a. the release of vesicles containing noradrenaline and ATP from varicosities.
b. fast excitatory junction potentials on vascular myocytes mediated by
α1-adrenoceptors.
c. a slow depolarization of vascular myocytes mediated by α1-adrenoceptors.
d. the hydrolysis of phosphoinositol bisphosphate (PIP2) in the myocyte
membrane.
e. the activation of vascular L-type Ca2 channels and/or non-selective
cation channels.
6. Vascular myocyte relaxation can be brought about by
a. adrenaline via an increase in intracellular cGMP.
b. the dephosphorylation of myosin heads by myosin light chain phosphatase.
c. a fall in the cytosolic free Ca2 concentration.
d. reduced sympathetic fiber activity.
e. vascular myocyte hyperpolarization.
7. Pharmacological agents that alter vascular tone include
a. adrenaline, which causes vasoconstriction in many tissues.
b. nitro dilators, such as glyceryl trinitrate, which raise intracellular cAMP.
c. sildenafil (Viagra), which raises intracellular cGMP.
d. losartan, which inhibits angiotensin II receptors to evoke vasodilatation.
e. nifedipine, which stimulates the sarcolemmal Ca2 pumps.
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