NSG 862: CV II | QUESTIOS AND
ANSWERS | LATEST UPDATE
What is Nitric Oxide (NO) and what does it do? -NO is a chemical messenger involved in:
*Homeostatic activity in the modulation of CV tone
*Platelet regulation
*Neurotransmitter function in the CNS
*GI smooth muscle relaxation
*Immune regulation
How can NO be given therapeutically, and what -inhalation
effect does it produce? - relaxation of the pulmonary arterial vasculature
How is nitric oxide (NO) synthesized? L-arginine (amino acid) by NO synthetase (enzyme)
How does NO cause vasodilation? 1. Diffuses into precapillary resistance arterioles where it induces
guanylate cyclase to increase cGMP concentration
- produces vasodilation
, How does cyclic GMP (cGMP) induce smooth -cGMP induces smooth muscle relaxation by multiple mechanisms,
muscle relaxation? including:
1. Inhibits calcium entry into the cell and decreases
intracellular calcium concentrations
2. Activates K channels--> hyperpolarization and relaxation of smooth
muscle
3.Stimulates a cGMP-dependent protein kinase G that activates myosin
light chain phosphatase, the enzyme that dephosphorylates myosin light
chains, which leads to smooth muscle relaxation
What happens to nitric oxide (NO) during stress, 1. As a result of stress, an inducible form of NO synthetase
and why is its half-time so short? can produce large amounts of NO, contributing to excessive
vasodilation
2. NO binds to the iron of heme-based proteins and is avidly bound
and
inactivated by hemoglobin
3. This leads to a half-time of less than 5 seconds under
normal physiologic conditions
Why does inhaled NO affect the pulmonary rapid uptake by hemoglobin
circulation but not the systemic circulation?
How do nitrovasodilators work? Nitrovasodilators (nitrates and nitroprusside) work through generation
of NO throughout the vasculature
What determines how much pulmonary -proportional to the degree of pulmonary vasoconstriction
arterial vasodilation NO causes?
*Someone with severe pulmonary HTN will have a greater response than
someone who does not.
When does NO have less effect on pulmonary if pulmonary vascular tone is not increased (such as in types of
vascular resistance? pulmonary hypertension other than “primary”)
How does inhaled NO usually improve Dilating vessels in alveoli- improving VQ matching
oxygenation?
ANSWERS | LATEST UPDATE
What is Nitric Oxide (NO) and what does it do? -NO is a chemical messenger involved in:
*Homeostatic activity in the modulation of CV tone
*Platelet regulation
*Neurotransmitter function in the CNS
*GI smooth muscle relaxation
*Immune regulation
How can NO be given therapeutically, and what -inhalation
effect does it produce? - relaxation of the pulmonary arterial vasculature
How is nitric oxide (NO) synthesized? L-arginine (amino acid) by NO synthetase (enzyme)
How does NO cause vasodilation? 1. Diffuses into precapillary resistance arterioles where it induces
guanylate cyclase to increase cGMP concentration
- produces vasodilation
, How does cyclic GMP (cGMP) induce smooth -cGMP induces smooth muscle relaxation by multiple mechanisms,
muscle relaxation? including:
1. Inhibits calcium entry into the cell and decreases
intracellular calcium concentrations
2. Activates K channels--> hyperpolarization and relaxation of smooth
muscle
3.Stimulates a cGMP-dependent protein kinase G that activates myosin
light chain phosphatase, the enzyme that dephosphorylates myosin light
chains, which leads to smooth muscle relaxation
What happens to nitric oxide (NO) during stress, 1. As a result of stress, an inducible form of NO synthetase
and why is its half-time so short? can produce large amounts of NO, contributing to excessive
vasodilation
2. NO binds to the iron of heme-based proteins and is avidly bound
and
inactivated by hemoglobin
3. This leads to a half-time of less than 5 seconds under
normal physiologic conditions
Why does inhaled NO affect the pulmonary rapid uptake by hemoglobin
circulation but not the systemic circulation?
How do nitrovasodilators work? Nitrovasodilators (nitrates and nitroprusside) work through generation
of NO throughout the vasculature
What determines how much pulmonary -proportional to the degree of pulmonary vasoconstriction
arterial vasodilation NO causes?
*Someone with severe pulmonary HTN will have a greater response than
someone who does not.
When does NO have less effect on pulmonary if pulmonary vascular tone is not increased (such as in types of
vascular resistance? pulmonary hypertension other than “primary”)
How does inhaled NO usually improve Dilating vessels in alveoli- improving VQ matching
oxygenation?
