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6 Cards in this Set
- Front
- Back
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Describe PANS regulation of CV function.
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explained multiple times already
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Explain why vagal nerve stimulation results in decreased HR at a much greater extent than an M receptor agonist or Ach
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a. Vagal nerve stimulation targets the nodal cells directly and activates Beta 1 receptors. However, if you administer an M receptor agonist or Ach, they will promote vasodilation by binding onto M3 receptors in smooth muscle which activate NO synthase producing NO → thereby decreasing blood pressure. The arterial baroreceptors will sense the decrease and try to increase CO by increasing HR (ANS reflex)
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Sketch a synapse between a postganglionic SANS nerve and a cardiac cell, and put in the steps involved in SANS neurotransmission, starting from neurotrans synthesis and ending with termination of neutrans activity.
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a. Neurotrans synthesis: “Tyra likes dope, not E” → Tyrosine → L-Dopa → Dopamine → Norepinephrine → Epinephrine
b. Neurotrans termination: reuptake into cells via transporters, COMT (outside cell) and MOA (inside cell) will degrade NE c. Autoreceptors- alpha-2 receptors can bind NE and inhibit further release of NE d. Heteroreceptors- M2 receptors on the synaptic terminal can bind ACh and therefore inhibit release of NE |
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Describe SANS regulation of CV function, and, for each major effect, name the receptor responsible for mediating the effect.
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a. Uses NE on nodal cells to increase activation of Ca channels (through Gs → adenyl cyclase → cAMP → pKA
i. Leads to increase in contractility b. Also increase If → increase HR c. Alpha receptors on arterioles promotes vasoconstriction d. Beta-2 receptors on skeletal muscle promotes vasodilation |
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Diagram the short-term and long-term systems responsible for protecting mean arterial blood pressure and, for each sympathetic and parasympathetic effect, indicate the receptor responsible for the reflex response.
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See picture
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Compare and contrast the effects of Epi and NE on BP and explain the basis of the differences between them
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a. NE → vasoconstriction via alpha-2 receptors on arterioles; vasoconstriction via alpha-2 receptors on venules/veins → increase venous return and therefore CO; increased contractility + HR on B-1 receptors in heart
b. Epi → activates same receptors as NE, but also B-2 in the skeletal muscles leading to vasodilation → thus, no change in HR usually observed. However, in high enough vasodilation, you could activate PANS reflex |
