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15 Cards in this Set
- Front
- Back
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ARB's block the AT1 receptor thereby inhibiting what are considered to be the more harmful angiotensin II effects during the development of pathologies such as Hypertension and HF. The AT2 receptor is still available for binding however and elicits more favorable effects. Name 3 ARB's
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Losartan
Valsartan Candesartan |
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ARB's have similar therapeutic effects to ACE inhibitors. Name these effects.
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Decreased Na reabsorption from the PCT, and TAL
Decreased Aldosterone secretion and therefore decrease Na reabsorption from the CD Decreased Vasoconstriction Decreased ADH secretion Decreased SNS output |
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What are 2 differences in effect between ACE inhibitors and ARB's?
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- ARB's have no effect on Bradykinin so no cough and no angioedema
- Angiotensin II is still being produced and at an increased amount bc of renin compensation. This is shunted to the AT2 receptor. |
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What are the adverse effects of ARB's?
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Same as ACE inhibitors but no cough or angioedema
- Increased renin release - Hyperkalemia with K sparing diuretics - teratogenicity - precipitate renal failure in patients with bilateral renal artery stenosis |
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Direct Renin Inhibitors are a new drug class that inhibit renin activity with no effect on bradykinin. Name an example of this type of drug.
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Aliskiren
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What are the 4 main mechanisms by which vascular tone is regulated?
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- Vascular Endothelium (Endothelin vs NO)
- ANS (SNS - Epi/NE - alpha1/beta2 -> net constriction) - Neurohormonal (Epi, NP, AngioII, ADH) - Local systems |
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What 2 mechanisms can cause Ca-mediated VSMC contraction?
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- Depolarization causing opening of L-type Ca channels in the Sarcolemma
- AT1 receptor stimulation will lead to downstream signaling and opening of Ca channels on SR |
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In the VSMC, how does Ca cause smooth muscle contraction?
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Ca binds Calmodulin
Ca-Cal complex activates MLCK which phosphorylates MLC Phosphorylation of MLC induces cross bridge formation with actin |
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What is a key component that differentiates smooth muscle cells from cardiac muscle cells?
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The presence of the Troponin complex in cardiac muscle cells.
Kinase system instead |
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In the VSMC, how does relaxation occur?
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NO permeates the cell membrane, activates Guanylyl Cyclase which increases cGMP production.
cGMP activates MLC-phosphatase which de-phosphorylates MLC |
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Describe the process by which NO is released from the Endothelial Cell.
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An agonist such as Ach or Bradykinin will bind to a receptor on the Endothelial Cell. This will cause Ca influx through L-type Ca channels and the SR. Ca binds to Calmodulin which activates eNOS which produces NO from Arg.
In addition, NO activates K channels inducing K efflux from the cell and hyper-polarizing the cell making it more difficult to depolarize and contract. |
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What is endothelin? What does it do?
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Synthesized by the endothelium and released to the smooth muscle cells. Activates ETA and ETB cells to induce smooth muscle contraction.
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Describe the feedback loop associated with Endothelin.
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It can bind an ETB receptor on endothelial cells and induce NO synthesis which causes relaxation.
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What increases endothelin expression?
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Angiotensin II, ADH and mechanical stress
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What decreases endothelin expression?
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NO, NP, Prostacyclins
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