a*********f
发帖数: 101 | 1 脑子有点不听使唤了，哪位能帮忙解释一下吗？谢谢。 | k**e
发帖数: 2728 | 2 wiki says:
Acetylcholine is normally released by the parasympathetic nervous system (PS
NS) at rest, and causes dilation of the coronary arteries. While acetylcholi
ne induces vasoconstriction of vascular smooth muscle cells through a direct
mechanism, acetylcholine also stimulates endothelial cells to produce nitri
c oxide (NO). NO then diffuses out of the endothelial cells, stimulating rel
axation of the nearby smooth muscle cells. In healthy arterial walls, the ov
erall indirect relaxation in
【在 a*********f 的大作中提到】
: 脑子有点不听使唤了，哪位能帮忙解释一下吗？谢谢。
| a******a
发帖数: 57 | 3 Hyperventilation leads to respiratory alkalosis, and decreased level of
hydrogen ion. For vascular smooth muscle cells, hydrogen ion antagonizes
calcium; therefore, decreased level of hydrogen results in enhaced muscle
contraction.
FYI http://circ.ahajournals.org/cgi/reprint/58/1/56.pdf | a*********f
发帖数: 101 | 4 谢谢您的回复。
那篇文献里提到：H+ Ca2+竞争transmembrane calcium transport system同一结合位
点。所以H+减少，and/or Ca2+增加会导致血管收缩。
但是BRS physiology 4th edition Page 185提到：H+ 和Ca2+ 竞争albumin结合位点.
所以呼碱时，H+减少，更多的free calcium将会与albumin结合，血浆free Calcium浓
度降低，导致tingling, numbness和muscle spasm.
是不是说free Calcium对骨骼肌和平滑肌的作用是不同的？
【在 a******a 的大作中提到】
: Hyperventilation leads to respiratory alkalosis, and decreased level of
: hydrogen ion. For vascular smooth muscle cells, hydrogen ion antagonizes
: calcium; therefore, decreased level of hydrogen results in enhaced muscle
: contraction.
: FYI http://circ.ahajournals.org/cgi/reprint/58/1/56.pdf
| a*********f
发帖数: 101 | 5 谢谢您的回复。
这是kaplan q bank里的一道题。
我记得kaplan pharmacology video里面说的和您提到的有点不同。
ACh对心脏的直接作用是负的变时变力变传导。副交感神经不直接支配血管。但是血管
内皮有M3型胆碱能受体。如果i.v. ACh，激活Gq，释放NO，导致血管舒张。
有没有可能是冠脉的自身调节作用。心输出量减少，心肌氧耗减少，所以冠脉收缩。
这与肾脏和脑的自我调节不同。肾脏和脑血管是灌注压增大，血管收缩，灌注压减少，
血管扩张。 | a******a
发帖数: 57 | 6 Skeletal muscle cells are innervated by neurons, and their contraction are
dominated by neuromuscular transmitters, eg Ach. Hypocalcemia can directly
increase neuronal excitablity, thus, leads to enhanced skeletal muscle
contraction. However, I do not personally know in much detail about how does
hypocalcemia alter neuronal excitability.
【在 a*********f 的大作中提到】
: 谢谢您的回复。
: 这是kaplan q bank里的一道题。
: 我记得kaplan pharmacology video里面说的和您提到的有点不同。
: ACh对心脏的直接作用是负的变时变力变传导。副交感神经不直接支配血管。但是血管
: 内皮有M3型胆碱能受体。如果i.v. ACh，激活Gq，释放NO，导致血管舒张。
: 有没有可能是冠脉的自身调节作用。心输出量减少，心肌氧耗减少，所以冠脉收缩。
: 这与肾脏和脑的自我调节不同。肾脏和脑血管是灌注压增大，血管收缩，灌注压减少，
: 血管扩张。
| w********b
发帖数: 356 | 7 Both endothelium and smooth muscle have receptors for Ach. The endothelium
receptors cause NO,PGI2 and EDHF production, producing endothelium-mediated
dilation. The smooth muscle receptors, however, cause contraction. At
lower concentrations of Ach, the endothelium receptors are activated and
produce dilation. At higher conc of Ach, the smooth muscle receptors are
activated and produce constriction. |
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