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+--- Thread: physio Q - mdkhayat (/showthread.php?tid=812128)
physio Q - mdkhayat - ArchivalUser - 08-08-2015
A drug that affects ion channel is given to an animal to determine its effect upon fluid intake due to angiotensin 2 .fluid intake due to angiotensin 2 and the drug is more then fluid intake with angiotensin 2 alone.
try to figure out the mechanism of drug.
1.activation of transient outward potasium currents
2.activation of voltage gated calcium currents
3.activation of voltage gated sodium currents
4.inhibition of delayed rectifying potasium currents
5.inhibition of cyclic AMP production
please explain
0 - ArchivalUser - 08-08-2015
increase fluid intake means it stimulate thirst centres with in brain.
here drug stimulates angiotensin 2 action.
intracellular ca stimulate angiotensin 2 action hence
2 may be the answer.
0 - ArchivalUser - 08-08-2015
angiotensin 2 stimulates thirst centres within brain.
0 - ArchivalUser - 08-08-2015
answer is 4.
can anybody explain?
0 - ArchivalUser - 08-08-2015
V2 receptor is a cAMP coupled.
remember, ADH action on V2 receptor will increase in cAMP==> activate protein kinase A this lead to insertion of water channel into the principle cells of the distal tubule.==> water retention.
inhibition of of V2 by a drug will have the opposite of the forementined above ==> thirst.
0 - ArchivalUser - 08-08-2015
if increse thirst due to renal effect then drug block angiotensin 2 effect.So more diuresis and more thirst.
see wiki
The role of the renin-angiotensin system[edit]
Angiotensin is involved in regulating aldosterone and is the core regulation.[11] Angiotensin II acts synergistically with potassium, and the potassium feedback is virtually inoperative when no angiotensin II is present.[12] A small portion of the regulation resulting from angiotensin II must take place indirectly from decreased blood flow through the liver due to constriction of capillaries.[13] When the blood flow decreases so does the destruction of aldosterone by liver enzymes.
Although sustained production of aldosterone requires persistent calcium entry through low-voltage-activated Ca2+ channels, isolated zona glomerulosa cells are considered nonexcitable, with recorded membrane voltages that are too hyperpolarized to permit Ca2+ channels entry.[2] However, mouse zona glomerulosa cells within adrenal slices spontaneously generate membrane potential oscillations of low periodicity; this innate electrical excitability of zona glomerulosa cells provides a platform for the production of a recurrent Ca2+ channels signal that can be controlled by angiotensin II and extracellular potassium, the 2 major regulators of aldosterone production.[2] Voltage-gated Ca2+ channels have been detected in the zona glomerulosa of the human adrenal, which suggests that Ca2+ channel blockers may directly influence the adrenocortical biosynthesis of aldosterone in vivo. [14]
0 - ArchivalUser - 08-08-2015
what's your answer? correct answer is 4.
may be related to depolarization of the cell.
0 - ArchivalUser - 08-08-2015
too many wording in this question make it sounds like too complicated. the question is very simple.
the key words to answer this question is thirst(increase water intake).
angiotensin II mechanism of action is increase of IP3 ==> inc in Ca2+
aldosterone is steroid hormone. no second messanger.
so the only action of drug that decrease in cAMP is blocking V2 receptor.
0 - ArchivalUser - 08-08-2015
yes then it is 4
drug blocks delayed rectifying potasium currents in collecting duct cell - inc k within cell (more positive charge)-inhibit Na absorption by collecting duct cell.
0 - ArchivalUser - 08-08-2015
prilosec,your choice is 5 ,but the answer is 4.