Question

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

Julian99

Membership Revoked
Removed
5+ Year Member
Joined
Dec 14, 2016
Messages
9
Reaction score
0
A study of a new antihypertensive drug is being conducted in experimental animals. It is found that one of its pharmacologic effects is a decrease in plasma renin activity and serum angiotensin II concentration. A possible mechanism of action that would produce this effect is blockade of which of the following?
(A) α1-Adrenoreceptor (B) β1-Adrenoreceptor (C) Angiotensin-converting enzyme (D) Angiotensin II AT1 receptor (E) Renal tubular Cl− reabsorption (F) Renal tubular Na+ reabsorption
why it is D, shouldn't it be C?
 
ACE comes from the lungs, and converts Angiotensin 1 to angiotensin 2

if the drug is affecting renin activity we are thinking a little farther back in the process of making Agtiotensin 1 from angiotensinogen

The drug may be in the class of Sartans as I believe that's the MOA

SOURCE: A plucky MS1 who did CV research for a few yrs


Sent from my iPhone using SDN mobile
 
A study of a new antihypertensive drug is being conducted in experimental animals. It is found that one of its pharmacologic effects is a decrease in plasma renin activity and serum angiotensin II concentration. A possible mechanism of action that would produce this effect is blockade of which of the following?
(A) α1-Adrenoreceptor (B) β1-Adrenoreceptor (C) Angiotensin-converting enzyme (D) Angiotensin II AT1 receptor (E) Renal tubular Cl− reabsorption (F) Renal tubular Na+ reabsorption
why it is D, shouldn't it be C?

I think the answer is B there are B1 receptors in the kidney, blocking them inhibit renin release
 
Top