A 55-year-old woman is treated with ramipril for primary (essential) hypertension. Her blood pressure decreases to normal value over several weeks of treatment. The patient seems to be compliant with her medication and experiences no significant side effects. She has no other medical issues and takes no other medications. She does not use tobacco, alcohol, or illicit drugs. Physical examination shows no abnormalities. Which of the following is the most likely combination of changes in response to this patient's treatment (AT = angiotensin) ?

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11ec160b_3c73_8df6_9249_6103a8e85e21_MD0001_00 The renin-angiotensin-aldosterone system (RAAS) is one of the most important neurohormonal systems, regulating arterial blood pressure and sodium and fluid content in the body. In response to decreased sodium, fluid volume, or arterial blood pressure, renin is released from the kidneys, converting angiotensinogen to angiotensin I. Subsequently, angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II. Angiotensin II then increases aldosterone secretion from the adrenal cortex, leading to increased sodium and fluid retention in the collecting tubules of the kidneys. Angiotensin II is also a potent vasoconstrictor that ultimately increases systemic vascular resistance and arterial pressure. Angiotensin II itself is involved in 2 negative feedback mechanisms that help regulate the RAAS. In short-loop negative feedback, elevated angiotensin II stimulates the angiotensin receptors on juxtaglomerular cells to inhibit renin release. In long-loop negative feedback, increased blood pressure and sodium levels (due to angiotensin II) eventually decrease renin release via intrarenal baroreceptor and macula densa pathways, respectively. ACE inhibitors such as ramipril block ACE and decrease the conversion of angiotensin I to angiotensin II, effectively blocking arteriolar vasoconstriction and aldosterone secretion. In addition to decreased blood pressure and sodium levels, decreased angiotensin II levels also interfere with negative feedback mechanisms, ultimately activating the RAAS to promote renin release. ACE is also responsible for the breakdown of bradykinin; therefore, ACE inhibitors lead to increased bradykinin levels, which are thought to cause the characteristic ACE inhibitor-induced cough. Educational objective: Angiotensin-converting enzyme (ACE) inhibitors block the effect of ACE, decreasing angiotensin II and aldosterone levels. By decreasing angiotensin II levels, ACE inhibitors directly interrupt negative feedback loops, thereby increasing renin and angiotensin I levels. ACE is also responsible for the breakdown of bradykinin; ACE inhibitors therefore increase bradykinin levels.

A 55-Year-Old Woman Is Treated with Ramipril for Primary (Essential)