What enzyme is known to increase blood pressure in the RAAS and promote inflammation/fibrosis?

Study for the Pathophysiology Pulmonary Exam. Explore detailed questions with hints and explanations. Prepare thoroughly for your exam and enhance your respiratory pathophysiology knowledge!

Multiple Choice

What enzyme is known to increase blood pressure in the RAAS and promote inflammation/fibrosis?

Explanation:
The correct choice highlights the significance of angiotensin-converting enzyme (ACE) in the renin-angiotensin-aldosterone system (RAAS). ACE is responsible for converting angiotensin I, an inactive precursor, into angiotensin II, which has profound effects on blood pressure regulation and promotes vascular and tissue inflammation and fibrosis. Angiotensin II, generated by the action of ACE, acts as a potent vasoconstrictor, narrowing blood vessels and thus increasing blood pressure. It also stimulates the adrenal glands to release aldosterone, which leads to sodium and water retention, further contributing to increased blood volume and pressure. Additionally, angiotensin II has pro-inflammatory effects, which can promote the development of fibrosis in various tissues, including the heart and lungs. While renin is the enzyme that initiates the RAAS cascade by converting angiotensinogen to angiotensin I, it does not directly influence blood pressure as tangibly as ACE does through the production of angiotensin II. ACE II, conversely, refers to a different isoenzyme that has opposing effects to ACE, often related to vasodilation and protective cardiovascular effects, thus not aligning with the intention of increasing blood pressure or promoting inflammation and fibrosis. Understanding

The correct choice highlights the significance of angiotensin-converting enzyme (ACE) in the renin-angiotensin-aldosterone system (RAAS). ACE is responsible for converting angiotensin I, an inactive precursor, into angiotensin II, which has profound effects on blood pressure regulation and promotes vascular and tissue inflammation and fibrosis.

Angiotensin II, generated by the action of ACE, acts as a potent vasoconstrictor, narrowing blood vessels and thus increasing blood pressure. It also stimulates the adrenal glands to release aldosterone, which leads to sodium and water retention, further contributing to increased blood volume and pressure. Additionally, angiotensin II has pro-inflammatory effects, which can promote the development of fibrosis in various tissues, including the heart and lungs.

While renin is the enzyme that initiates the RAAS cascade by converting angiotensinogen to angiotensin I, it does not directly influence blood pressure as tangibly as ACE does through the production of angiotensin II. ACE II, conversely, refers to a different isoenzyme that has opposing effects to ACE, often related to vasodilation and protective cardiovascular effects, thus not aligning with the intention of increasing blood pressure or promoting inflammation and fibrosis.

Understanding

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