Hypertension & Kidney Disease

• Persistent Elevation:
  Chronic high levels of angiotensin II are linked to high blood pressure, chronic kidney disease, and conditions that activate the renin–angiotensin system (RAS).

Inflammatory Effects

• Pro-Inflammatory Role:
  Angiotensin II is pro-inflammatory and might contribute to endothelial dysfunction in autoimmune vasculitis or chronic inflammatory states.

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Pharmacologic Intervention & RAS Underactivity

• Pharmacologic Intervention:
  Use of ACE inhibitors or ARBs will reduce angiotensin II levels.
• RAS Underactivity:
  Rare conditions with reduced renin production may lead to low angiotensin II.

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Age-Related and Pregnancy Influences on RAS

• Aging Effects:
  Changes in vascular reactivity and kidney function with aging may alter baseline angiotensin II.
• Physiologic Adjustments in Pregnancy:
  Pregnancy can influence RAS components, though typically in a well-regulated manner.

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Renin–Angiotensin–Aldosterone System (RAAS)

All these markers are components of the Renin–Angiotensin–Aldosterone System (RAAS), which regulates blood pressure, fluid balance, and electrolyte homeostasis:

• Renin is produced by the kidneys and initiates the process by converting angiotensinogen into angiotensin I.
• Angiotensin I serves as a precursor that is converted by Angiotensin Converting Enzyme (ACE) into the active Angiotensin II.
• Angiotensin II is a potent vasoconstrictor that also stimulates the adrenal cortex to secrete Aldosterone.
• Aldosterone, measured in both blood and urine, acts on the kidneys to enhance sodium and water retention, thereby increasing blood volume and pressure.

Together, these components work in a coordinated cascade to maintain cardiovascular stability and fluid balance.

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