angiotensinkinon

Angiotensinkinon is not a standard term in current physiology or pharmacology. It does not denote a clearly defined molecule in reputable nomenclature. If you encounter the term, it is most likely a misspelling or a mistaken reference to components of the renin–angiotensin system, especially angiotensinogen, the liver-derived precursor of angiotensin peptides.

The renin–angiotensin system regulates blood pressure, electrolyte balance, and fluid homeostasis. Angiotensinogen is cleaved by renin to form angiotensin I; angiotensin-converting enzyme (ACE) then converts angiotensin I into angiotensin II, the principal effector peptide. Angiotensin II acts on AT1 and AT2 receptors to cause vasoconstriction, aldosterone release, sodium retention, and sympathetic activation. A counter-regulatory axis exists via angiotensin (1-7) and the Mas receptor, which tends to oppose some effects of angiotensin II.

Clinical relevance: The renin–angiotensin system is a major therapeutic target in hypertension, heart failure, chronic kidney disease, and some forms of diabetic nephropathy. Pharmacologic agents include ACE inhibitors, angiotensin II receptor blockers (ARBs), and direct renin inhibitors, which reduce the production or action of angiotensin II.

In sum, the term angi otensinkinon is not standardized; for reliable information, consider angiotensinogen or the angiotensin peptides within the renin–angiotensin system. If a specific source uses the term, it should be consulted to determine the intended concept.