Kininase II

Kininase II, also known as angiotensin-converting enzyme (ACE), is a crucial enzyme in the Renin-Angiotensin System (RAS) that plays a significant role in regulating blood pressure and fluid balance within the body. This enzyme is responsible for the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor that increases blood pressure. Additionally, kininase II degrades bradykinin, a peptide that promotes vasodilation and lowers blood pressure. Therefore, kininase II has a dual role in the physiological regulation of blood pressure and fluid balance.

Function

Kininase II is found in various tissues, including the lungs, kidneys, and heart, reflecting its systemic impact on blood pressure regulation. By converting angiotensin I to angiotensin II, it not only increases blood pressure through vasoconstriction but also stimulates the release of aldosterone from the adrenal gland. Aldosterone promotes sodium and water retention by the kidneys, further increasing blood pressure. The degradation of bradykinin by kininase II reduces its vasodilatory effect, complementing the blood pressure-raising actions of angiotensin II.

Clinical Significance

Given its pivotal role in blood pressure regulation, kininase II is a target for antihypertensive drugs, particularly ACE inhibitors. These drugs block the activity of kininase II, leading to decreased levels of angiotensin II and increased levels of bradykinin. This results in vasodilation, reduced blood volume, and, consequently, lower blood pressure. ACE inhibitors are widely used in the treatment of hypertension, heart failure, and chronic kidney disease.

Genetics

The gene encoding kininase II is located on chromosome 17q23.3. Variations in this gene can affect the activity of the enzyme, potentially influencing an individual's susceptibility to hypertension and the effectiveness of ACE inhibitors.

Research Directions

Research into kininase II continues to explore its broader implications in cardiovascular health, including its role in heart failure, kidney disease, and metabolic syndrome. Understanding the genetic and molecular mechanisms underlying its activity may lead to the development of more targeted therapies for cardiovascular diseases.

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