Renina

Renina, widely known in English as renin, is an aspartyl protease enzyme produced by the juxtaglomerular cells of the kidney. It catalyzes the rate-limiting step of the renin–angiotensin–aldosterone system (RAAS) by cleaving angiotensinogen to form angiotensin I, a decapeptide that is subsequently converted to angiotensin II, a potent vasoconstrictor and stimulant of aldosterone release. Through this pathway, renina helps regulate blood pressure, electrolyte balance, and fluid homeostasis.

Renina is synthesized as prorenin, an inactive precursor secreted by juxtaglomerular cells. Prosegment removal yields active renin, though prorenin can also be activated non-proteolytically or by receptor binding in certain tissues. Circulating levels can be measured as plasma renin activity or direct renin concentration, depending on assay methodology.

Renina release is tightly regulated by multiple signals. Sympathetic nervous system activity, via beta-1 adrenergic receptors, increases renin secretion. Decreased renal perfusion pressure and reduced delivery of sodium chloride to the macula densa stimulate release as well. Angiotensin II provides negative feedback by inhibiting further renin production.

Clinical relevance of renina centers on its role in hypertension and electrolyte disorders. Plasma renin activity or direct renin concentration are used to evaluate hypertensive states and suspected mineralocorticoid disorders. Renin-secreting tumors, though rare, cause secondary hypertension. Treatments targeting the RAAS include ACE inhibitors, angiotensin II receptor blockers, and direct renin inhibitors such as aliskiren.

In humans, the kidney is the primary source of circulating renin, with smaller amounts produced in other tissues. Dysregulation of renin contributes to disorders of blood pressure and electrolyte balance, and ongoing research continues to clarify its broader physiological and pathological roles.