The kidney is the core target organ of the renin-hypertensin system. Endogenous hypertensin participates in the regulation of renal hemodynamics, water-electrolyte metabolism, and glomerular filtration function. By precisely modulating the RAAS pathway, angiotensin injection can improve pathological renal conditions and protect renal function. It is mainly used in the treatment of renal diseases such as postoperative complications of hereditary polycystic kidney disease and sepsis-associated acute kidney injury, and demonstrates unique advantages especially in patients with refractory hypotension complicated with renal dysfunction.

1.1 Treatment of Refractory Hypotension After Hereditary Polycystic Kidney Disease Surgery

Autosomal recessive polycystic kidney disease (ARPKD) is a rare hereditary cystic kidney disorder. In severe cases, massive enlargement of bilateral kidneys compresses the thoracic and abdominal cavities, requiring bilateral nephrectomy to relieve symptoms.

Postoperative hypotension is a common severe complication in pediatric patients, particularly in anephric infants, where traditional vasopressors often yield unsatisfactory results. As a potent vasoconstrictor, the product activates the AT1 receptor on vascular endothelium, constricting systemic arterioles and increasing vascular resistance, thereby rapidly elevating mean arterial pressure (MAP).

1.2 Adjunctive Therapy for Sepsis-Associated Acute Kidney Injury

Sepsis-associated acute kidney injury (SA-AKI) is a frequent complication in critically ill patients. Its core pathological mechanism is systemic inflammatory response induced by sepsis, leading to renal vasodilation and hypoperfusion, followed by decreased glomerular filtration function. The product improves renal hemodynamics by constricting renal blood vessels and elevating glomerular perfusion pressure, while inhibiting systemic inflammatory response, alleviating renal tissue damage, and assisting in the restoration of renal function.

The core pathological basis of myocardial infarction and coronary heart disease is coronary atherosclerosis, vascular stenosis or occlusion, leading to myocardial ischemia and hypoxia, myocardial injury, and even necrosis. Through mechanisms including anti-inflammation, inhibition of cardiomyocyte apoptosis, and improvement of myocardial remodeling, angiotensin injection plays a vital role in acute-phase treatment of myocardial infarction and secondary prevention of coronary heart disease, reducing the risk of long-term cardiovascular events and improving prognosis.

2.1 Acute-Phase Treatment of Acute Myocardial Infarction

Following acute myocardial infarction (AMI), myocardial ischemia and hypoxia trigger severe inflammatory response, cardiomyocyte apoptosis, and myocardial fibrosis, resulting in impaired cardiac function. Continuous intravenous infusion of hypertensin IV injection significantly inhibits the secretion of inflammatory factors (e.g., TNF-α, IL-1β), reduces cardiomyocyte apoptosis, improves mitochondrial function, and alleviates oxidative stress and DNA damage in cardiomyocytes, thereby reducing infarct size and preserving myocardial function.

2.2 Secondary Prevention of Coronary Heart Disease

The core goal of secondary prevention for coronary heart disease is to reduce the risk of cardiovascular events such as recurrent myocardial infarction, heart failure, and sudden cardiac death. By regulating the RAAS pathway, the product inhibits vascular smooth muscle cell proliferation, reduces atherosclerotic plaque formation, improves endothelial function, and attenuates inflammatory response, thus slowing the progression of coronary heart disease and lowering the risk of long-term cardiovascular events.

I. Initial Exploration (1898–1934)

The discovery of angiotensin originated from research on the relationship between the kidney and blood pressure. In 1898, Finnish physiologists Tigerstedt and his assistant Bergman at the Karolinska Institute first injected kidney extracts into rabbits and observed a marked rise in arterial vascular pressure. They named this pressor renal substance "renin", establishing an initial link between the kidney and vascular pressure regulation, though the mechanism of renin and its downstream products remained unclear.

Research progressed slowly for decades until 1934, when pathologist Harry Goldblatt successfully established an experimental hypertensive animal model by clamping the renal artery of dogs, confirming that renal ischemia induces sustained hypertension and suggesting the kidney secretes a circulating pressor substance, laying a critical experimental foundation for the subsequent discovery of hypertensin.

II. Key Breakthrough (1939)

In 1939, two independent research teams achieved simultaneous breakthroughs. Led by Eduardo Braun Menéndez at the University of Buenos Aires, a team used Goldblatt's model to isolate a pressor plasma substance from venous blood of ischemic kidneys, naming it "hypertensin" and verifying it as the product of an enzymatic reaction between renin and a plasma substrate. Concurrently, a team led by Irving H. Page at Eli Lilly Laboratories in Indianapolis accidentally discovered that renin reacts with plasma to produce a potent vasoconstrictor during renin purification, naming it "angiotonin". In 1943, they confirmed the enzymatic nature of this reaction and designated the plasma substrate as renin substrate.

III. Unified Nomenclature and Systematic Elucidation (1958 and Beyond)

As the two teams had identified the same substance under different names, Eduardo Braun Menéndez and Irving H. Page reached an agreement at a University of Michigan conference in 1958, unifying the terms "hypertensin" and "angiotonin" into "hypertensin", formally establishing its official name. Subsequently, scientists isolated various hypertensin subtypes, clarified its synthetic pathway, and gradually refined the regulatory mechanism of the renin-hypertensin system, providing clear targets for subsequent drug development and driving innovations in the treatment of hypertension, heart failure, and related diseases.