A clinical approach in regression of glomerulosclerosis.

Abstract

The role of the renin angiotensin system (RAS) in hypertension and end organ damage has long been recognized. Angiotensin 1 converting enzyme inhibitors (ACEI) are superior to other antihypertensive agents in protecting the kidney against progressive deterioration, even in normotensive persons. Like ACEI, angiotensin II type 1 receptor antagonists (AT1RA) ameliorate or even reverse glomerulosclerosis in rat animal models. These findings suggest that Angiotensin II (Ang II) has nonhemodynamic effects in progressive renal disease. The RAS is now recognized to be linked to induction of plasminogen activator-inhibitor-1 (PAI-1), possibly via the AT4 receptor, thus promoting both thrombosis and fibrosis. Interactions of the RAS with aldosterone and bradykinin may have an impact on both blood pressure and tissue injury. The beneficial effect on renal fibrosis of inhibiting the RAS likely reflects the central role that angiotensin has in regulating renal function and structure by its various actions. This article explores the interaction of the renin angiotensin aldosterone system with PAI-1, and the potential significance of these interactions in the pathogenesis of progressive renal disease and remodeling of renal sclerosis.

• Authors: Marilena Stoian, Gabriela Radulian, Delia Chiţac, E Simion, V Stoica
• Journal: Romanian journal of internal medicine = Revue roumaine de medecine interne (Rom J Intern Med) Vol. 45 Issue 2 Pg. 215-8 ( 2007) ISSN: 1220-4749 [Print] Germany
• PMID: 18333378 (Publication Type: Journal Article, Review)

Chemical References

• Angiotensin II Type 1 Receptor Blockers
• Angiotensin-Converting Enzyme Inhibitors
• Plasminogen Activator Inhibitor 1
• Angiotensin II
• Aldosterone

Topics

• Aldosterone (physiology)
• Angiotensin II (physiology)
• Angiotensin II Type 1 Receptor Blockers (therapeutic use)
• Angiotensin-Converting Enzyme Inhibitors (therapeutic use)
• Animals
• Disease Models, Animal
• Disease Progression
• Glomerulosclerosis, Focal Segmental (drug therapy, physiopathology)
• Humans
• Plasminogen Activator Inhibitor 1 (metabolism)
• Rats
• Renin-Angiotensin System (physiology)