title: [Role of the kallikrein kinin system and its interrelationship with vasoactive systems in pregnancy].
abstract: Glomerular hyperfiltration and increased sodium reabsorption are key factors for the development of the fetus and placenta in pregnancy. These adjustments result from hemodynamic and renal factors involving vasoactive systems. It was demonstrated in rats that activation of KKS precedes the installation of glomerular hyperfiltration as aprotinin prevents the increase in glomerular filtration. In addition, individual or associated inhibition of specific kallikrein kinin system effectors, prostaglandins (PGs) and nitric oxide (NO), confirm the glomerular filtration rate dependence of KKS during pregnancy. It was also found that the renin-angiotensin system (RAS) contributes to glomerular hyperfiltration as this is affected by the administration of RAS blockers. The peak of hyperfiltration maximum inhibition was obtained by the blockade of both systems (KKS and RAS). In addition, strategies used to alter the glomerular hyperfiltration and increased sodium reabsorption during pregnancy, showed abnormalities in the development of the fetus and placenta, fewer offspring, more fetus resorptions and intrauterine growth retardation. KKS inhibitors associated with RAS or nitric oxide blockers showed the greatest impact. As a consequence, it was demonstrated that KKS plays a central role in the adaptation phenomenom that accompanies normal pregnancy. The interplay of KKS with several vasoactive systems, seem to arrange a network involved in the hemodynamic adaptations to allow the proper development of pregnancy and the fetus and placenta.
authors: Servicio de Nefrología Experimental, Instituto de Investigaciones Médicas Alfredo Lanari, Universidad de Buenos Aires. elioddo@yahoo.com.ar
authors: Elisabet
authors: E
authors: Oddo
authors: Elvira E
authors: EE
authors: Arrizurieta
mesh_terms: D000818:Animals; D007611:Aprotinin / Q000494:pharmacology; D005260:Female; D005919:Glomerular Filtration Rate / Q000502:physiology*; D016234:Kallikrein-Kinin System / Q000187:drug effects / Q000502:physiology*; D007668:Kidney / Q000098:blood supply / Q000503:physiopathology; D007678:Kidney Glomerulus / Q000098:blood supply; D009569:Nitric Oxide / Q000037:antagonists & inhibitors; D011247:Pregnancy; D011453:Prostaglandins / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D012084:Renin-Angiotensin System / Q000502:physiology*; D015842:Serine Proteinase Inhibitors / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism*; D012965:Sodium Chloride / Q000494:pharmacology; D014664:Vasodilation / Q000502:physiology
chemical_list: D011453:Prostaglandins; D015842:Serine Proteinase Inhibitors; D009569:Nitric Oxide; D012965:Sodium Chloride; D007611:Aprotinin; D012964:Sodium