Stimulation of the renal kallikrein-linin system by vasoactive substances and its relationship to the excretion of salt and water.
Large doses of angiotensin when infused intravenously or into the renal artery cause natriuresis. The initial effect is release of prostaglandin (probably PGE) and this leads to release of kallikrein. This latter step can be inhibited by noradrenaline. Activation of the kallikrein/kinin system is followed by release of a large molecular weight natriuretic hormone which is absent in glomerulonephritis. A small molecular weight hormone follows the large one and probably effects natriuresis by inhibition of renal Na/K ATPase. This inhibition is reversed by noradrenalint or renal nerve stimulation. Natriuresis is the result of a chain reaction and not a single specific natriuretic hormone.
D000818:Animals; D004285:Dogs; D007213:Indomethacin / Q000494:pharmacology; D007444:Inulin / Q000378:metabolism; D007610:Kallikreins / Q000502:physiology*; D007668:Kidney / Q000187:drug effects / Q000502:physiology*; D007705:Kinins / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology; D009994:Osmolar Concentration; D012964:Sodium / Q000378:metabolism / Q000652:urine; D014556:Urine; D010130:p-Aminohippuric Acid / Q000378:metabolism
D007705:Kinins; D007444:Inulin; D012964:Sodium; D007610:Kallikreins; D009638:Norepinephrine; D007213:Indomethacin; D010130:p-Aminohippuric Acid