The Macula Densa and Juxtaglomerular Body in Cirrhosis

Plasma renin substrate sensitivity to oestrogens and oestrogen metabolism in cirrhosis

“…** Statistical difference (P < 0.01) between the mean values for normal and cirrhotic adults. Our finding that PRS is increased after oral administration of Moxestrol is in agreement with observations made with oestrogen derivatives in rats [5-71 and with oestrogen-containing oral contraceptives in women [8- Overconsumption of renin substrate could be considered a likely explanation as the plasma renin concentration in cirrhosis is probably high [21] ; however, in malignant arterial hypertension the plasma renin activity is high, and yet PRS remains normal or high [22]. Diminished synthesis of renin substrate is therefore a more likely explanation and is consistent with the decreased production of various plasma proteins produced by the liver, such as albumin [23] and coagulation proteins [24], in patients with cirrhosis.…”

Intrarenal Distribution of Plasma Flow in Cirrhosis as Measured by Transit Renography: Relationship with Plasma Renin Activity, and Sodium and Water Excretion

“…The mechanism whereby hyponatraemia increases renin secretion is probably related to sodium delivery to the macula densa of the distal tubule (Davis & Freeman, 1976). Patients with cirrhosis and hyponatraemia may have hypertrophy and hyperplasia of the juxtaglomerular apparatus (Reeves, Lowenstein & Sommers, 1963). Whether a redistribution of plasma or blood flow to the longer juxtamedullary nephrons is ever a cause of sodium retention has been a subject of much debate (Horster & Thurau, 1968;Stein, Ferris, Huprich, Smith & Osgood, 1971;Blanz, Wallin, Rector & Seldin, 1972;Bruns, Alexander, Riley & Levinsky, 1974).…”

Aspects of ascites

“…However, renal blood flow may be reduced in spite of a normal or raised cardiac output (Lancestremere et al, 1962) and this could activate the renin-angiotensin system which in turn stimulates aldosterone production. Renin levels have been shown to be greatly raised in patients with ascites (Brown et al, 1964) and the juxtaglomerular apparatus is hypertrophied (Reeves, Lowenstein & Sommers, 1963). Alternatively a 'volume receptor' may exist in a site which is relatively dehydrated by the continual loss of fluid into the peritoneal cavity.…”