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1. The intrarenal distribution of plasma flow was determined with a technique based on the analysis of the transit time of sodium o-[131I]-iodohippurate through the kidney in 43 patients with cirrhosis with near-normal total renal perfusion. 2. Twenty-five of the patients had an abnormal pattern of transit times, suggesting a redistribution of plasma flow from outer cortical to juxtamedullary nephrons. 3. Plasma renin activity ranged from below normal to six times normal and high values were found only in patients showing an abnormal pattern of transit times. The latter was also found to be related to sodium retention and a reduced renal capacity to excrete free water.

1. The effect of inhibition of prostaglandin synthesis on urinary excretion of free dopamine, a catecholamine thought to act as a renal natriuretic hormone, was examined in six normal women. 2. The volunteer subjects were treated with indomethacin (2 mg day−1 kg−1) for 7 days. This regimen produced an immediate and significant but transient decrease in urinary sodium excretion, averaging about 80 mmol over a period of 3 days. 3. Urinary dopamine excretion during the control period was not different from that during the entire period of indomethacin treatment. 4. It is concluded that indomethacin does not affect urinary dopamine excretion. The change in intrarenal nervous release of dopamine in response to the sodium retention induced by indomethacin may have been too small to make a significant contribution to total urinary dopamine excretion.

1. Infusion of angiotensin II antagonist failed to restore the blood pressure of short-term Goldblatt 2-kidney hypertensive rats to normal levels before and after sodium restriction. 2. The blood pressure of both normal and sodium-restricted Goldblatt 2-hypertensive rats remained elevated 6 h after bilateral nephrectomy. 3. The residual hypertension found during antagonist infusion and after bilateral nephrectomy is not maintained by the renin—angiotensin system or sodium retention.

1. Hypertension-prone Dahl S rats on either low or high NaCl diets have less than half the concentration of prostaglandin E2 (PGE2) in quick-frozen renal papillae compared with that of hypertension-resistant Dahl R rats. 2. A 4% high NaCl diet doubles the concentration of PGE2 in the renal papillae compared with the effect of a moderately low (0.3%) NaCl diet. 3. A diet with 16% linoleic acid triples the PGE2 concentration in S papillae and increases it 2.5 times in R papillae, compared with a diet with 1.5% linoleic acid. 4. The 16% linoleic acid diet also delays the onset of NaCl-induced hypertension and prevents about half of the ultimate rise in blood pressure. 5. The low PGE2 concentration in the renal papillae of S rats could contribute to a tendency toward sodium retention and thereby encourage NaCl-induced hypertension. 6. Thiazides greatly increase sodium and water excretion in isolated kidneys from pre-hypertensive S rats perfused with blood at a normotensive arterial inflow pressure. This effect would allow brisk natriuresis without the need for hypertensive arterial pressures and could thereby reduce blood pressure in NaCl-related hypertension.