Urinary high density lipoprotein in minimal change glomerular disease and chronic glomerulopathies.

Serum lipids and lipoproteins and urinary apolipoprotein A (Apo A) were determined in two groups of patients. One group consisted of 11 children (ages ranging from 4 to 14 years) with minimal change glomerular disease. The other group consisted of 13 patients, eight less than 19 years old five adults, with different types of chronic glomerulopathy. Elimination of urinary lysozyme was a feature of chronic glomerulopathies, and creatinine clearances were also significantly lower in this group. Patients with chronic glomerulopathies had significantly lower HDL cholesterol and Apo A concentrations in their sera. In contrast, urinary Apo A concentrations were significantly higher in patients with chronic glomerulopathies, who also showed significantly lower urinary protein selectivities. Lipoprotein electrophoresis of urines containing Apo A showed distinct high-density lipoprotein (HDL) fractions, suggesting that HDL is eliminated in the urine as a result of increased glomerular permeability. This is also supported by a correlation coefficient of 0.77 between the selectivity indices and the ratio of urinary Apo A to total proteinuria. The determination of urinary Apo A appears to give valuable diagnostic information in patients with glomerular disease. According to our results the absence of urinary Apo A is very suggestive of minimal change glomerular disease.

Gastrin and the ultrastructure of G cells after stimulation with acetylcholine.

The effect of intragastric administration of acetylcholine on serum and antral gastrin concentrations of rats has been examined using a radioimmunoassay and quantitative electron microscopy. Exposure of the stomach of rats, previously fasted for 24h, to 2% acetylcholine for either 0.5 or 2h resulted in a significant 4--5 fold increase in serum gastrin concentrations to levels similar to those found in fed animals. Such treatment produced no detectable change in antral gastrin concentration or in the number or electron density of secretory granules in the G cells. This lack of detectable change in the G cells was not unexpected since our calculations suggest that less than 10% of the total gastrin stored in the antrum is released over 2h as a result of the stimulation with acetylcholine. The proportion of electron-lucent secretory granules was, however, markedly increased by prolonged fixation in aldehydes. The increase was similar in both ACh stimulated and control animals. These results indicate that the ultrastructural appearance of G cell secretory granules in influenced far more by the conditions of fixation than by the release of gastrin. They therefore cast considerable doubt on the hypothesis that gastrin is released by molecular dispersion from the granules.

Role of sodium intake in the antihypertensive effect of propranolol.

Twelve hypertensive patients had measurements of body weight, blood pressure, plasma renin activity, and plasma volume during periods of normal sodium intake and acute sodium depletion. After receiving propranolol orally for four to 14 weeks, repeat measurements were obtained under identical conditions of sodium intake. During normal sodium intake, propranolol therapy was associated with a decrease in plasma renin activity, a variable tendency to an increase in body weight and plasma volume, and a decrease in mean arterial pressure of 5 mm Hg (NS). During sodium restriction, blood pressure was decreased significantly from that observed during normal sodium intake and propranolol added a further significant decrease of 8 mm Hg (P less than .01). Blood pressure reductions obtained with sodium depletion and acute diuretic therapy were approximately the same with or without propranolol. The increase in plasma renin activity expected with sodium depletion and diuretic therapy was not blunted by propranolol.

Relationship between changes in plasma gastrin and lower oesophageal sphincter pressure after meals.

Changes in plasma gastrin and lower oesophageal sphincter pressure were measured in 20 subjects after a standard protein meal. Significant increases in both gastrin and sphincter pressure were seen. Peak gastrin response occurred an average of 19-5 minutes and peak lower oesophageal sphincter response 40-0 minutes after the meal. Both gastrin and sphincter pressure showed a wide spectrum of response. In 5 subjects there was no appreciable rise (less than 5 pg/ml) in plasma gastrin after the meal, and 3 of these had symptoms of oesophageal reflux. In this group there was only a small but nervertheless significant rise in lower oesophageal sphincter pressure (mean pressure rise 18-0 per cent of fasting value, p less than 0.05). Greater increases in sphincter pressure (mean rise 54-2 per cent, p less than 0.005) were seen in subjects with a moderate (up to 50 pg/ml) rise in plasma gastrin, and those with the most marked gastrin response (less than 50 pg/ml) showed the greatest rise in pressure (mean rise 80-3 per cent, p less than 0.0025). These results suggest that endogenous plasma gastrin is the main stimulus to the rise in lower oesophageal sphincter pressure after food. Subjects with a poor gastrin response to the meal have only a small increase in sphincter pressure and as a result may be more liable to develop gastro-oesophageal reflux.