Warren D. Davidson

Comparison of the Effects of Human and Porcine Gastrin on Isolated Gastric Mucosa of the Bullfrog

Summary Synthetic human gastrin stimulates HCl secretion by the isolated gastric mucosa of the bullfrog. On a molar basis, human gastrin is about 1/2 as potent as pentagastrin and about 1/200 as potent as porcine gastrin. Maximal secretory response to human gastrin, pentagastrin, and porcine gastrin occurred at 2.5 7 × 10-6, 2.5 × 10−6 or 2.5 × 10−5M, and 2.5 × 10−8 M, respectively.

Action of Pancreozymin-Cholecystokinin on the Isolated Gastric Mucosa of the Bullfrog∗

Summary Pancreozymin-cholecystokinin stimulates acid secretion by the isolated gastric mucosa of the bullfrog. On a molar basis it is 2-3 times as potent as pentagastrin; porcine gastrin is 25-35 times as potent as pancreozymin-cholecystokinin. The maximal secretory responses to porcine gastrin, pentagastrin, and pancreozymin-cholecystokinin were achieved at 2.5 × 10-8, 2.5 × 10-6, and 2.5 × 10-6 M, respectively.

Production of potassium depletion by benzothiadiazine compounds

Abstract Secondary hyperaldosteronism was simulated in seven patients by the administration of desoxycorticosterone acetate (DCA) in doses of 30 mg. per day. In these patients the sodium-retaining properties of this agent appeared to be independent of total exchangeable sodium. The combined administration of hydrochlorothiazide and DCA resulted in a significantly greater kaliuretic effect than that of the sum of the two given separately. Similar results were obtained with other benzothiadiazine compounds. In conditions associated with secondary hyperaldosteronism, i.e., portal cirrhosis with ascites, nephrosis and malignant hypertension, the benzothiadiazine derivatives are likely to produce moderate to severe potassium epletion. Claims that one benzothiadiazine compound causes less potassium depletion than another are meaningless unless endogenous aldosterone secretion is considered.

Effects of varying rates of sodium excretion on Na22 kinetics.

Summary Biological decay curves of Na22 excretion showed good correlation with urinary sodium excretion during alteration of sodium excretion by sodium chloride, DCA and hydrochlorothiazide over periods of 3 to 7 days. During these short intervals, biological decay curves of serum radioactivity and serum specific activity were too variable to allow correlation with urinary sodium excretion. Daily total exchangeable sodium shows a progressive rise and cannot be used to reflect acute changes in sodium balance.