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The quantitative relation of calcium and protein secretion was studied on the isolated perfused canine pancreas at different secretory states of hydrokinetic and ecbolic stimulation and various extracellular Ca++-concentrations. 1. Calcium and protein secretion are correlated at both ecbolic and hydrokinetic stimulation as well as by biological or synthetic secretion. 2. Enzyme-associated calcium was estimated at 35 nmol/mg protein and did not vary under differing stimulatory and secretory conditions. 3. During variable concentrations of synthetic secretin basal protein and calcium concentrations in the pancreatic juice show a hyperbolic relationship to the respective rates of fluid secretion. At flow rates beyond 3 ml/5 min the calcium concentrations asymptotically tend to 0.46 mEq/l while protein concentrations nearly decrease to zero. Moreover, the y-intercept of the regressionline correlating the calcium and protein concentrations gives with 0.48 mEq/l Ca++ additional evidence of the existence and magnitude of an enzyme-independent calcium fraction, which seems to remain constant over the whole range of secretory rates. 4. The omission of perfusate calcium does not abolish the calcium-protein correlation either at hydrokinetic or at ecbolic stimulation, but diminishes the enzyme-independent calcium fraction. 5. Enhancing perfusate Ca++-concentrations augments calcium output byt fails in stimulating enzyme secretion. It is concluded that at exclusively hydrokinetic stimulation basal secreted protein with a definite amount of chelated calcium is diluted by variable rates of pancreatic juice containing enzyme independent Ca++ at a constant concentration. During different secretory states of hydrokinetic or ecbolic stimulation the respective proportions of enzyme associated and independent calcium vary, and thus determine changes in the calcium-protein ratios. Extracellular calcium can only influence the non-protein-bound calcium fraction of the pancreatic juice presumably by diffusion from the extracellular fluid through the ductal epithelium rather than by an active secretory mechanism.
H Teufel, and
P Stock, and
H Rohrmoser, and
M M Forell
October 1971,
The Journal of clinical investigation,
H Teufel, and
P Stock, and
H Rohrmoser, and
M M Forell
July 1974,
Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme,
H Teufel, and
P Stock, and
H Rohrmoser, and
M M Forell
February 1972,
The Journal of physiology,
H Teufel, and
P Stock, and
H Rohrmoser, and
M M Forell
June 1978,
Diabetologia,
H Teufel, and
P Stock, and
H Rohrmoser, and
M M Forell
October 1973,
Gut,
H Teufel, and
P Stock, and
H Rohrmoser, and
M M Forell
October 1967,
Journal of the Royal College of Surgeons of Edinburgh,
H Teufel, and
P Stock, and
H Rohrmoser, and
M M Forell
January 1978,
European surgical research. Europaische chirurgische Forschung. Recherches chirurgicales europeennes,
H Teufel, and
P Stock, and
H Rohrmoser, and
M M Forell
January 1991,
Pancreas,
H Teufel, and
P Stock, and
H Rohrmoser, and
M M Forell
May 1967,
Gastroenterology,
H Teufel, and
P Stock, and
H Rohrmoser, and
M M Forell
September 1973,
The Journal of clinical investigation,
