Gastric Inhibition of the Drinking Response

Montgomery, A. V.; Holmes, Joseph H.

doi:10.1152/ajplegacy.1955.182.2.227

Cited by 20 publications

(6 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In dogs the drinking induced by hypertonic saline infusions is inhibited by balloon-distention of the stomach, but ·only if the distention precedes the infusion by at least 20 minutes (23). Distention immediately prior to the infusion does not inhibit drinking.…”

Section: Tastementioning

confidence: 96%

Digestive System

Mellinkoff¹

1957

Annu. Rev. Physiol.

View full text Add to dashboard Cite

Section: Tastementioning

confidence: 96%

Digestive System

Mellinkoff¹

1957

Annu. Rev. Physiol.

View full text Add to dashboard Cite

“…A third reason is that all previous workers measured the amount of water drunk rather than the net fluid intake. In a rapid drinker like the dog this may be reasonable, though there is the complication of temporary gastro-pharyngeal satiation (Montgomery & Holmes, 1955). In a slow drinker such as the rat, however, non-urinary loss of water during the drinking period will appreciably alter the amount of water available for diluting the injected substance.…”

Section: Dand9cription Of a Typical Experimentsmentioning

confidence: 99%

Drinking by nephrectomized rats injected with various substances

Fitzsimons¹

1961

The Journal of Physiology

126

View full text Add to dashboard Cite

Gilman (1937), experimenting on normal dogs, observed that hypertonic solutions of sodium chloride, which cause cellular dehydration, gave rise to more drinking than hypertonic solutions of urea, which do not cause loss of cell water. He concluded that thirst is due to cellular dehydration.Experiments on dogs by Holmes & Gregersen (1950a, b) in which a variety of substances were given, confirmed that osmotically effective solutes cause most drinking and by implication most thirst, and Adolph, Barker & Hoy (1954) showed that sodium chloride was twice as powerful as urea in causing normal rats to drink. In both species, however, no simple quantitative relationship was found between the amount of substance injected and the amount of water drunk.In the present work it was thought that the analysis would be simplified if the kidneys were removed, because there could be no renal response to the substance, which could therefore act until neutralized by drinking, and the quantitative relation between the amount of substance injected and water drunk could thus be investigated. It was hoped that the cellular dehydration hypothesis of drinking would be tested in this way. METHODS Male albino rats, weighing between 150 and 400 g, were most commonly used in these experiments, but some female rats and a small number of hooded rats and ginger rats of both sexes were used also. Food (Diet 41, Bruce & Parkes, 1949) was available until the beginning of the experiment and water was available before and during the experiment from a drinking meter which enabled the time course of drinking to be recorded (Fitzsimons, 1958).Experimental procedure Each animal was anaesthetized with open ether and the external jugular vein catheterized by a soft polyvinyl chloride tube, outside diameter 1 mm. The tip of the catheter was advanced to the right atrium to miniimize the complication of dead space when injections were being made. The catheter was brought subcutaneously to the back of the neck and about 2 cm was left projecting through a stab wound in the skin. The catheter, which was filled with 0*9 % sodium chloride solution, was closed with a small plug.Bilateral nephrectomy was then carried out through a dorsal incision. A clean surgical technique was employed, but no aseptic precautions were taken because the experiments 36-2

show abstract

“…Indeed, they figure prominently in various models of drinking behavior (Mc-Farland, 1971;Oately, 1967;Toates & Oately, 1970). Support for orogastric control has come, in large part, from canine studies which showed that stomach distension, produced either by water preloads or by inflated balloons, inhibited drinking (Montgomery & Holmes, 1955;Towbin, 1949).…”

mentioning

confidence: 99%

Orogastric determinants of drinking in rats: Interaction between absorptive and peripheral controls.

Hall¹,

Blass²

1977

Journal of Comparative and Physiological Psychology

View full text Add to dashboard Cite

Water intake of water-deprived rats, drinking with absorption prevented by pyloric occlusion, was compared with that of rats drinking normally. Drinking without absorption, under the control of only orogastric factors, was not graded in response to varied deprivation (Experiment 1). Orogastric controls effectively inhibited intake after absorbed water, but not isotonic saline, preloads (Experiment 2). The extent of orogastric inhibition was directly related to absorbed preload volume (Experiment 3). With large absorbed water preloads (9 ml), intakes with and without absorption were equal. Normal function of orogastric controls may thus be based on their interaction with absorption, which progressively enhances peripheral inhibition of drinking.

show abstract

Gastric Inhibition of the Drinking Response

Cited by 20 publications

References 0 publications

Digestive System

Digestive System

Drinking by nephrectomized rats injected with various substances

Orogastric determinants of drinking in rats: Interaction between absorptive and peripheral controls.

Contact Info

Product

Resources

About