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K. A. MUNDAY
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SUMMARY

1. Xenopus laevis responds to injected adrenaline by an increase in the level of blood sugar. This increased blood sugar is apparently derived from liver and not from muscle glycogen.

2. Blood-sugar levels of Xenopus equilibrated on a black background (BB) and on a white background (WB) are statistically different throughout 6 months' starvation (P<0·05). On prolonged starvation for 14–16 months the lower blood-sugar level recorded in WB animals is not statistically different from that in BB animals (P> 0·10).

3. Xenopus shows a marked excitation hyperglycaemia, which is thought to be due to secretion of endogenous adrenaline. This hyperglycaemia is greatest in animals kept on a white background.

4. Xenopus equilibrated on black and white backgrounds show different hyperglycaemic responses to similar doses of adrenaline (P < 0·01). Compared with their own 'control-distilled water injection' levels, WB animals show an increase of blood sugar 40% higher than BB animals.

5. If melanophore-expanding hormone ('B') is an effective agent in decreasing the hyperglycaemic response to adrenaline, the greater effective level of circulating hormone in BB animals, together with their relatively reduced glycaemic response, supports the view that endogenous 'B' hormone plays a role in normal carbohydrate metabolism.

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K. A. MUNDAY
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G. F. BLANE
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1. Transiently high plasma sodium and low potassium levels have been recorded in rats exposed to severe cold (0° C) for periods of up to 48 hr. At the same time the whole blood haematocrit value was reduced. No such changes occurred in similarly exposed adrenalectomized rats.

2. The Na/K ratio of urine produced by rats during the first 12 hr of exposure was found to be abnormally low, i.e. suggestive of sodium retention with potassium loss.

3. A rapid increase in urinary 17-oxosteroid (17-KS) output was shown to occur in rats exposed to cold, but the level falls to subnormal levels within 36–48 hr and remains subnormal even though the cold stress continues to act.

4. These observations have been tentatively interpreted as evidence of early adrenal hyperactivity with release of hormones of the 'mineralocorticoid-type' during the acute stress caused by cold.

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N. T. DAVIES
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K. A. MUNDAY
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B. J. PARSONS
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A study was made of the effects of cyclic AMP, theophylline, cycloheximide, puromycin and actinomycin D on the stimulation by angiotensin of fluid transport by sacs of rat colon mucosa.

Cyclic AMP and theophylline, added together or separately, had no effect on fluid transport by colon sacs, suggesting that the stimulation of fluid transport after the application of angiotensin is not mediated through cyclic AMP. Cycloheximide and puromycin (used at concentrations which block colon protein synthesis by 50–90%) had no effect on fluid transport by control colon sacs, but completely blocked the stimulatory response of the colon to angiotensin. In contrast, actinomycin D (at a concentration which significantly inhibits RNA synthesis) did not affect fluid transport in control or angiotensin-stimulated colon sacs. The results are discussed in relation to the possibility that protein synthesis, at the stage of translation, is involved in the action of angiotensin on fluid transport by the colon.

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N. T. DAVIES
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K. A. MUNDAY
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B. J. PARSONS
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Fluid transfer by isolated everted sacs of rat jejunum, ileum and intact colon prepared from adrenalectomized-nephrectomized rats 48 h after operation was reduced when compared with that of sacs prepared from untreated controls (P < 0·001). Angiotensin at 10−10 g/ml significantly (P < 0·01) stimulated fluid transfer by intestinal sacs prepared from the adrenalectomized-nephrectomized rats; all three regions of gut were equally sensitive.

Fluid transfer was similarly reduced in stripped colon sacs prepared from adrenalectomized-nephrectomized rats. Angiotensin had a dose-dependent biphasic action on fluid transfer by stripped colon sacs: low concentrations (10−11 and 10−12 g/ml) stimulated (P < 0·05), whilst high concentrations (10−9 and 10−8 g/ml) inhibited fluid transfer (P < 0·01). Histological examination of the colon preparations showed that the stripping procedure removed the ganglia, indicating that both angiotensin effects were due to direct action on the colon mucosa.

The significance of these results is discussed in relation to the role of angiotensin in the control of salt and fluid transport by the mammalian kidney and other epithelial tissues.

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JENNIFER E. BOLTON
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K. A. MUNDAY
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B. J. PARSONS
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A study has been made of the effects of protein synthesis inhibitors on the responses of rat jejunum in vivo to intravenous infusions of angiotensin. Actinomycin D, an inhibitor of the transcription stage of protein synthesis, was without effect on the stimulation of fluid transport which follows the infusion of low doses of angiotensin. Cycloheximide, an inhibitor of the translation stage of protein synthesis, blocked the stimulatory response to angiotensin, but was without effect on the inhibitory response to high doses of the hormone. It is concluded that low (physiological) doses of angiotensin stimulate fluid transport by a mechanism involving protein synthesis at a stage later than transcription whereas high doses of the hormone inhibit fluid transport by a process which does not require protein synthesis.

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K. A. MUNDAY
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B. J. PARSONS
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JUDITH A. POAT
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GHISLAINE A. D'AURIAC
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P. MEYER
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Department of Physiology and Biochemistry, University of Southampton, Southampton, S09 3TU and *Department of Physiology and Pharmacology, INSERM U7, Hopital Necker, 75015 Paris, France

(Revised manuscript received 21 January 1976)

Angiotensin has a number of actions which include stimulation of sodium transport by rat colon and kidney (Parsons & Munday, 1972). Attempts to implicate cyclic AMP as a mediator of angiotensin responses have proven inconclusive. Kaplan (1965), Davies, Munday & Parsons (1972) and Munday, Parsons & Poat (1972) were unable to mimic angiotensin responses with cyclic AMP derivatives or theophylline, whereas Coviello (1973) and Hornych, Meyer & Milliez (1973) obtained angiotensin-like effects following the application of cyclic AMP. The possible involvement of cyclic AMP in the responses of intestine and kidney has been re-assessed using direct measurements of adenyl cyclase activities and tissue cyclic AMP concentrations in two independent laboratories.

Fluid and sodium transport was measured in stripped sacs of

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K. A. MUNDAY
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B. J. PARSONS
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JUDITH A. POAT
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D. J. SMITH
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The presence of calcium in the fluid in which intestinal or kidney tissue is incubated is required for the tissue to respond to angiotensin. Everted sacs of rat colonic mucosa exhibited an increased rate of fluid transport in the presence of angiotensin; this response was lost when the serosal fluid, but not the mucosal fluid, was calcium-free. Angiotensin-stimulated transport was maintained when calcium was replaced with strontium or barium, but was lost when calcium was exchanged for magnesium. Similarly, calcium ions were required in the incubation fluid of rat kidney cortex slices to demonstrate angiotensin-enhanced sodium transport. These observations are discussed in relation to the possible roles of divalent cations in the mechanism of action of angiotensin.

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P. G. DOREY
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K. A. MUNDAY
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B. J. PARSONS
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JUDITH A. POAT
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MARY E. UPSHER
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A study has been made of the effects of chemical sympathectomy and ganglion blockade on the responses of rat jejunum in vivo to intravenous doses of angiotensin and noradrenaline capable of stimulating fluid transport. Pretreatment with 6-hydroxydopamine (chemical sympathectomy) or pentolinium tartrate (ganglion blockade) abolished the stimulatory actions of angiotensin II but left the responses to noradrenaline unimpaired. Dopamine, like noradrenaline, stimulated fluid transport but this response required very high dopamine infusion rates, was refractory to the dopamine antagonist sulpiride and was inhibited by the α-blocker phentolamine.

The possible interaction between angiotensin and the intestinal sympathetics is discussed with reference to control of extracellular fluid volume.

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