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J T Fitzsimons

Publications and source records attributed to J T Fitzsimons.

At least 37 records · Page 2Linked to original sources
PubMed1983

Em localization of atpase on microtubules of isolated cilia from Tetrahymena vorax.

1. Isolated cilia were prepared from Tetrahymena vorax using the local anaesthetic dibucaine in the deciliation step. 2. ATPase was cytochemically localized on microtubules of isolated cilia using the Washstein-Meisel incubation; deposition of lead phosphate indicated the sites of enzyme activity. 3. Mild fixation conditions gave optimum localizations. Satisfactory results were attained using 0.5% glutaraldehyde with a fixation time of 30 min. 4. An increase in ATPase activity, as judged by lead phosphate precipitation, was observed when cytochemical incubations were increased from 5 min to 1 hr. An incubation time of 15 min gave optimum results. 5. No advantage was gained with incubation times over 1 hr as diffusion of reaction product may occur. 6. No ATPase activity was observed in control incubations where the enzyme substrate ATP was omitted. 7. Purified cilia preparations provide useful starting material for the study of microtubular ATPase.

Adenosine Triphosphatases↗
PubMed1983

Renin-induced sodium appetite: effects on sodium balance and mediation by angiotensin in the rat.

1. Injection of pig renin or purified renin from the mouse submaxillary gland into the preoptic region or third ventricle of the rat caused thirst within a minute or so of injection followed shortly afterwards by increased sodium appetite. Renin from two widely different sources produced identical responses.2. The stimulating effect of renin on intake of water and hypertonic (2.7%) NaCl was continuous and persisted for at least a week after the largest (265 ng) dose of purified renin.3. The stimulating effect was also very large. A single preoptic injection of less than 0.75 pmol (26.5 ng) purified mouse renin caused mean intakes of 250.4 +/- 26.2 ml water and 44.8 +/- 12.5 ml 2.7% NaCl by five naive rats in 24 h. After the largest dose (265 ng) intakes of water and 2.7% NaCl reached about 80% and 20% body weight respectively.4. Weekly injections of renin resulted in progressively larger intakes of NaCl and water in response to the injections.5. Even after repeated injections, carbachol did not stimulate sodium appetite. The stimulating effect on water intake was quickly over and showed no progressive increase with repeated injections. Overnight intake of water was generally depressed after carbachol.6. Preoptic injection of renin caused some increase in sodium excretion but this was small compared with the stimulating effect on sodium appetite.7. Detailed temporal analysis of fluid and sodium balance shows that the increased intakes of water and 2.7% NaCl were not secondary to renin-induced urinary losses. Increased intakes of water and 2.7% NaCl caused by renin resulted in the rats going into and remaining in positive fluid and sodium balance throughout the 24 h experiment.8. Renin-induced sodium appetite and thirst were inhibited by the converting enzyme inhibitors teprotide or captopril, or by the angiotensin antagonist saralasin. Inhibition was longer lasting after captopril. Carbachol-induced thirst was unaffected.9. In conclusion, renin injected into the preoptic region or third ventricle is a potent stimulus to sodium appetite as well as thirst. The effect is mediated by local generation of angiotensin II and it is not secondary to increased urinary loss.

Angiotensin II↗
PubMed1983

Renin dependence of captopril-induced drinking after ureteric ligation in the rat.

In experiments lasting 8 h, low (0.5 mg kg-1) or medium (5 mg kg-1) subcutaneous doses of the angiotensin-converting enzyme inhibitor captopril were mildly dipsogenic in sham-operated rats, much more so in rats subjected to bilateral ureteric ligation and not at all in bilaterally nephrectomized rats. Rats with ligated ureters drank enough water to gain weight during the experiments. All other groups lost weight. The enhanced responsiveness of rats with ligated ureters, despite fluid retention, shows that captopril-induced drinking was not secondary to increased renal fluid loss. Ureteric ligation alone which caused some increase in renin secretion was mildly dipsogenic compared with sham operation. Captopril caused further increases in plasma renin concentration and more drinking suggesting that the captopril response is renin-dependent. The failure of the nephrectomized rat to drink after captopril also shows that the response is renin-dependent. The highest dose (50 mg kg-1) of captopril did not at first stimulate drinking, though water intake increased later. Slowness to drink was not the result of general depression of behaviour since drinking in response to subcutaneous hypertonic NaCl or intracranial angiotensin II was not inhibited by the highest dose. Slowness to drink after the highest dose was attributable to blockade of converting enzyme centrally as well as peripherally. This meant that the increased circulating angiotensin I resulting from peripheral blockade of converting enzyme was only slowly converted to angiotensin II in the brain. When cerebral conversion of angiotensin I was prevented by a single intracranial injection of 25 micrograms captopril, drinking in response to the lower doses of captopril was also inhibited in normal rats and in rats with ligated ureters. The same intracranial dose of captopril also inhibited drinking in response to intracranial injections of renin or angiotensin I, but not angiotensin II. The time course of inhibition of renin-induced drinking was similar to that of inhibition of subcutaneous captopril-induced drinking. In conclusion, subcutaneous captopril causes increased water intake through activation of the renal renin-angiotensin system, an effect that is enhanced when the system has already been partly activated by ureteric ligation. Increased circulating angiotensin I resulting from blockade of peripheral converting enzyme must be converted to angiotensin II in the brain in order to stimulate drinking. Drinking is not the consequence of increased fluid loss.

Angiotensins↗
PubMed1983

Cathepsin D and calcium-activated protease activities in skeletal muscle of normal and protein-deficient pregnant rats.

The role which two proteolytic enzymes (cathepsin D, CD and calcium-activated protease, CAP) might play in the early anabolic and subsequent catabolic phases of skeletal muscle protein metabolism was investigated in rats fed normal and protein-deficient (50 g/kg) diets. Enzyme measurements were performed on crude homogenate and subcellular fractions of mixed thigh muscle. In normal pregnancy there was no evidence that the changes in muscle protein mass which occurred were assisted by changes in the activities of CD or CAP. CAP activity was, however, reduced throughout protein-deficient pregnancy. Electron micrographs of gastrocnemius muscle samples taken on day 21 of pregnancy suggested increased lysosome numbers in the protein-deficient animals. However, the specific activity of CD in the muscle microsomal-mitochondrial fraction from these animals showed decreased specific activity. Thus, neither CD nor CAP play any major role in releasing amino acids from maternal skeletal muscle for placental and fetal use during protein deficiency. Changes in CAP activity in early pregnancy may indirectly help to protect the fetus from protein deficiency by allowing maternal protein mass to accumulate early in pregnancy for catabolism and use at a later stage.

Animals↗
PubMed1982

The effects of lipid fluidity on the rotational diffusion of complex I and complex III in reconstituted NADH-cytochrome c oxidoreductase.

NADH-ubiquinone oxidoreductase (Complex I) can be recombined with ubiquinol-cytochrome c oxidoreductase (Complex III) to reconstitute NADH-cytochrome c oxidoreductase. Two modes of interaction have been found. In one, the Complexes interact stoichiometrically in one to one molar ratios to give a binary Complex I-III unit. In the other, the kinetics of NADH-cytochrome c oxidoreductase are characteristic of 'Q-pool' behaviour seen in intact mitochondria and submitochondrial particles in which the Complexes need not interact directly but can do so via a pool of mobile ubiquinone. Stoichiometric behaviour is found when only boundary layer or annular lipid is present or the lipid is in the gel phase. The lipid is immobile on the ESR time scale and protein rotational diffusion, measured by saturation transfer ESR, is very slow. Q-pool behaviour is found when mobile extra-annular lipid phase is also present. Protein rotational diffusion is rapid and characteristic of a fully disaggregated state. We have also used freeze-fracture electron microscopy of reconstituted NADH-cytochrome c oxidoreductase to monitor protein aggregation and lateral phase separation of lipids and proteins under various conditions. We discuss our findings in relation to models for lateral interactions between respiratory chain enzymes.

Animals↗
PubMed1982

The effects of changes in osmolality and sodium concentration on angiotensin-induced drinking and excretion in the pigeon.

1. The pigeon drank copiously after a short latency in response to intracerebro-ventricular (I.C.V.) infusion of angiotensin II dissolved in isotonic NaCl. There were small, insignificant increases in urinary excertion so that the increased water intake caused the pigeon to go into positive fluid balance. Water was chosen in preference to 0.3 M-NaCl, which was also available to drink in these experiments.2. I.C.V. infusion of angiotensin dissolved in water, or in isotonic or hypertonic solutions of non-eletrolytes, or in KCl or CaCl(2) resulted in about half the water intake produced by angiotensin dissolved in isotonic NaCl.3. I.C.V. infusion of hypertonic NaCl alone caused drinking. I.C.V. infusion of angiotensin dissolved in hypertonic NaCl caused an amount of water to be drunk that was a simple addition of the amounts drunk in response to angiotensin dissolved in isotonic NaCl and to the extra amount of NaCl.4. Drinking in response to I.C.V. infusion of two other dipsogenic peptides, eledoisin and physalaemin, was similarly affected by the composition of the solutions in which they were dissolved.5. The pigeon also drank in response to intravenous (I.V.) infusion of angiotensin II dissolved in isotonic NaCl. Urine flow and sodium excretion increased markedly so that the pigeons just maintained fluid balance.6. In contrast to the reduction in intake when angiotensin was infused I.C.V. dissolved in hypertonic non-electrolytes, I.V. infusions of angiotensin dissolved in hypertonic non-electrolytes caused enhanced drinking, compared with the corresponding infusions of angiotensin dissolved in isotonic NaCl.7. Drinking induced by I.V. infusion of angiotensin was little affected by simultaneous I.C.V. infusion of isotonic or hypertonic sucrose, or water, but it was increased by simultaneous I.C.V. infusion of hypertonic NaCl.8. Drinking responses were partly additive when angiotensin was given by simultaneous I.C.V. and I.V. infusion.9. The increased urine flow and electrolyte excretion in response to I.V. infusion of angiotensin were little affected by simultaneous I.C.V. infusion of angiotensin.10. These experiments suggest that in the pigeon there may be separate sets of receptors in the cerebral ventricles for initiating drinking, one set responding to angiotensin, another to hypertonic NaCl. Outside the blood-brain barrier, and accessible to blood-borne substances, there may also be separate sets of receptors, one set responding to angiotensin, another to increases in effective osmolality of the blood.

Angiotensin II↗
PubMed1982

Pulmonary vein-atrial junction stretch receptors and the inhibition of drinking.

A chronically implanted inflatable balloon was used to produce distension of a left pulmonary vein at its junction with the left atrium in trained conscious dogs. Balloon inflation caused a fall in the amounts of water drunk in response to injection of isoproterenol, infusion of hypertonic NaCl, or overnight water deprivation. There was also a significant increase in heart rate, but arterial, central venous, and left atrial pressures were unaltered. Blockade of the left vagosympathetic nerve prevented the inhibitory action of distension of a pulmonary vein on water intake in response to injection of isoproterenol. In experiments where the balloon was left inflated for 24 h, distension also caused a fall in the spontaneous daily water intake, whereas food intake was unaffected. Despite the fall in water intake, urine flow increased so that the dog went into negative fluid balance. In conclusion, distension of a pulmonary vein at its junction with the left atrium causes reduction in both spontaneous and induced water intake, and this inhibition is not secondary to circulatory changes or fluid retention by the kidney. The action of the receptors concerned may complement the actions of the same or similar receptors on renal function whose effects have been observed previously in acute experiments in anesthetized animals and here for the first time in conscious animals.

Animals↗
PubMed1982

Angiotensin does contribute to drinking induced by caval ligation in rat.

In small (0.5 mg/kg) subcutaneous doses, the angiotensin-converting enzyme inhibitor, captopril, greatly enhanced drinking in response to caval ligation in the rat. Drinking was not secondary to urinary water loss since the rats developed a substantial positive fluid balance. High (50 mg/kg) subcutaneous doses of captopril reduced drinking to a level below that following caval ligation alone. This effect could be mimicked by giving repeated intracerebroventricular injections of captopril (total amount 110 micrograms) to rats treated with the lower subcutaneous dose of captopril. With this combination, therefore, not only did the lower dose enhancement disappear, the basal caval ligation drinking response was also reduced with a total dose of captopril of less than 2% of the higher subcutaneous dose alone. These results show that, when conversion of angiotensin I to angiotensin II is prevented in the brain as well as systemically, drinking in response to caval ligation is reduced although not entirely prevented. The original report that such drinking is multifactorial, depending on angiotensin as well as nonangiotensin mechanisms, is confirmed.

Angiotensin I↗
PubMed1981

Drinking and changes in blood pressure in response to angiotensin II in the pigeon Columba livia.

1. Angiotensin II is as potent a stimulus to drink in pigeons as it is in mammals. There are striking similarities in the action of this peptide in pigeons and mammals. 2. Angiotensin II injected intracranially, I.V. or I.P. consistently caused short-latency and vigorous drinking in pigeons but no other behaviour. Drinking was completed rapidly and intakes were very large, sometimes in excess of 10% of the bird's body weight. 3. The latency to drink and the amount drunk were dose dependent for all routes of injection. Angiotensin II was most effective when injected directly into the brain. As little as 10(-4) mol angiotensin II injected into the cerebral ventricles caused birds to drink. 4. The rapid cessation of drinking after intracranial injection of angiotensin II was not caused by rapid loss of activity of the peptide in the brain but by the actual ingestion of the water. 5. The brain sites most sensitive to the dipsogenic action of angiotensin II in the pigeon were the dorsal and ventral third ventricle, the tissue adjacent and anterior to these sites, and the lateral ventricles. The lateral hypothalamic area was only slightly less sensitive. Negative sites for drinking were found in the lateral forebrain and the hind brain. These findings are similar to those in mammals. 6. Pigeons drank during I.V. infusion of as little as 16 X 10(-12) mol angiotensin II kg-1 min-1. This was near the threshold for increasing arterial pressure in pigeons and is near the threshold for drinking in rats and dogs. 7. The Asn1, Asp1, Val5 and Ile5 analogues of angiotensin II were equipotent as stimuli to drink but a wide range of other peptides and drugs injected into the brain failed to increase water intake. An exception was eledoisin which was, comparing molecule with molecule, only 10-100 times less potent than angiotensin II in the pigeon. 8. Injections of angiotensin II into brain sites which caused drinking failed to alter heart rate or arterial pressure in pigeons. 9. This and other recent studies demonstrate the wide phylogenetic distribution of the dipsogenic action of angiotensin II and support the idea that the control of water intake is an important physiological function of the renin-angiotensin system in vertebrates.

Angiotensin II↗
PubMed1981

Drinking and changes in blood pressure in response to precursors, fragments and analogues of angiotensin II in the pigeon Columba livia.

1. The pigeon drank as vigorously in response to intracranial injection of synthetic renin substrate and angiotensin I as to angiotensin II. 2. Mammalian renin injected into the brain caused the water-replete pigeon to drink but it was a less effective dipsogen than in the mammal. As in the mammal, renin-induced drinking was slower in onset and continued for longer than angiotensin-induced drinking. 3. The converting enzyme inhibitor SQ 20881 attenuated drinking in response to intracranial renin, synthetic renin substrate and angiotensin I but enhanced intracranial angiotensin II-induced drinking. Therefore drinking induced by the intracranial injection of precursors of angiotensin II is mediated through local generation of angiotensin II. 4. I.V. injection of angiotensin I was as effective as angiotensin II in causing the pigeon to drink, but synthetic renin substrate was less effective. I.V. doses of angiotensin I and II had to be about 100 times greater than the intracranial doses in order to produce similar intakes. 5. Angiotensin I and II were equally effective pressor agents by I.V. injection in the pigeon but synthetic renin substrate was much less effective. I.V. SQ 20881 inhibited the pressor response to I.V. synthetic renin substrate or angiotensin I but enhanced the angiotensin II-induced response. 6. Aliphatic position 8-substituted analogues of angiotensin II which are competitive antagonists of angiotensin II-induced drinking and pressor responses in the mammal in antagonist:agonist mole ratios as low as 10:1, failed to reduce drinking in response to intracranial synthetic renin substrate or angiotensin II, although not themselves agonists, nor did they prevent the pressor to infusion of angiotensin II even with antagonist:agonist mole ratios as high as 10,000:1. 7. Shortening the angiotensin octapeptide from the N-terminus caused a progressive reduction in intracranial dipsogenic activity. Activity was completely abolished by removing the C-terminal phenylalanine. 8. These results demonstrate that in pigeons, as in mammals, it is angiotensin II which is the biologically active peptide in the control of drinking behaviour and blood pressure by the renin-angiotensin system. Precursors of angiotensin II can be converted to the octapeptide in the avian brain as well as in the circulation. The angiotensin receptors for drinking and blood pressure responses are similar to each other in the pigeon and they are very similar but not identical with the angiotensin receptors for the dipsogenic, pressor and myotropic actions of angiotensin II in mammals.

Angiotensin II↗
PubMed1981

Renin-dependence of drinking induced by partial aortic obstruction in the dog.

1. Inflation of a balloon implanted in the abdominal aorta above the level of the renal arteries was used to produce partial obstruction to aortic blood flow in trained, conscious mongrel dogs.2. Following inflation, heart rate and arterial blood pressure downstream from the point of inflation fell, whilst arterial blood pressure upstream from the point of inflation rose. Central venous pressure was unaltered.3. In sixteen out of eighteen experiments, balloon inflation led to drinking. Inflations maintained for 3 days led to a sustained increase in daily water intakes, but intakes of 0.9% NaCl were unaltered when both water and 0.9% NaCl were available to drink.4. There was a significant inverse correlation between the amount drunk in the first 60 min following balloon inflation and the ratio of the change in the arterial pressure upstream of the obstruction to the change in pressure downstream of the obstruction.5. In experiments where the inflation was maintained for 90 min, there was no further drinking between the 60th and 90th min. In experiments where the inflation was released after 60 min, there was another bout of drinking between the 60th and 90th min.6. Plasma renin activity and plasma renin concentration both rose following balloon inflation. Drinking following balloon inflation was abolished by infusion of the competitive angiotensin II antagonist saralasin.7. Inflation of an aortic balloon to a size that produced drinking in other experiments also led to a reduction in urinary water and electrolyte loss in fluid pre-loaded dogs.8. In conclusion, water intake in response to partial aortic obstruction above the level of the kidneys is caused by renin released from the kidneys. However, the dipsogenic effectiveness of the endogenous renin released is reduced as a result of the simultaneous increase in arterial pressure above the obstruction.

Animals↗
PubMed1980

Angiotensin and other peptides in the control of water and sodium intake.

Several neuroactive peptides have been implicated in thirst and sodium appetite in different species; three peptides are considered here. The best established of these is the octapeptide angiotensin II, which when administered systemically or intracranially causes completely normal drinking behaviour in all vertebrates tested, including many mammals, four or five birds, one reptile and one bony fish. In the rat, in which the original experiments were carried out, injection of a few femtomoles of angiotensin II caused a brisk drinking response within a minute or so of injection at a time of day when the animal would usually be resting. The response is usually completed within 10 min and after the larger doses the amounts of water taken may approach what the animal would normally drink in the course of 24 h. Another response to intracranial angiotensin, seen so far only in the rat, is an increase in sodium appetite. This is slower in onset than thirst, lasts for many hours and the response tends to become greater with repeated injections of hormone. Naturally occurring increases in sodium appetite may be caused by angiotensin generated by the action of cerebral isorenin. A second neuroactive peptide that affects thirst is the undecapeptide eledoisin, which is found in the salivary glands of certain Mediterranean cephalopods. Eledoisin and, to a lesser extent, substance P, with which it is related, are potent intracranial dipsogens in the pigeon, producing behaviour that is indistinguishable from that produced by angiotensin. However, in contrast to the stimulatory action of angiotensin on drinking behaviour in all other vertebrate species tested, these substances specifically depress drinking in the rat. A third peptide that has been implicated in thirst is antidiuretic hormone (ADH). This hormone has a profound but indirect effect on water intake in diabetes insipidus. In the dog, however, ADH in physiological amounts may influence thirst mechanisms by direct action on the central nervous system. In this species, but not in the rat, ADH lowers the threshold of thirst in response to osmotic stimulation and also to infusion of angiotensin. Of these three peptides, and others not mentioned here, angiotensin II has the best claim to be regarded as a neuroactive peptide. It alone is always dipsogenic when injected into the brain and it also stimulates sodium appetite. Whether the effects of angiotensin, on thirst and sodium appetite should be regarded as manifestations of the activity of a classical endocrine system, of a paracrine system, of a neurotransmitter system, or of all of these, cannot be decided at present. But these actions of angiotensin, when considered with its other actions on the distribution and conservation of body fluid, show that the hormone is intimately concerned in extracellular fluid volume control.

Angiotensin II↗
PubMed1980

Renin-like effects of NGF evaluated using renin-angiotensin antagonists.

Intracranial injection of angiotensin II (AII) or activation of the cerebral isorenin-angiotensin system with intracranial renin causes an immediate thirst and a delayed sodium appetite in the rat. Nerve growth factor (NGF), a polypeptide trophic factor for peripheral sympathetic and sensory neurones, has also been reported to be a potent stimulus to thirst and sodium appetite when injected into the brain of the rat. Lewis et al. drew attention to the marked similarity between the effects of 2.5S NGF and renin on thirst and sodium appetite and suggested that the NGF responses were mediated by the cerebral isorenin-angiotensin system. We report here that NGF-induced thirst and sodium appetite, as well as increased blood pressure and increase ornithine decarboxylase activity in the brain and liver, depend on the formation of AII (see also ref. 6).

Angiotensin II↗
PubMed1980

Increased sodium appetite in the rat induced by intracranial administration of components of the renin-angiotensin system.

1. Intracranial injections of components of the renin-angiotensin system in rats in normal water and Na balance caused an immediate thirst followed by a progressive increase in Na appetite during a test session which lasted 18 h. The effect on water and Na intake was dose-dependent. 2. Long-term (7 day) infusions of angiotensin II into the third cerebral ventricle at rates of 1 or 10 pmol h-1 produced large and sustained increases in intake of water and 2 . 7% NaCl. Intakes sometimes exceeded 100 ml 2 . 7% NaCl per day but quickly fell to normal when the infusion was stopped. 3. Intracranial injection or infusion of carbachol caused a transient increase in water intake but had no effect on the intake of NaCl. 4. The Na appetite induced by intracranial injection of angiotensin was specific for Na since rats offered a choice of water and equimolar concentrations of NaCl and KCl took only water and NaCl. This resembles the pattern seen in Na-depleted rats. 5. Increased Na appetite was not secondary to increased water intake since it occurred when only 2 . 7% NaCl was available to drink. 6. Increased Na appetite was not secondary to natriuresis since, first, the angiotensin-stimulated rats went into positive Na balance, secondly, intracranial renin did not cause increased Na excretion in Na-loaded rats and thirdly, anureic rats showed a significant Na appetite in response to renin. 7. These results suggest that angiotensin in the brain may play a role in the development of Na appetite.

Angiotensin II↗
PubMed1980

Arousal of a specific and persistent sodium appetite in the rat with continuous intracerebroventricular infusion of angiotensin II.

1. Prolonged exposure of the brain of the normal Na-replete rat to angiotensin II produced a marked and persistent Na appetite. In a first series of experiments, short-term, repeated systemic injections of isoprenaline or renin (both of which raise circulating angiotensin levels), and repeated intracranial injections of angiotensin II evoked increased ingestion of 2 . 7% NaCl. In the second series of experiments, continuous infusions of angiotensin II directly into the brain evoked extremely large intakes of 3% NaCl. 2. In addition to large intakes of hypertonic NaCl some rats drank daily volumes of water that exceeded their body weight. 3. Not only did the animals drink large volumes of 3% NaCl some rats drank daily volumes of water that exceeded their body weight. 3. Not only did the animals drink large volumes of 3% NaCl during continuous angiotensin II infusion, but after termination of the infusion they continued to ingest NaCl at a rate comparable to that of the adrenalectomized rat. In most of the animals the persistent NaCl intake diminished over several days, but other animals continued to drink NaCl for as long as their intake was measured (up to 7 months). 4. The response to continuous infusion of angiotensin II was dose-dependent. Both water and 3% NaCl intake increased over a dose range of 6 ng h-1 to 6000 ng h-1. The persistence of the sodium appetitite was also dose-dependent across the same range of doses. 5. Angiotensin-induced salt appetite is specific for Na. Animals did not drink 0 . 5 M-NH4Cl and only occasionally drank minimal amounts of 0 . 5 M-KCl during continuous infusion. 6. The large water turnover was not responsible for the Na appetite. Rats given access to 3% NaCl only during infusion of angiotensin copiously. Animals that were not infused but were given saccharine-flavoured water in order to increase their water intakes did not drink 3% NaCl offered at the same time even though fluid intake was high. Rats that did not receive intracranial infusions but were infused intragastrically with volumes of water equal to or exceeding the amounts that were drunk during angiotensin infusion did not drink the 3% NaCl but did drink some water. 7. Records of the drinking by rats infused with angiotensin show that firstly the onset of drinking after the start of angiotensin infusion varied from animal to animal, secondly, NaCl drinking was not temporally linked to water intake, although this was observed occasionally, and thirdly, most of the drinking occurred during the night although angiotensin was infused continuously throughtout the nychthemeron. 8. Therefore, increases in angiotensin levels, probably with other factors such as increased levels of aldosterone or ACTH, result in Na appetite. The hormonal changes may alter the animals' preception of salt making it more acceptable. By means that are not yet understood the increased accceptability of salt persists after the termination of angiotensin infusion.

Angiotensin II↗
PubMed1980

Drinking and antidiuresis in response to reductions in venous return in the dog: neural and endocrine mechanisms.

1. In order to investigate the mechanisms of hypovolaemic thirst and sodium appetite an inflatable balloon in the upper abdominal inferior vena cava was used to produce acute, graded and reversible reductions in venous return to the heart in conscious dogs. 2. Reducing venous return caused a fall in central venous, arterial and pulse pressures. Heart rate and venous pressure upstream from the point of inflation rose. 3. Within 6--28 min of inflating the balloon the dogs started drinking. The amount drunk in a 1 h experiment was significantly correlated with the changes in central venous and arterial pressures. 4. More prolonged obstruction to venous return led to a sustained increase in water intake and the development of a sodium appetite. 5. Plasma renin activity and concentration rose following caval obstruction. 6. Drinking in response to reductions in venous return was reduced, but not abolished, by simultaneous infusion of the competitive angiotensin II antagonist saralasin acetate. 7. When the left vagosympathetic nerve was blocked at the same time as balloon inflation the response was enhanced. 8. Urine flow fell after partial obstruction of the vena cava. Therefore drinking led to the development of a positive fluid balance. 9. We have shown that hypovolaemia is a potent and quantitatively defined stimulus to drinking in the dog and that the renal renin-angiotensin system makes an important contribution to it.

Animals↗