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Biomedical subjects

B J Rolls

Publications and source records attributed to B J Rolls.

At least 127 records · Page 7Linked to original sources
PubMed1977

Drinking following intracarotid infusions of hypertonic solutions in dogs.

Eight dogs were prepared with bilateral carotid loops and trained to stand quietly in a modified Pavlov stand. In each of the dogs, 0.3, 0.45, and 0.6 M NaCl were infused, split between the two carotids at a rate of 0.6 ml-kg-1-min-1 for 10 min and the effect on drinking assessed. A graded increase in drinking was obtained with increased osmolality of the saline (R = 0.59, N = 32, P less than 0.001). Infusion of 0.3 M NaCl was associated with an increase in jugular venous osmolality, but no significant increase in systemic osmolality. Intravenous infusion of 0.3 M NaCl at 0.6 ml-kg-1-min-1 had no effect on drinking. Intracarotid infusion of 0.3 M sucrose in 0.15 M NaCl stimulated drinking to a similar extent as 0.3 M NaCl, whereas intracarotid 0.3 M urea in 0.15 M NaCl had no effect. Increasing the systemic plasma osmolality by infusing 1.04 M NaCl intravenously stimulated drinking, an effect which was abolished by removing the central osmotic stimulus with intracarotid infusions of water. These results are compatible with a central osmoreceptor theory of thirst.

Animals↗
PubMed1977

Thirst following water deprivation in dogs.

Eight dogs were prepared with unilateral carotid loops, and trained to stand quietly in a modified Pavlov stand. They were deprived of water for 24 h, which significantly depleted both the cellular and extracellular fluid (ECF) compartments. When they were allowed access to water for 5 min, they promptly drank amounts sufficient to make up their fluid deficits. Infusion of water into the unilateral carotid loop to reduce the cerebral blood osmolality to normal did not consistently reduce drinking because of inadequate mixing in the Circle of Willis. The eight dogs were then prepared with bilateral loops and deprived of water. Infusion of water at 0.6 ml-kg-1-,min-1 reduced the jugular plasma osmolality to control levels but did not affect systemic osmolality and reduced the drinking by 72%. Intracarotid infusion of water at differing rates reduced drinking in a dose related fashion. Intravenous infusion of 0.15 M NaCl in an amount designed to expand the ECF volume to normal reduced drinking by 27%. Expansion of the ECF volume plus bilateral intracarotid infusion of water to remove the central osmotic stimulus completely inhibited drinking. It is concluded that drinking following water deprivation in dogs is controlled by both central osmotic and by extracellular fluid volume factors, and that the osmotic factor is the more important. The drinking stopped well before these fluid deficits, as judged by body fluid analysis, had been restored. Some other mechanisms, therefore, must be involved in satiety.

Animals↗
PubMed1975

The relationship between elevated water intake and oedema associated with congestive cardiac failure in the dog.

1. In the dog constriction of the thoracic region of the inferior vena cava increases water intake and extracellular and plasma fluid volumes. 2. Restriction of water intake to the pre-operative level for 2 weeks reduces the measured extracellular fluid volume to the pre-operative level. 3. Administration of the competitive angiotensin inhibitor, saralasin acetate, to two dogs in congestive cardiac failure following thoracic caval constriction markedly reduced their water intake. 4. These results suggest that increased fluid intake is probably important in the aetiology of the oedema associated with congestive cardiac failure, probably through the renin-angiotensin system.

Angiotensin II↗
PubMed1971

The effect of intravenous infusion of antidiuretic hormone on water intake in the rat.

1. In rats the continuous I.V. infusion of ADH at rates up to 6.0 mu. kg(-1) min(-1) decreased drinking caused by water deprivation, by a 10% increase in osmotic pressure, and by caval ligation.2. Infusion of ADH at rates between 0.07 and 6.0 mu. kg(-1) min(-1) never potentiated drinking nor did it significantly affect the 24 hr water intake of rats that were in water balance at the start of the experiment.3. Urine output was slowed by a rate of infusion (13.0 muu. kg(-1) min(-1)) which was approximately 150 times smaller than the lowest rate which was found to decrease water intake.4. Since the rates of infusion of ADH which directly affect water intake and urine flow are so different, it is unlikely that ADH is a general homoeostatic hormone which controls both thirst and urine output in the rat.

Animals↗
PubMed1970

Drinking induced by injection of angiotensin into the rain of the rat.

1. When applied directly to the brain, angiotensin II amide, as either the valine(5) octapeptide, causes rats in normal fluid balance to drink water.2. The drinking response to angiotensin injections is copious, rapid, repeatable within the same test session, and stable over months of testing in the same animal.3. The response is motivationally potent and specific. After injection the animals move directly to the source of water and drink. There is typically no preliminary hyperactivity or subsequent depression. The animals do not eat, gnaw or exhibit other behaviours that are not normally seen during spontaneous drinking. The injections rouse sleeping animals to drink and interrupt eating in animals deprived of food for two days.4. The region of the brain that is most sensitive to angiotensin includes the anterior hypothalamus, the preoptic region, and the septum including the nucleus accumbens.5. Intracranial renin elicited drinking. Bradykinin and vasopressin did not, nor did adrenaline, noradrenaline or aldosterone. In the most sensitive region, sites positive for angiotensin also yielded drinking to carbachol.6. Responses were obtained with 5 ng (ca. 5 p-mole) and occurred reliably with 50 ng angiotensin or more. The dose-response curve for amount drunk rose from 5 to 100 ng and levelled off thereafter. Angiotensin is therefore the most potent dipsogen known and is effective at doses that are reasonably within the concentration range for circulating endogenous angiotensin.7. Injections into the sensitive region of doses of angiotensin that were effective for drinking did not produce peripheral haemodynamic changes in lightly anaesthetized rats.8. This work strengthens the suggestion that angiotensin is a natural hormone of drinking behaviour that participates in extracellular thirst by its release from the kidney and subsequent direct action on a specific chemoreceptive region in the anterior diencephalon and limbic lobe.

Aldosterone↗
PubMedDate not supplied

Effects of dietary fat, nutrition labels, and repeated consumption on sensory-specific satiety.

This study investigated whether energy from fat, nutrition information, and/or repeated consumption of a palatable snack food affects the development of sensory-specific satiety (SSS). Participants (51 males and 44 females) ate an afternoon snack of potato chips in a laboratory for two 10-day (Monday-Friday) sessions in a repeated measures, cross-over design. In one 10-day session, participants were given regular, full-fat potato chips (22.2 kJ/g; 150 kcal/oz) and, in the other, they were given potato chips made with olestra (11.8 kJ/g; 80 kcal/oz), a non-absorbable fat replacer. Information about the fat and energy content of the chips was provided to half the participants, while the other half was not informed. In both sessions, participants were instructed to consume the potato chips ad libitum. Initial ratings of sensory properties of the two types of chips did not differ significantly. In SSS tests, participants rated sensory properties of the chips and four test foods (turkey, strawberry yogurt, cookie, and carrot) on days 1, 5, and 10 of the 10-day sessions. Following consumption, ratings of pleasantness of taste and texture and prospective consumption of both types of chips declined compared to the test foods. Further analyses showed that the development of SSS was not affected by the fat and energy content of the chips, the provision of nutrition information, or repeated consumption.

Adult↗