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Biomedical subjects

J T Fitzsimons

Publications and source records attributed to J T Fitzsimons.

At least 73 records · Page 4Linked to original sources
PubMed1977

Cellular and extracellular dehydration, and angiotensin as stimuli to drinking in the common iguana Iguana iguana.

1. After water deprivation, the iguana promptly drank slightly more than enough water to restore the body fluids to isotonicity even under conditions of hypervolaemia. 2. In response to systemic injections of hypertonic solutions of NaCl and sucrose, the iguana drank and retained enough water to dilute the injected load to isotonicity irrespective of whether water was offered immediately or after 3 hr, and irrespective of whether the solute was administered I.V. or I.P. 3. Hypertonic solutions to glucose, urea, sorbitol and KCl caused little drinking. 4. The long latencies to drinking after hypertonic loads, which were not dependent on the nature of the solute, the route of administration or the dosage, were shown not to be a result of slow distribution of the solute throughout the body fluids. 5. Clearance of injected solutes via renal and extra-renal (nasal salt gland) routes was negligible during the 6 hr experimental period. 6. Measurements of plasma [Na], haematocrit, osmotic pressure and inulin space showed that the iguana drank, in response to cellular dehydration, enough water to restore the intracellular fluid volume to normal. 7. We conclude that, in response to substances which dehydrate cells, the iguana regulates its body osmolality precisely and efficiently provided it is able to do so by drinking. In this respect the responses of the iguana are similar to those of the nephrectomized rat since, in the short term, both rely exclusively on drinking to restore cellular water to normal. 8. The iguana also drinks in response to extracellular dehydration produced by hyperoncotic peritoneal dialysis, and in response to I.P. angiotensin II.

Angiotensin II↗
PubMed1976

Motility in normal and filamentous forms of Rhodospirillum rubrum.

By suitable choice of medium, Rhodospirillum rubrum has been grown both in normal (length 2 mum) and filamentous (length up to 60 mum) forms. Both forms were highly motile, and negatively-stained preparations showed bipolar flagellated cells, with an average of seven flagella at each pole. Motion consisted of a series of runs and tumbles, the ditribution of run time-lengths being Poissonian. Both forms tumbled in response to dark shock and showed negative chemotaxis to oxygen. The observation that the motility pattern was very similar in normal and filamentous forms makes chemical control of tumbling unlikely and favours a system involving membrane potentials.

Chemotaxis↗
PubMed1975

The relative importance of central nervous catecholaminergic and cholinergic mechanisms in drinking in response to antiotensin and other thirst stimuli.

1. Intracranial or subcutaneous doses of atropine or atropine methyl nitrate that were fully effective at preventing drinking in response to intracranial carbachol did not block angiotensin-induced drinking. 2. The nicotinic antagonist dihydro-beta-erythroidine given intracranially affected neither angiotensin- nor carbachol-induced drinking. 3. The dopaminergic antagonists haloperidol and spiroperidol injected intracranially blocked angiotensin-induced drinking but did not affect carbachol-induced drinking. 4. Angiotensin- and carbachol-induced drinking were unaffected by alpha- or beta-adrenergic antagonists except at toxic doses. 5. Destruction of catecholaminergic neurones with 6-hydroxydopamine markedly reduced angiotensin-induced drinking, but had relatively little effect on carbachol-induced drinking. 6. Intracranial haloperidol reduced the amount of water drunk in response to overnight deprivation of water, but did not affect feeding in response to overnight starvation or to intracranial noradrenaline. 7. Drinking following overnight water deprivation was unaffected by intracranial alpha- or beta-adrenergic antagonists. 8. Preventing dopaminergic transmission with intracranial haloperidol decreased the water to food ratio of the rat's intake after overnight starvation, whereas increasing the dopamine levels with the combination of FLA-63 and L-DOPA increased the ratio. 9. Intraventricular dopamine in large amounts caused the water-replete rat to drink. 10. It is concluded that among the many functions of dopaminergic systems in the brain is a role in the control of water intake, and that these systems participate in an important way in drinking in response to angiotensin.

Acetylcholine↗
PubMed1974

Drinking and antidiuresis elicited by isoprenaline in the dog.

1. Isoprenaline hydrochloride injected subcutaneously or infused intravenously caused drinking and simultaneous antidiuresis in the dog. The minimal effective dose was between 20 and 50 mug per dog.2. Isoprenaline-induced drinking was prevented by the beta-adrenergic antagonist propranolol and enhanced by the alpha-antagonist phentolamine.3. Ganglionic blockade with pentolinium or with hexamethonium did not interfere with the response.4. A delay of 1 hr after injection of 100 mug isoprenaline, before drinking was permitted, did not significantly reduce the amount of water subsequently drunk. A preload of water approximately equal to the volume of water normally drunk caused a greater reduction in water intake in some dogs.5. Isoprenaline caused an increase in heart rate and pulse pressure which lasted for between 1 and 3 hr according to dose. Central venous pressure fell, but mean arterial pressure was little altered. Haemodynamic changes preceded drinking by about 5 min.6. Infusion of isoprenaline caused drinking in the bilaterally nephrectomized dog.7. We conclude that isoprenaline is a potent stimulus to drinking in the dog and that the effect is not exclusively mediated by the renin-angiotensin system.

Animals↗