HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Costales, M Articles by Vijande, M Search for Related Content PubMed PubMed Citation Articles by Costales, M Articles by Vijande, M

Partly occluding the abdominal aorta between the renal arteries caused the rat to drink steadily increasing amounts of 2.7% NaCl when this solution and water were available. The increase in NaCl intake preceded the increase in water intake that also occurred after aortic occlusion, and intakes of both fluids were reaching maximal values 1-2 weeks after operation. The amounts of fluid drunk during the day increased greatly. This change in the pattern of drinking, together with the rise in fluid intake and the drop in food intake meant that drinking was less associated with feeding than it is in the normal rat. The rats went into fluid and electrolyte deficit within 24 h of partial aortic occlusion and remained in deficit for about a week (the duration of the balance experiment) despite increasing intakes of NaCl and water. Renal function was unimpaired during the first 2 weeks, and the abnormal signs were mainly and rapidly reversed by removal of the ischaemic kidney or administration of the angiotensin converting enzyme inhibitor, captopril. Therefore polydipsia and increased sodium appetite in the first 2 weeks after aortic occlusion were likely to have been caused by fluid deficit, with increased renin secretion from the ischaemic kidney contributing to both behaviours. Arterial blood pressure rose immediately after aortic occlusion, before the onset of increased drinking. Up to 3 weeks after operation the incidence and severity of the hypertension did not appear to depend on the spontaneous changes in intake of water or hypertonic NaCl.

This article has been cited by other articles:

				J. T. FITZSIMONS Angiotensin, Thirst, and Sodium Appetite Physiol Rev, July 1, 1998; 78(3): 583 - 686. [Abstract] [Full Text] [PDF]