Regulation of water and electrolyte metabolism during dehydration and rehydration in camels
General Material Designation
[Thesis]
First Statement of Responsibility
A. A. Al-Qarawi
Subsequent Statement of Responsibility
R. L. H. Engen, Walter H.
.PUBLICATION, DISTRIBUTION, ETC
Name of Publisher, Distributor, etc.
Iowa State University
Date of Publication, Distribution, etc.
1997
PHYSICAL DESCRIPTION
Specific Material Designation and Extent of Item
99
DISSERTATION (THESIS) NOTE
Dissertation or thesis details and type of degree
Ph.D.
Body granting the degree
Iowa State University
Text preceding or following the note
1997
SUMMARY OR ABSTRACT
Text of Note
The present study was undertaken to examine the effect of severe dehydration and rapid rehydration in electrolytes and body fluids homeostasis on the arabian camel (Camelus dromedarius), and to find out which pathway is responsible for the secretion of aldosterone in the dehydrated camel; either the renin-angiotensin axis or ACTH axis. In the first experiment ten dromedary camels were studied for a total of 29 days; 7 days under control conditions, 15 days of water deprivation and 7 days of rehydration in Bureidah (Saudi Arabia) during summer, 1996. Plasma electrolyte concentrations, plasma osmolality, packed cell volume (PCV), blood hemoglobin concentrations, plasma concentrations of glucose, creatinine, blood urea nitrogen (BUN), total protein, plasma renin activity (PRA), angiotensin II, aldosterone, arginine-vasopressin (AVP), adrenocorticotropic hormone (ACTH) and cortisol concentrations were determined during both periods. During the second trial adrenocorticotropic hormone (ACTH) and enalapril, an angiotensin-converting enzyme inhibitor (ACE-I), were utilized in two separate experiments during dehydration and control (hydration) periods. Enalapril (0.2 mug/kg) induced a sharp decrease in plasma (Na and an increase in plasma (K concentrations (P < 0.05) in the dehydrated camels but not in the control camels. Plasma osmolality decreased significantly in both dehydrated and control camels after ACE-I administration. ACE-I induced a sharp decrease in plasma angiotensin II and aldosterone concentrations (P < 0.05) in the dehydrated camels. In the control camels however, ACE-I induced a decrease in plasma aldosterone concentrations but not in plasma angiotensin II. Plasma renin activity (PRA) increased significantly in the dehydrated camels. In the second experiment, 0.4 IU/kg ACTH administration had no significant effect on plasma electrolytes and osmolality on the dehydrated and control camels. The administration of ACTH induced a sharp increase in plasma cortisol concentrations in the dehydrated and control camels. Plasma aldosterone concentrations however, increased only in the dehydrated camels. The present study clearly shows that both angiotensin II and ACTH stimulate aldosterone secretion during dehydration in camels. However, due to the parallel increase in PRA, plasma angiotensin II and plasma aldosterone in dehydrated camels without any parallel changes in plasma cortisol or ACTH, the effect of angiotensin II on aldosterone secretion seems to be dominant over ACTH.