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Am J Physiol Regul Integr Comp Physiol 279: R271-R277, 2000;
0363-6119/00 $5.00
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Vol. 279, Issue 1, R271-R277, July 2000

Octreotide-induced drinking, vasopressin, and pressure responses: role of central angiotensin and ACh

I. Hajdu1,2, F. Obál Jr.1, J. Gardi2,3, F. Laczi3, and J. M. Krueger2

1 Department of Physiology and 3 Endocrine Unit, University of Szeged, A. Szent-Györgyi Medical Center, Szeged, Hungary; and 2 Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, Washington State University, Pullman, Washington 99164-6520

The involvement of central angiotensinergic and cholinergic mechanisms in the effects of the intracerebroventricularly injected somatostatin analog octreotide (Oct) on drinking, blood pressure, and vasopressin secretion in the rat was investigated. Intracerebroventricular Oct elicited prompt drinking lasting for 10 min. Water consumption depended on the dose of Oct (0.01, 0.1, and 0.4 µg). The drinking response to Oct was inhibited by pretreatments with the intracerebroventricularly injected angiotensin-converting enzyme inhibitor captopril, the AT1/AT2 angiotensin receptor antagonist saralasin, the selective AT1 receptor antagonist losartan, or the muscarinic cholinergic receptor antagonist atropine. The dipsogenic effect of Oct was not altered by prior subcutaneous injection of naloxone. Oct stimulated vasopressin secretion and enhanced blood pressure. These responses were also blocked by pretreatments with captopril or atropine. Previous reports indicate that the central angiotensinergic and cholinergic mechanisms stimulate drinking and vasopressin secretion independently. We suggest that somatostatin acting on sst2 or sst5 receptors modulates central angiotensinergic and cholinergic mechanisms involved in the regulation of fluid balance.

somatostatin; muscarinic; cholinergic; thirst; blood pressure; rat


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