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Physiological increases in cortisol inhibit basal vasopressin release in conscious dogs. Am J Physiol 1994 Jun;266(6 Pt 2):R1744-51

Date

06/01/1994

Pubmed ID

8024023

DOI

10.1152/ajpregu.1994.266.6.R1744

Scopus ID

2-s2.0-0028042565   24 Citations

Abstract

Glucocorticoid deficiency leads to elevated plasma vasopressin (AVP), while chronic endogenous hypercortisolism may inhibit osmotically stimulated AVP, suggesting that glucocorticoids may be feedback inhibitors of AVP secretion. We evaluated the effect of physiological increases in cortisol (65 mg/day iv) for 7 days on basal AVP and oxytocin (OT) in five conscious, male dogs. Cortisol increased from 1.3 +/- 0.1 to 5.0 +/- 0.8 micrograms/dl during infusion. Basal plasma AVP significantly decreased from 3.5 +/- 0.2 to 2.6 +/- 0.3 pg/ml during cortisol infusion. Plasma OT, osmolality, and sodium did not change while arterial pressure decreased (from 107 +/- 3 to 102 +/- 2 mmHg) on days 4 and 6. Increases in cortisol led to a physiologically significant, nonosmotic decrease in AVP. The effect was specific to AVP and independent of changes in arterial pressure. Glucocorticoid administration significantly decreased basal AVP within 24 h, which is comparable to the negative feedback control of adrenocorticotropic hormone. The inverse relationship between cortisol and AVP may account for the nonosmotic change in AVP in patients with disorders of glucocorticoid secretion.

Author List

Papanek PE, Raff H

Authors

Paula Papanek PhD, MPT, LAT, FACSM Associate Professor & Director of Exercise Science in the Exercise Science & Physical Therapy department at Marquette University
Hershel Raff PhD Professor in the Medicine department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Adrenocorticotropic Hormone
Animals
Arginine Vasopressin
Blood Glucose
Blood Pressure
Dogs
Hydrocortisone
Infusions, Intravenous
Male
Oxytocin
jenkins-FCD Prod-387 b0ced2662056320369de4e5cd5f21c218c03feb3