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Vasopressin Receptor Regulation in Maintaining Potassium Homeostasis in a Sus scrofa Model of Hemorrhagic Shock
Author(s) -
Uyehara Catherine F T,
Kajiura Lauren N,
Murata LeeAnn M,
Wong Sara A,
Ichimura Wayne M,
Hernandez Claudia A,
Sarkar Joy,
Rowland Michael R
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.962.1
Subject(s) - vasopressin , arginine vasopressin receptor 2 , medicine , endocrinology , receptor , vasopressin receptor , homeostasis , kidney , resuscitation , chemistry , biology , antagonist , anesthesia
We previously showed that elevated potassium (K)levels seen with severe hemorrhage appear to stimulate enhanced vasopressin(VP) release, and that in turn, elevated VP levels help correct hyperkalemia by increasing renal tubular K secretion. We thus tested whether brain VP receptors controlling vasopressin release were regulated synergistically with kidney VP receptors whichmodulated renal K excretion. We hypothesized that brain VP receptor up‐regulation may enable positive feedback for K‐stimulated augmentation of VP responsiveness in hemorrhage, and that renal VP receptor expression would reflect VP receptor mediated action on renal K excretion. Thus, in anesthetized Yorkshire cross pigs (n=35) we compared plasma VP (pVP) and plasmaK (pK) before, at the end of hemorrhage (30 ml/kg over 20 minutes), and after resuscitation, against mRNA expression of V1aR, V1bR, and V2R receptors in brain and kidney tissues collected after resuscitation. Multiple regression analysis showed that increased pVP at the end of hemorrhage positively correlated (p<0.05) with expression of V1aR and V1bR in the hypothalamus, V1bR in the anterior pituitary, and V2R in the renal cortex. Plasma K levels at the end of resuscitation were negatively correlated (p<0.05) with renalcortex V2R expression. In a different group of control animals that did not undergo hemorrhage, pVP and pK remained unchanged throughout. Results suggest that an up‐regulation of V1a and V1b receptors in the brain contributed to an amplified VP response in hemorrhage. In addition, VP appears to stimulate renal V2R expression to lower pK levels and maintain K homeostasis via a renal V2R‐mediated negative feedback mechanism. Support or Funding Information This project was supported by U.S. Army Medical Resarch and Materiel Command Congressionally Directed Medical Research Program grant #DAMD17‐03‐1‐0072. The views expressed in this abstract are those of the authors and do not reflect the official policy or position of the Department of the Army, Department of Defense, or the U.S. Government.