This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hupf, H. Articles by Schunkert, H. Search for Related Content PubMed PubMed Citation Articles by Hupf, H. Articles by Schunkert, H. Related Collections Gene expression Autonomic, reflex, and neurohumoral control of circulation Endothelium/vascular type/nitric oxide

(Circulation Research. 1999;84:365-370.)
© 1999 American Heart Association, Inc.

Rapid Communication

Evidence for a Vasopressin System in the Rat Heart

Harald Hupf, Daniela Grimm, Günter A. J. Riegger, Heribert Schunkert

From the Medizinische Klinik und Poliklinik für Innere Medizin II, Universität Regensburg, Germany.

Correspondence to Prof H. Schunkert, MD, Klinik und Poliklinik für Innere Medizin II, Universität Regensburg, Franz-Josef-Strauss-Allee, D-93042 Regensburg, FRG. E-mail heribert.schunkert{at}klinik.uni-regensburg.de

Abstract—Traditionally, a hypothalamo-neurohypophysial system is thought to be the exclusive source of arginine vasopressin (AVP), a potent antidiuretic, vasoconstricting, and growth-stimulating neuropeptide. We have identified de novo synthesis of AVP in the heart as well as release of the hormone into the cardiac effluents. Specifically, molecular cloning of sequence tags amplified from isolated, buffer-perfused, and pressure-overloaded rat hearts allowed the detection of cardiac AVP mRNA. Subsequent experiments revealed a prominent induction of AVP mRNA (peak at 120 minutes, 59-fold, P<0.01 versus baseline) and peptide (peak at 120 minutes, 11-fold, P<0.01 versus baseline) in these isolated hearts. Newly induced vasopressin peptide was localized most prominently to endothelial cells and vascular smooth muscle cells of arterioles and perivascular tissue using immunohistochemistry. In addition to pressure overload, nitric oxide (NO) participated in these alterations, because inhibition of NO synthase by N-nitro-L-arginine methyl ester markedly depressed cardiac AVP mRNA and peptide induction. Immediate cardiac effects related to cardiac AVP induction in isolated, perfused, pressure-overloaded hearts appeared to be coronary vasoconstriction and impaired relaxation. These functional changes were observed in parallel with AVP induction and largely prevented by addition of a V₁ receptor blocker (10^-8 mol/L [deamino-Pen¹, O-Me-Tyr², Arg⁸]-vasopressin) to the perfusion buffer. Even more interesting, pressure-overloaded, isolated hearts released the peptide into the coronary effluents, offering the potential for systemic actions of AVP from cardiac origin. We conclude that the heart, stressed by acute pressure overload or NO, expresses vasopressin in concentrations sufficient to cause local and potentially systemic effects.

Key Words: gene expression • pressure overload • heart • nitric oxide • vasoconstriction

This article has been cited by other articles:

				C. B. Overgaard and V. Dzavik Inotropes and Vasopressors: Review of Physiology and Clinical Use in Cardiovascular Disease Circulation, September 2, 2008; 118(10): 1047 - 1056. [Full Text] [PDF]

				J. Gutkowska, M. Miszkurka, B. Danalache, N. Gassanov, D. Wang, and M. Jankowski Functional arginine vasopressin system in early heart maturation Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2262 - H2270. [Abstract] [Full Text] [PDF]

				N. Gassanov, M. Jankowski, B. Danalache, D. Wang, R. Grygorczyk, U. C. Hoppe, and J. Gutkowska Arginine Vasopressin-mediated Cardiac Differentiation: INSIGHTS INTO THE ROLE OF ITS RECEPTORS AND NITRIC OXIDE SIGNALING J. Biol. Chem., April 13, 2007; 282(15): 11255 - 11265. [Abstract] [Full Text] [PDF]

				S. R. Goldsmith and M. Gheorghiade Vasopressin Antagonism in Heart Failure J. Am. Coll. Cardiol., November 15, 2005; 46(10): 1785 - 1791. [Abstract] [Full Text] [PDF]

				J. ANTUNES-RODRIGUES, M. DE CASTRO, L. L. K. ELIAS, M. M. VALENCA, and S. M. McCANN Neuroendocrine Control of Body Fluid Metabolism Physiol Rev, January 1, 2004; 84(1): 169 - 208. [Abstract] [Full Text] [PDF]

				M. Naitoh, J. Risvanis, L. C. Balding, C. I. Johnston, and L. M. Burrell Neurohormonal antagonism in heart failure; beneficial effects of vasopressin V1a and V2 receptor blockade and ACE inhibition Cardiovasc Res, April 1, 2002; 54(1): 51 - 57. [Abstract] [Full Text] [PDF]

				H.-J. Weig, K.-L. Laugwitz, A. Moretti, K. Kronsbein, C. Stadele, S. Bruning, M. Seyfarth, T. Brill, A. Schomig, and M. Ungerer Enhanced Cardiac Contractility After Gene Transfer of V2 Vasopressin Receptors In Vivo by Ultrasound-Guided Injection or Transcoronary Delivery Circulation, April 4, 2000; 101(13): 1578 - 1585. [Abstract] [Full Text] [PDF]

				B. K. Brar, A. K. Jonassen, A. Stephanou, G. Santilli, J. Railson, R. A. Knight, D. M. Yellon, and D. S. Latchman Urocortin Protects against Ischemic and Reperfusion Injury via a MAPK-dependent Pathway J. Biol. Chem., March 17, 2000; 275(12): 8508 - 8514. [Abstract] [Full Text] [PDF]

				K.-L. Laugwitz, H.-J. Weig, A. Moretti, E. Hoffmann, P. Ueblacker, I. Pragst, K. Rosport, A. Schomig, and M. Ungerer Gene Transfer of Heterologous G Protein-Coupled Receptors to Cardiomyocytes : Differential Effects on Contractility Circ. Res., April 13, 2001; 88(7): 688 - 695. [Abstract] [Full Text] [PDF]