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      Gonadotropin-Releasing Hormone Increases Plasma Catecholamines and Blood Pressure in Toads

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          Synthetic gonadotropin-releasing hormone (GnRH) was injected intravenously into conscious, adult toads ( Bufo marinus) to elucidate the nervous and cardiovascular actions of the hormone. GnRH (0.001–1.0 nmol·kg^<sup>1</sup>) produced dose-dependent increases in mean arterial blood pressure and pulse pressure, beginning within 3 min after injection. These pressor responses to GnRH were specific to the hormone since they could be inhibited reversibly by [D-pGlu<sup>1</sup>, D-Phe<sup>2</sup>, D-Trp<sup>3,6</sup>]-GnRH. Arterial plasma concentrations of unconjugated catecholamines increased simultaneously with the rise in blood pressure following GnRH injection: the half-maximal pressor dose of GnRH (0.1 nmol·kg<sup>–1</sup>) caused a 3-fold increase in plasma noradrenaline and a 20-fold increase in plasma adrenaline concentrations. Pretreatment of toads with an α-adrenergic antagonist, prazosin, and a β-adrenergic antagonist, propranolol, abolished the pressor responses to GnRH. We conclude that GnRH mobilizes catecholamines, which act through α- and β-adrenergic mechanisms to raise blood pressure. Thus, endogenous GnRH or GnRH-like peptides may coordinate the pituitary, nervous and cardiovascular mechanisms which prepare toads for seasonal reproductive activity.

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          Author and article information

          S. Karger AG
          28 March 2008
          : 39
          : 5
          : 437-441
          Department of Physiology, College of Medicine, University of Saskatchewan, Saskatoon, Canada
          124017 Neuroendocrinology 1984;39:437–441
          © 1984 S. Karger AG, Basel

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          Pages: 5
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