Gonadotropin-releasing hormone increases plasma catecholamines and blood pressure in toads.
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 X kg-1) 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-pGlu1, D-Phe2, D-Trp3,6]-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 X kg-1) caused a 3-fold increase in plasma noradrenaline and a 20-fold increase in plasma adrenaline concentrations. Pretreatment of toads with an alpha-adrenergic antagonist, prazosin, and a beta-adrenergic antagonist, propranolol, abolished the pressor responses to GnRH. We conclude that GnRH mobilizes catecholamines, which act through alpha- and beta-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.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D002024:Bufo marinus; D004305:Dose-Response Relationship, Drug; D004837:Epinephrine / Q000097:blood*; D005260:Female; D008297:Male; D009638:Norepinephrine / Q000097:blood*; D010906:Pituitary Hormone-Releasing Hormones / Q000494:pharmacology*; D011224:Prazosin / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000187:drug effects
D010906:Pituitary Hormone-Releasing Hormones; D011433:Propranolol; D009638:Norepinephrine; D011224:Prazosin; D004837:Epinephrine