Centrally mediated increased sympathetic activity is not important in the genesis of ACTH-induced hypertension in sheep

• Published in: Clinical and experimental pharmacology & physiology Vol. 16; no. 7; p. 607
• Main Authors: Spence, C D, Mathai, M, Mills, E H, Coghlan, J P, Whitworth, J A, Scoggins, B A
• Format: Journal Article
• Language: English
• Published: Australia 01.07.1989
• Subjects: Adrenocorticotropic Hormone; Animals; Blood Pressure - drug effects; Clonidine - pharmacology; Female; Heart Rate - drug effects; Hypertension - chemically induced; Hypertension - physiopathology; Injections, Intravenous; Methyldopa - pharmacology; Sheep; Sympathetic Nervous System - physiopathology; Vascular Resistance - drug effects
• ISSN: 0305-1870
• DOI: 10.1111/j.1440-1681.1989.tb01611.x

1. Adrenocorticotrophin (ACTH) administration to sheep produces a rapid adrenally dependent hypertension which is maximal after 3 days and associated with increased cardiac output (CO) and heart rate (HR), while calculated total peripheral resistance remains unchanged. 2. This study investigated the proposal that a centrally mediated increase in sympathetic activity is important in the development of ACTH-induced hypertension. 3. Concomitant intravenous infusions of either clonidine (60 micrograms/kg per day) or methyldopa (60 mg/kg per day) with ACTH (5 micrograms/kg per day) failed to inhibit the increase in mean arterial pressure (MAP) observed with ACTH. 4. In a separate experiment clonidine abolished the increase in CO and HR but not the pressor response associated with ACTH administration. 5. These results do not support a role for centrally mediated increase in sympathetic activity in the genesis of ACTH-induced hypertension.