Alterations in osmotic but not pressor responses to ACTH by optic recess lesions in sheep.
This study examines whether neural structures in the region of the optic recess of the third ventricle may be involved in the genesis of adrenocorticotrophic hormone (ACTH)-induced hypertension in sheep. Five sheep were prepared with lesions in an area of the forebrain that included the organum vasculosum of the lamina terminalis (OVLT) and surrounding periventricular tissue. In these animals the dipsogenic response to systemically infused hypertonic sodium chloride (NaCl) was abolished. ACTH treatment (20 micrograms/kg/day) for 5 days caused an increase in mean arterial pressure (MAP) of 19 mm Hg, a response identical to that seen in normal sheep. With ACTH treatment, increases in plasma osmolality were greater than normal, but polydipsia did not occur in the lesioned sheep. In six other sheep with lesions either lateral or anterior to the optic recess of the third ventricle, the dipsogenic response to hypertonic NaCl and pressor response to ACTH were normal. These studies establish that in ACTH-treated sheep the integrity of the anterior ventral part of the third ventricle is not essential for the development of the hypertension. This is in contrast to the finding in other models of experimental hypertension in the rat.
D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D002552:Cerebral Ventricles / Q000502:physiology*; D004326:Drinking / Q000187:drug effects; D005260:Female; D006973:Hypertension / Q000139:chemically induced; D007032:Hypothalamus, Anterior / Q000502:physiology; D011301:Preoptic Area / Q000502:physiology; D012756:Sheep; D014882:Water-Electrolyte Balance / Q000187:drug effects*
D000324:Adrenocorticotropic Hormone