title: Hypothalamic digitalis-like substance is released with sodium-loading in rats.
abstract: Role of the hypothalamic digitalis-like substance (EDLS) on the hypertension associated with an excess intake of sodium and the releasing mechanism were investigated. The blood pressure in rats fed with a sodium diet increased significantly after 4 weeks of the treatment compared to the control rats fed with a regular diet, which was accompanied by increased urinary output of the EDLS. Electrical lesions of the AV3V area in the hypothalamus significantly decreased both the urinary EDLS level and the blood pressure elevated by the sodium-loading. With the immunohistochemistry using digoxin antibody, the immunoreactives were localized in the neurons of paraventricular and supraoptic nuclei and some other hypothalamic areas, and were also seen in the nerve fibers distributed in the basal hypothalamus, infundibulum, and pituitary posterior lobe. Assuming that the CSF sodium is responsible for the release of EDLS, hypertonic NaCl (2.5 M) was infused into the lateral ventricle for 30 minutes. Blood pressure increased gradually, attaining peak rises about 30 minutes later. The plasma content of the EDLS was significantly greater in the hypertonic NaCl group than the control group treated with either the artificial CSF or 2.5 M of urea solution. On the other hand, the hypothalamic content decreased with the infusion of the hypertonic saline. Furthermore, the continuous intracerebroventricular infusions of the hypertonic NaCl with osmotic minipumps in conscious rats significantly increased the arterial pressure after 6 days. Thereby, the plasma level of the EDLS was significantly greater than the control rats that received only the artificial CSF.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: 2nd Department of Medicine, Kyoto Prefectural University of Medicine, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Takahashi
authors.forename: M
authors.initials: M
authors.lastname: Matsusawa
authors.forename: K
authors.initials: K
authors.lastname: Suga
authors.forename: I
authors.initials: I
authors.lastname: Ikegaki
authors.forename: M
authors.initials: M
authors.lastname: Nishimura
authors.forename: M
authors.initials: M
authors.lastname: Yoshimura
authors.forename: N
authors.initials: N
authors.lastname: Ihara
authors.forename: H
authors.initials: H
authors.lastname: Yamada
authors.forename: Y
authors.initials: Y
authors.lastname: Sano
mesh_terms: D000818:Animals; D004071:Digitalis Glycosides / Q000276:immunology*; D007027:Hypothalamic Diseases / Q000378:metabolism; D007031:Hypothalamus / Q000276:immunology*; D007150:Immunohistochemistry; D007276:Injections, Intraventricular; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012462:Saline Solution, Hypertonic / Q000494:pharmacology; D012964:Sodium / Q000494:pharmacology*; D013997:Time Factors
chemical_list: D004071:Digitalis Glycosides; D012462:Saline Solution, Hypertonic; D012964:Sodium