The Vasopressor Response to Centrally Administered Ouabain

• Published in: Circulation research Vol. 55; no. 6; pp. 773 - 779
• Main Authors: Caldwell, R William, Songu-Mize, Emel, Bealer, Steven L
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD American Heart Association, Inc 01.12.1984; Lippincott
• Subjects: Animals; Biological and medical sciences; Cardiotonic agents; Cardiovascular system; Diastole - drug effects; Epinephrine - blood; Hexamethonium; Hexamethonium Compounds - pharmacology; Injections, Intraventricular; Medical sciences; Nephrectomy; Ouabain - pharmacology; Pharmacology. Drug treatments; Phentolamine - pharmacology; Propranolol - pharmacology; Rats; Rats, Inbred Strains; Renin - blood; Saralasin - pharmacology; Vasoconstrictor Agents - pharmacology; Vertebrata; Cardiotonic agent; Mammalia; Rat; Digitalis; Animal; Rodentia; Central nervous system; Intracerebral administration; Arterial pressure; Cerebral ventricle
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/01.RES.55.6.773

Ouabain (80 γgAg) injected into the lateral cerebroventricles (ICV) of rats produced a prompt and sustained increase in arterial blood pressure. A diastolic blood pressure increase of about 40 mm Hg began within 10 minutes of injection and lasted at least 1 hour. This dose of ouabain had no effect on arterial pressure when given intravenously. The vasopressor response to intracerebroventricularly administered ouabain was not blocked by prior intravenous administration of phentolamine (1 γg/kg) or hexamethonium (3 mg/kg). However, continuous intravenous infusion of saralasin (2 mg/kg per min) prevented the pressor response to intracerebroventricularly administered ouabain. In addition, bilateral nephrectomy, adrenalectomy, pretreatment with intravenously administered propranolol (2 mg/kg) or captopril (10 mg/kg) abolished the increase in blood pressure evoked by intracerebroventricularly administered ouabain. Plasma renin and epinephrine levels at the peak of the pressor response to intracerebroventricularly administered ouabain were respectively, about 2.5- and 2-fold higher than in control rats. Our data indicate that ouabain administered into the central nervous system produces a hypertensive effect which does not primarily involve peripheral α-adrenergic receptors, but appears to be due to angiotensin II produced by renin of renal origin. These data suggest that digitalis agents can interact with sites in the central nervous system to induce a release of renin from the kidney; this release appears to involve activation of β-adrenergic receptors by catecholamines from the adrenal medulla, perhaps through a direct adrenal-kidney vascular network.