Increased levels of
octopamine in
adrenergic nerve terminals and plasma have been implicated in the circulatory and renal disturbances of chronic
hepatic failure. Little is known about its renal actions in normal animals. In the present study, DL-
octopamine was administered both i.v. and into one renal artery of anaesthetized dogs in doses ranging between 25-200 micrograms/min (1.6-20 micrograms/kg/min).
Octopamine was hypertensive in doses of 100 micrograms/min and more and this change was associated with a significant decrement in GFR and renal perfusion. This
amine also exerted a direct tubular effect since decreased excretion of
sodium and water occurred in the absence of blood pressure or renal perfusional changes when given i.v. When given into one renal artery
octopamine produced only an ipsilateral antidiuresis and antinatriuresis, in the absence of any change to GFR or renal perfusion.
Lithium clearances suggest that
octopamine acts beyond the proximal tubule in altering the tubular reabsorption of
salt and water. Because
octopamine was found to increase blood pressure in the presence of a hypertensive infusion of
noradrenaline, it is likely that this
amine exerts a primary pharmacological effect rather than liberating
noradrenaline from nerve terminals. Saline expansion (7%
body weight), acute biliary obstruction, chronic
cirrhosis with
ascites, and chronic thoracic caval constriction with the production of
ascites all abolish the effect of
octopamine when administered at 100 micrograms/min. Though
octopamine may directly influence renal perfusion, its possible role in
liver disease remains uncertain.