La. Barker et al., Acute presser actions of ouabain do not enhance the actions of phenylephrine or norepinephrine in anesthetized rats, J CARDIO PH, 37(3), 2001, pp. 339-348
Citations number
43
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
The inhibition of high-affinity isoforms of the Na+,K+-ATPase by nanomolar
levels of ouabain has been proposed to enhance the actions of vasoconstrict
or agents that act via a Ca+2-dependent mechanism. The present study tested
this hypothesis by evaluating the effects of ouabain (6 and 18 mug/kg, i.v
.) on the vasopressor actions of phenylephrine and norepinephrine in anesth
etized, reflex-blocked rats. In separate groups of animals, dose-response c
urves for increases in diastolic pressure produced by phenylephrine were ge
nerated after the administration of saline (control), ouabain (18 mug/kg),
L-omega-N-nitro arginine methyl ester (L-NAME, 3 mu mol/kg) and angiotensin
II (15 ng/kg per min). Treatment with ouabain (18 mug/kg) produced an incr
ease in diastolic pressure of 19 +/- 3 mm Hg but did not significantly alte
r the potency or maximal response produced by phenylephrine. In contrast. t
reatment with angiotensin II and L-NAME, agents known to enhance the action
s of alpha -adrenoceptor agonists, increased the potency of phenylephrine.
In animals in which the presser actions of norepinephrine were evaluated be
fore and after the administration of ouabain (6 mug/kg), ouabain did not al
ter the presser response to norepinephrine. Blockade of alpha -adrenoceptor
s with phentolamine was found to attenuate as well as partially reverse the
increase in diastolic pressure produced by ouabain. These observations sug
gest that ouabain produces a presser response by actions on sympathetic ner
ve endings as well as on vascular smooth muscle and that these actions do n
ot alter the sensitivity to phenylephrine or norepinephrine.