• 1 January 1982
    • journal article
    • research article
    • Vol. 220  (2) , 375-381
Abstract
Renal (cortex and medulla) and splanchnic (duodenum, liver, pancreas and spleen) blood flows were measured with 25-.mu. radioactive microspheres in anesthetized, open-chest dogs. The effects of nicotine (36 .mu.g/kg per min i.v.) before and after selective .alpha.-adrenergic blockade (phenoxybenzamine, 1 mg/kg i.v.) and before and after combined .alpha.- and .beta.-adrenergic blockade (phenoxybenzamine, 1 mg/kg i.v. and propranolol, 1 mg/kg i.v.) were evaluated. Before adrenergic blockade, nicotine increased arterial pressure (+82%) but had heterogeneous directional effects on regional blood flows: pancreas (-64%), duodenum (-33%), kidney cortex (-31%), kidney medulla (-17%), liver (+5%) and spleen (+71%). Vascular conductance was reduced in kidney cortex (-61%), kidney medulla (-57%), duodenum (-59%), liver (-46%) and pancreas (-79%) and was not altered in spleen. Selective .alpha.-adrenergic blockade prevented the hypertensive response to nicotine, but heterogeneous changes in regional flows persisted: pancreas (-40%), spleen (-40%), kidney medulla (-35%), kidney cortex (-31%), liver (+50%) and duodenum (+74%). After combined .alpha.- and .beta.-adrenergic blockade, nicotine increased systemic arterial pressure (+75%) and decreased vascular conductance in all tissues. Results indicate a heterogeneous influence of nicotine in renal and splanchnic circulations associated with regional differences in activities of .alpha.- and .beta.-adrenergic receptors and a potent nonadrenergic vasoconstrictor response in these circulations to nicotine after blockade of .alpha.- and .beta.-adrenergic receptors.