SMOKING ATTENUATES THE VASOCONSTRICTOR RESPONSE TO NORADRENALINE IN TYPE-I DIABETIC-PATIENTS AND NORMAL SUBJECTS - POSSIBLE RELEVANCE TO DIABETIC NEPHROPATHY

Exaggerated vascular reactivity has been implicated in the pathogenesi s of diabetic nephropathy, and several studies suggest that smoking ac celerates its progression. We therefore assessed the vasoactive effect s of smoking by comparing noradrenaline-induced vasoconstriction in do rsal hand-veins between smoking and non-smoking groups of Type I diabe tic patients with and without microalbuminuria and in non-diabetic sub jects. Smokers had a significantly higher dose causing 50% vasoconstri ction (reduced sensitivity to noradrenaline) in all three groups: micr oalbuminuric diabetic smokers vs. nonsmokers, 20.2(4.6) (SEM) vs. 6.6( 2.3) ng min(-1) (P=002); normoarbuminuric, 76.9(29.4) vs. 22.8(9.1) ng min(-1) (P=0.03); non-diabetic subjects, 97.8(30.0) vs. 38.0(12.8) ng min(-1) (P=0.01). Both microalbuminuric diabetic groups showed signif icantly greater sensitivity to noradrenaline-induced vasoconstriction than the other smoking and non-smoking groups, respectively (P<0.01). Vasoconstrictor responses to noradrenaline are attenuated in smokers, possibly due to alpha-adrenoceptor down-regulation. Smoking could incr ease urinary albumin losses and accelerate renal damage through catech olamine surges which raise systemic and, perhaps, intraglomerular bloo d pressure. This hypothesis deserves further consideration.