Objective-To examine the effects of substance P (endothelium dependent vaso
dilator) and glyceryl trinitrate (endothelium independent vasodilator) on e
picardial coronary arteries in patients with normal coronary angiograms and
patients with coronary artery disease.
Design-Intracoronary infusions of normal saline, the receptor mediated nitr
ic oxide stimulant substance P (5.6 and 27.8 pmol/min each for five minutes
), and glyceryl trinitrate (250 mu g bolus) were given in 24 patients with
coronary artery disease and stable angina, and in nine patients with normal
angiograms. The diameter of proximal and distal coronary segments was meas
ured by computerised quantitative angiography
Results-Proximal segments of patients with coronary artery disease dilated
less than those of patients with normal angiograms in response to 27.8 pmol
/min substance P (mean (SEM): 7.9 (1.3)% upsilon 15 (2.3)% respectively, p
< 0.01). The proximal segments of diseased arteries also dilated less than
those of "normal)) arteries in response to glyceryl trinitrate (10.2 (1.6)%
upsilon 18.4 (2.9)%, respectively, p < 0.01). The responses of distal segm
ents to substance P and glyceryl trinitrate were similar in the two patient
groups. There were correlations tall p < 0.001) between the coronary diame
ter after substance P and after glyceryl trinitrate in normal proximal segm
ents (r = 0.94) and normal distal segments (r = 0.64), in diseased proximal
segments (r = 0.95) and diseased distal segments (r=0.89), and for coronar
y stenoses (r = 0.93).
Conclusions-Proximal segments of patients with coronary disease dilated les
s than the proximal segments of ((normal)) patients in response to substanc
e P and glyceryl trinitrate. The response to substance P is substantial and
closely correlated with the response to glyceryl trinitrate in both ('norm
al)) patients and those with coronary disease. This suggests that although
the probmal segments of diseased coronary arteries have a reduced capacity
to dilate in response to direct stimulation of smooth muscle cell relaxatio
n, they retain much of their endothelium dependent vasodilator function.