Comparison of nitroprusside and nitroglycerin in inhibition of angiotensin II and other vasoconstrictor-mediated contraction in human coronary bypass conduits.
OBJECTIVE
To compare the effect of nitroprusside (SNP) and nitroglycerin (NTG) on angiotensin II (ANGII), endothelin-1 (ET-1), and alpha1-adrenoceptor (phenylephrine, PE)-mediated contraction in internal mammary artery (IMA).


METHODS
Human IMA segments (n=120) taken from 37 patients were studied. Concentration-relaxation curves for SNP and NTG were established in IMA precontracted with these vasoconstrictors. Concentration-contraction curves were also constructed in IMA rings incubated with SNP and NTG (0.1 and 1 microM) for 10 min.


RESULTS
Both SNP and NTG caused full relaxation with similar EC50s except NTG was four-fold more potent than SNP in PE-induced contraction (-7.92 +/- 0.06 vs -7.32 +/- 0.2 log M, mean +/- s.e. mean, P<0.01; 95% confidence interval for the difference of the means: 0.19, 1.01 log M). Pretreatment with SNP (0.1 and 1 microM) significantly depressed the contraction by ANGII from 56.6 +/- 7.7% (of 100 mM K+-contraction) to 18.3 +/- 8.6% and 3.9 +/- 2.1% (P=0.0001). In four rings treated with SNP, the contraction to ANGII was abolished whereas NTG did not depress ANGII-mediated contraction. Pretreatment with SNP (1 microM), but not NTG, significantly depressed the magnitude of the PE-induced contraction from 4.7 +/- 1.2 to 1.7 +/- 0.4 g (P<0.05). Treatment with both SNP and NTG significantly increased the EC50 (-5.09 +/- 0.17 log M, P=0.0007 for SNP and -5.40 +/- 0.06 log M, P=0.02 for NTG). Pretreatment with SNP did not significantly change either the magnitude or the EC50 of the ET-1-induced contraction.


CONCLUSIONS
SNP may be advantageous compared with NTG in preventing coronary arterial graft contraction. However, once grafts have constricted to ANGII, alpha1-adrenoceptor agonists, and ET-1, NTG may be only marginally advantageous.
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G W
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Grantham Hospital, Department of Surgery, University of Hong Kong, Hong Kong.
Yang
C Q
CQ
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000804:Angiotensin II / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D001026:Coronary Artery Bypass; D019332:Endothelin-1 / Q000494:pharmacology; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D008323:Mammary Arteries / Q000187:drug effects* / Q000502:physiology; D005996:Nitroglycerin / Q000494:pharmacology*; D009599:Nitroprusside / Q000494:pharmacology*; D014661:Vasoconstriction / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology*
D000316:Adrenergic alpha-Agonists; D019332:Endothelin-1; D014665:Vasodilator Agents; D000804:Angiotensin II; D009599:Nitroprusside; D005996:Nitroglycerin