Effects of nitric oxide and sodium nitroprusside on the intrinsic elastic properties of pressurized rat coronary artery.
The study was designed to assess the influence of either nitric oxide (NO) or sodium nitroprusside and the absence of endothelium on the intrinsic elastic properties of coronary arteries from WKY rats. For this purpose, segments of the right interventricular coronary were mounted in an arteriograph where wall thickness and internal diameter were continuously monitored while intraluminal pressure was controlled in the absence of flow. To study the passive properties, pressure-diameter relationships were determined by measuring the corresponding internal diameter for each stepwise increase in intraluminal pressure. Thus, wall stress, strain and incremental elastic modulus (Einc) were assessed in the following experimental conditions: control, incubation with nitro-L-arginine methyl ester (L-NAME, 100 microM) or L-NAME + L-arginine (L-arg, 100 microM), incubation with sodium nitroprusside (SNP, 100 microM), endothelium removal (CHAPS). The Einc-stress relationship was not significantly different in the different experimental conditions, but values of Einc plotted as function of strain were significantly decreased after L-NAME incubation and partly reversed after L-arg addition. The same effect was observed after endothelium destruction but to a lesser extent. After SNP incubation, values of Einc were significantly decreased for small values of strain and increased for high values of this parameter. These results show that NO synthase inhibition induced, for a given strain, a decrease of elastic modulus in coronary arteries. It can be speculated that functional antagonism exerted by NO against spontaneous contractile tone was reduced. Thus, the smooth muscle cells were in a greater state of activation and probably more strongly involved in the intrinsic elastic properties of this preparation. However, an unexplained effect of NO on wall stiffness cannot be excluded. Conversely, SNP increased the initial diameter and induced an initial decrease in stiffness followed by a subsequent increase. After endothelium destruction, stiffness was significantly decreased compared to control conditions. It can be concluded that NO modulates the intrinsic elastic properties of the coronary arteries through smooth muscle cell relaxation. Furthermore, results with SNP support the hypothesis that the lower the state of activation of the smooth muscle cells, the higher the elastic modulus of the arterial wall in this coronary artery preparation.
Pourageaud
F
F
Laboratoire de Pharmacodynamie, Faculté de Pharmacie, Université de Bordeaux II, France.
Freslon
J L
JL
D000818:Animals; D001120:Arginine / Q000494:pharmacology; D003331:Coronary Vessels / Q000502:physiology*; D004730:Endothelium, Vascular / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D066298:In Vitro Techniques; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D009599:Nitroprusside / Q000494:pharmacology*; D051381:Rats; D011921:Rats, Inbred WKY; D014655:Vascular Resistance
D004791:Enzyme Inhibitors; D009599:Nitroprusside; D009569:Nitric Oxide; D001120:Arginine; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester