1. The mechanical and pharmacological properties of small pulmonary arteries (100–300 μm normalized lumen diameter) were directly compared with those of the left main pulmonary artery (1–2 mm) from the rat. The active and passive length-tension characteristics and responses to a variety of agonists and antagonists were dependent on arterial diameter.

2. Maximum contractile function was obtained in both groups of vessels when stretched so as to give an equivalent transmural pressure of 30 mmHg. This is substantially lower than that found for systemic vessels, and reflects the normal low pulmonary arterial pressure.

3. Noradrenaline was a powerful vasoconstrictor in large but not small pulmonary arteries (P> 0.001). In contrast, bradykinin produced a significantly greater response in the small arteries (P < 0.001). In comparison with large pulmonary arteries, small arteries were more sensitive to noradrenaline (P<0.05) and 5-hydroxytryptamine (P < 0.001), less sensitive to endothelin-1 (P> 0.001) and had the same sensitivity to prostaglandin F.

4. The mechanism that maintains the low arterial tone of the pulmonary circulation is unknown, but it may involve the release of relaxing factors from the endothelium. In this preparation, basal resting tone could not be demonstrated in either large or small arteries.

5. Acetylcholine-induced relaxation of pre-contracted pulmonary arteries was reduced or absent in the small artery, despite histological evidence of an intact endothelium. In large arteries pre-contracted with prostaglandin F, acetylcholine (100 μmol/l) caused 88.2% relaxation compared with 25.2% in the small artery.

6. These results suggest that it would be unwise to extrapolate from results obtained either in large pulmonary artery preparations or in perfused lungs to what may occur in the functionally important resistance arteries.

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