The effects of hypoxia on resting and K-stimulated tension were tested on small rings of rat pulmonary and mesenteric resistance arteries (SPA and SMA, respectively) and on the large branches of the main pulmonary artery (LPA). Reduction of PO2 from approximately 135 Torr to less than 40 Torr slowly increased SPA and LPA resting tension but did not affect SMA tension. The increases in SPA and LPA tension during hypoxia were reversible and were dependent on external Ca2+. Verapamil, 10(-6) M, inhibited the hypoxic pulmonary vasoconstriction by 53-78%. The hypoxia-contracted SPA and LPA were relaxed by 2-4 microM cromakalim; these relaxations were reversed by 2 microM glibenclamide. Hypoxia attenuated the K-stimulated tension (delta TK) in both SPA and SMA at all external K+ concentrations ([K+]o = 10-100 mM) without affecting the shapes of the respective [K+]o-tension curves. However, the SPA curve was located much farther to the left on the [K+]o axis than the SMA curve. [K+]o congruent to 13 mM evoked a half-maximal increase in SPA tension; maximal delta TK was observed at [K+]o greater than or equal to 30 mM. In contrast, [K+]o less than 20 mM induced a negligible increase in SMA tension, whereas 35-40 mM K+ activated about one-half of the increase in tension elicited by 100 mM K+. The LPA [K+]o-tension curve in normoxia was intermediate between the SMA and SPA curves, but hypoxia shifted the LPA curve to the left: delta TK was augmented at [K+]o less than 20 mM and attenuated at high [K+]o.(ABSTRACT TRUNCATED AT 250 WORDS)