Objective: To observe the reactivity of isolated pulmonary artery rings from rats with chronic hypoxic pulmonary hypertension (HPH) to protein kinase.C (PKC) activator.
Methods: Pulmonary artery rings from adult rats exposed to normobaric hypoxia for two weeks and normal rats were isolated for measurement of isometric contractions to PMA, the specific activator of PKC. Responses were examined as follows: (1) The maximal response (P(1)) to 0.5 micromol/L PMA and the time required to achieve a half-maximal response to 0.5 micromol/L PMA (t(1/2)); (2) Dose-response curve in response to PMA (0.01 - 10.0 micromol/L) and the dose of PMA that produced a contractile response as 50% of the maximal response (P(0)) to 80 mmol/L KCl (EC(50) KCl).
Results: P(1) of hypoxic group (34.3 +/- 2.4) P(0)% was greater than that of normal group [(26.2 +/- 2.9) P(0)%, n = 6, P < 0.05)], t(1/2) and EC(50) KCl of hypoxic group [(27 +/- 7) min, and (0.7 +/- 0.1) micromol/L] were smaller than those of normal group [(32 +/- 5) min, n = 6, P < 0.05, and (6.0 +/- 0.2) micromol/L, n = 12, P < 0.05].
Conclusions: The reactivity of pulmonary artery rings from hypoxic rats to PMA was enhanced, which indicates that protein kinase C may have an important role in the development of HPH.