Prostacyclin-induced contraction of isolated aortic strips from normal and spontaneously hypertensive rats (SHR)

Abstract

Prostacyclin (PGl 2) (500-5,000 ng/ml) produced a concentration-dependent increase in contractile tension of isolated thoracic aortic strips (AS) from normotensive (WKY) and spontaneously hypertensive rats (SHR). No significant differences were noted between this response to PGl 2 in these two groups. Lower concentrations of PGl 2 (10 pg/ml — 100 ng/ml) caused neither contraction nor relaxation of agonist-contracted tissue. PGl 2 (500-5,000 ng/ml) did not relax KCl or methoxamine contracted AS. In concentrations above 100 ng/ml, PGl 2 caused a further increase in tension in KCl-depolarized preparations. The constrictor effect of PGl 2 on AS was attenuated by verapamil pretreatment or removal of extracellular Ca ++ from the physiological buffer. This inhibitory effect of Ca ++ deficiency on the PGl 2 response was significantly greater in AS from SHR compared to WKY tissue. The stable metabolite of PGl 2, 6-keto PGF 1a, caused a weak constrictor effect (40% of KCl reference contraction) over the concentration range 1,000–5,000 ng/ml. Contraction induced by PGl 2 was not prevented by pretreatment with antagonists of adrenergic, histamine, serotonin or cholinergic receptors. The contraction response of the rat AS to PGl 2 is similar to that reported for porcine coronary artery and rabbit aortic tissues in vitro.