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

Prostacyclin (PGI2) (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 PGI2 in these two groups. Lower concentrations of PGI2, (10 pg/ml - 100 ng/ml) caused neither contraction nor relaxation of agonist-contracted tissue. PGI2 (500-5,000 ng/ml) did not relax KCl or methoxamine contracted AS. In concentrations above 100 ng/ml, PGI2 caused a further increase in tension in KCl-depolarized preparations. The constrictor effect of PGI2 on AS was attenuated by verapamil pretreatment or removal of extracellular Ca++ from the physiological buffer. This inhibitory effect of Ca++ deficiency on the PGI2 response was significantly greater in AS from SHR compared to WKY tissue. The stable metabolite of PGI2, 6-keto PGF1a, caused a weak constrictor effect (40% of KCl reference contraction) over the concentration range 1,000-5,000 ng/ml. Contraction induced by PGI2 was not prevented by pretreatment with antagonists of adrenergic, histamine, serotonin or cholinergic receptors. The contraction response of the rat AS to PGI2 is similar to that reported for porcine coronary artery and rabbit aortic tissues in vitro.