[Contribution of the vascular interstitial matrix to induced contraction by angiotensin II. In vitro studies on the rabbit aorta, mesenteric artery and vein].

This study examines the contribution of hyaluronan, a rich anionic glycoprotein, to angiotensin-II-induced contraction (AII: 10(-11) to 10(-8) M) of endothelium-free strips of aorta, mesenteric artery and vein obtained from normal rabbits. Tissues are treated with hyaluronidase (HYAL: 1 mg/ml) during 60 min before being mounted in organ baths superfused with normal Krebs solution for isotonic contraction. Isotonic contraction of the mesenteric artery to the four highest doses of AII is reduced by 50 to 60% following HYAL treatment, compared to the normal contraction curve (0.01 < p < 0.001). Isotonic contraction of the aorta and mesenteric vein to AII is not influenced by HYAL. Isometric contraction curves of the three tissues to AII are not modified by HYAL. In additional experiments, the Krebs solution was selectively enriched in calcium (3.8 mM/l) and in sodium (160 mEq/l) to verify if the effect of HYAL is associated with interstitial washing in the concentration of these cations, because of the hyaluronan digestion. In fact, the calcium-rich superfusion is associated with complete correction of the HYAL-induced reduction of the mesenteric artery isotonic contraction. The sodium-rich superfusion failed to normalize the depressed mesenteric artery contraction. Since HYAL only affected isotonic contraction of the resistance artery (mesenteric), it is likely that the interstitial space of this tissue contains more hyaluronan than the aortic or mesenteric vein matrix, or that HYAL only affected the smooth muscle cell population involved in the circular tonus of the resistance vessel. Correction of the abnormality by calcium enrichment of the Krebs solution suggests that a relative diminution and/or a redistribution of this important cation, obtained following the interstitial degradation of hyaluronan.