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PGE2 verstarkt an isoliert perfundierten Kaninchennieren und Meerschweinchenlungen die Wirkung von Histamin auf den Perfusionsdruck. Gleiches wurde auch mit Metiamid, einem H2-Rezeptorblocker, beobachtet. Anhand dieser Befunde wird die mogliche Rolle von c-AMP bei dieser Verstarkerwirkung diskutiert.

Angiotensin converting enzyme activity was found to be significantly decreased in the isolated perfused lung from zinc-deficient rats when compared with that of controls. Addition of zinc ion to the superfusion medium did not cause a recovery in this decreased activity of the enzyme. It is postulated that zinc deficiency probably produces a structural change in the lung angiotensin converting enzyme.

Impromidine and dimaprit, two newly-synthesized histamine H2-receptor agonists, have been shown to produce a prostaglandin-mediated contraction in the isolated rat stomach fundus.

Crude kallikrein (Padutin®), but not pure kallikrein, when preincubated with angiotensin I caused a potentiation of the myotropic effect of decapeptide on the isolated continuously superfused rabbit aortic strip. Addition of converting enzyme inhibitor, SQ 20881, to the medium inhibited this potentiation. The potentiation by crude kallikrein of the myotropic effect of angiotensin I is probably due to the conversion of decapeptide to octapeptide angiotensin II. This study indicates that Padutin is not a pure kallikrein preparation and probably contains a kininase fraction which causes the conversion of angiotensin I.

The distribution of histamine receptors was studied in the isolated perfused vascular bed of the cat terminal ileum. The results indicated that the depressor effect of histamine is mediated through the stimulation of metiamide-sensitive H2-receptors, while the pressor effect of the amine is mediated by the stimulation of mepyramine-sensitive H1-receptors.