The canine posterior vena cava was excised and divided into three embryologically distinct segments: segment A (supradiaphragm), segment B-C (intrahepatic and that between liver and renal veins), and segment D (infrarenal). Circular and longitudinal strips were cut from each segment, suspended in Krebs bicarbonate solution and isometric tensions were recorded. The responses to six vasoactive agents, as well as transmural neural stimulation were studied. Maximum tension and ED50 were obtained for norepinephrine, epinephrine, acetylcholine, bradykinin, histamine and 5-hydroxytryptamine (5-HT). The responses were not only quantitatively, but qualitatively different among the three segments. Bradykinin constricted the strips in A and B-C but not in D. 5-HT (less than 10(-5) M) caused a dose-dependent contraction in A and D through its direct stimulating action, while in C, a contractile response appeared only after administration of a higher dose of 5-HT. This was due to an indirect sympathomimetic action of the agent. Segment B-C, which histologically contained massive longitudinal muscle bundles in the outer layer of the wall, exhibited spontaneous, rhythmic contractions. The existence of a cholinergic excitatory innervation, in addition to adrenergic, was demonstrated in C by transmural neural stimulation.

Acetylcholine↗

PubMed1978

Effects of adenosine triphosphate and prostaglandins on vascular adrenergic transmission.

The effects of prostaglandins (PGs) on the adrenergic neuroeffector transmission and their relationship to the action of ATP were investigated. This was in view of the putative negative feedback mediated by ATP or a related purine compound, and the reported stimulation of PG synthesis by adenine nucleotides. The central ear artery and saphenous vein of the rabbit were isolated and their contractile responses to adrenergic nerve stimulation monitored. These responses were markedly reduced by PGE1 and PGE2 and significantly augmented by indomethacin and aspirin, suggesting the occurrence of the PGE-mediated negative feedback. PGF2a facilitated the response of the vein but was without affect on the artery, while arachidonic acid was facilitatory on the former and inhibitory on the latter. Possibly a PGF2a-like substance is formed in the presence of arachidonic acid and, in the vein, masks the effect of any PGE. ATP depressed the arterial and venous contractile response to adrenergic nerve stimulation. This inhibition was not significantly affected by indomethacin or aspirin. It was enhanced in the artery and diminished in the vein by arachidonic acid, but only to the extent of algebraic sum of the effects of ATP and the acid. It seems possible that the purine- and PGE-mediated feedback mechanisms are independent and parallel pathways.

Adenosine Triphosphate↗

PubMed1978