Effect of endothelium on the actions of sympathetic and sensory nerves in the perfused rat mesentery.

  title={Effect of endothelium on the actions of sympathetic and sensory nerves in the perfused rat mesentery.},
  author={Y J Li and Sue Piper Duckles},
  journal={European journal of pharmacology},
  volume={210 1},
  • Y. LiS. Duckles
  • Published 7 January 1992
  • Biology, Medicine
  • European journal of pharmacology

Electrophysiological effects of activating the peptidergic primary afferent innervation of rat mesenteric arteries

The results suggest that CGRP released from primary afferent axons hyperpolarizes vascular smooth muscle by activating glibenclamide‐sensitive K+ channels and indicates that an unknown factor released by the primary afferential axons increases e.j.p. amplitude.

Involvement of sensory nerves in vasodilator responses to acetylcholine and potassium ions in rat hepatic artery

The results suggest that C GRP is a nerve‐derived hyperpolarizing factor in the rat hepatic artery and the ability of ouabain to disclose a CGRP‐mediated neurogenic relaxation must be considered when this agent is used as a pharmacological tool.

The effect of endotoxin on sympathetic responses in the rat isolated perfused mesenteric bed; involvement of nitric oxide and cyclo‐oxygenase products

The data suggest that endotoxin impairs the release of noradrenaline and that this effect is secondary to increased production of nitric oxide and prostanoids, possibly by the endothelium.

Differential actions of anandamide, potassium ions and endothelium-derived hyperpolarizing factor in guinea-pig basilar artery

It is indicated that EDHF is neither anandamide nor potassium ions in this artery, and EDHF-mediated vasorelaxation in the guinea-pig isolated basilar artery does not seem to involve Na+/K+-ATPase, sensory nerves or gap junctions.



Endothelial cells inhibit the vascular response to adrenergic nerve stimulation by a receptor-mediated mechanism.

Data suggest that endothelial cells modulate the effect of perivascular neurotransmitters by a receptor-mediated mechanism in the case of the sympathetic innervation and would be more relevant at low levels of transmitter release and will be minimized during intense sympathetic stimulation.

Vasoconstrictor response induced by 5-hydroxytryptamine released from vascular adrenergic nerves by periarterial nerve stimulation.

5-HT is taken up by vascular adrenergic nerve endings in vitro and it is released by nerve stimulation, resulting in vasoconstriction, which suggests that 5-HT may contribute to the maintenance of local vascular tone through this mechanism in vivo.

Endothelium inhibits norepinephrine release from adrenergic nerves of rabbit carotid artery.

Observations indicate that the endothelium metabolizes norepinephrine, acts as a physical barrier to its overflow into the blood vessel lumen, and inhibits the release of the adrenergic transmitter from adrenergic nerves.

Capsaicin-induced vasodilatation of human coronary arteries in vitro is mediated by calcitonin gene-related peptide rather than substance P or neurokinin A.

CGRP but not SP mimics the vasodilatory effects of capsaicin on human coronary arteries, which suggests that CGRP rather than SP is likely to mediate the relaxatory effects seen upon activation of cardiac sensory nerves.

Dual effects of capsaicin on responses of the rabbit ear artery to field stimulation

The results suggest that the dual effects of Cap on stimulation‐induced contractions of rabbit ear artery may arise from the release of multiple mediators that act prejunctionally to modulate NA release.

The effect of perivascular denervation on endothelium-dependent relaxation to acetylcholine

In the arterial beds from capsaicin treated rats there was a depression of the ability of Acetylcholine to produce endothelium dependent relaxation, but no change in endothelia-dependent relaxation to ACh was found in 6-hydroxydopamine treated rats.

Calcitonin gene-related peptide and vasodilator nerves in large cerebral arteries of cats.

Results suggest that CGRP is involved in the TNS-induced vasodilator response of the large cerebral arteries of the cat, which was of nonadrenergic, noncholinergic origin.