Propofol-induced relaxation of rat mesenteric arteries: evidence for a cyclic GMP-mediated mechanism.

@article{Liu1998PropofolinducedRO,
  title={Propofol-induced relaxation of rat mesenteric arteries: evidence for a cyclic GMP-mediated mechanism.},
  author={R. Liu and M G Lang and Thomas Felix L{\"u}scher and Manuel Kaufmann},
  journal={Journal of cardiovascular pharmacology},
  year={1998},
  volume={32 5},
  pages={
          709-13
        }
}
Experiments were designed to evaluate whether guanosine 3',5'-cyclic monophosphate (cGMP)-mediated mechanisms contribute to vasodilation via propofol in rat mesenteric resistance arteries. Ring segments were suspended in the myograph system for isometric tension recording, and responses to propofol were tested in the presence and absence of methylene blue (MB), an inhibitor of guanylate cyclase. At concentrations > or = 1 microM, propofol caused concentration-dependent relaxation of vessel… 

The Mechanisms of Propofol-Mediated Hyperpolarization of In Situ Rat Mesenteric Vascular Smooth Muscle

It is suggested that propofol induces hyperpolarization and relaxation in denervated, small mesenteric vessels by activation of KCa and KATP channels, which may be mediated byactivation of NO and cGMP, but not cAMP, second messenger pathways.

The effects of propofol on vascular function in mesenteric arteries of the aging rat.

  • F. GragasinS. Davidge
  • Medicine, Biology
    American journal of physiology. Heart and circulatory physiology
  • 2009
Propofol causes relaxation in small mesenteric arteries in an endothelial-dependent and independent manner and increases ACh-induced relaxation in aged arteries, which leads to overall vascular relaxation.

Propofol Stimulates Ciliary Motility via the Nitric Oxide–Cyclic GMP Pathway in Cultured Rat Tracheal Epithelial Cells

Results show that propofol stimulates CBF via the NO–cGMP pathway in rat tracheal epithelial cells, suggesting a possible advantage of prop ofol in decreasing respiratory risk.

Protein Kinase C Isoforms Distinctly Regulate Propofol-induced Endothelium-dependent and Endothelium-independent Vasodilation

Propofol can increase the PKC-mediated availability of nitric oxide but inhibit the novelPKC-regulated Ca2+-sensitization, which provides a novel explanation for the mechanism of propofol-induced vasodilation.

Propofol and thiopental attenuate the contractile response to vasoconstrictors in human and porcine coronary artery segments.

The data indicate that propofol and thiopental relax isolated coronary segments in a dose-dependent manner, and that there is no evidence that these effects are dependent of endothelial factors.

Inhibition of Ca2+-induced relaxation by oxidized tungsten wires and paratungstate.

Recent studies of rat mesenteric arteries using a wire myograph detected decreased Ca2+ and acetylcholine-induced relaxation responses. Preliminary experiments indicated the reduced responses were

Propofol Inhibits Human Platelet Aggregation Induced by Proinflammatory Lipid Mediators

Propofol emulsion and propofol in ethanol produced similar inhibition of platelet aggregation induced by LPA, PAF, and U46619 in a dose-dependent fashion, which appears to act distal to platelet receptors, inositol phosphate 3, and phospholipase C.

Mechanisms of cellular synchronization in the vascular wall. Mechanisms of vasomotion.

A new chloride channel is demonstrated and characterized in vascular SMCs, which has properties necessary to coordinate SMCs in the vascular wall and that bestrophin protein could be the molecular substrate for this current, which is suggested to be essential for the cGMP-dependent calcium-activated chloride current.

Effects of General Anesthetics on Regulation of the Peripheral Vasculature

Current knowledge about the effects of general anesthetics on both the extrinsic intrinsic regulatory mechanisms of peripheral vascular control and the large number and complexity of these known mechanisms has made it extremely difficult to determine which are significant.

General Anesthetics and Vascular Smooth Muscle Direct Actions of General Anesthetics on Cellular Mechanisms Regulating Vascular Tone

Vascular actions of general anesthetics are reviewed and their underlying mechanisms, their in vivo relevance, and the future of research for general anesthetic vascular pharmacology are discussed.

References

SHOWING 1-10 OF 25 REFERENCES

Propofol-Associated Dilation of Rat Distal Coronary Arteries Is Mediated by Multiple Substances, Including Endothelium-Derived Nitric Oxide

It is concluded that propofol has a direct vasodilatory effect on distal coronary arteries in rats and is primarily endothelium-dependent and is mediated by multiple substances, including nitric oxide (NO) and a vasodILatory prostanoid.

Effects of propofol on isolated rabbit mesenteric arteries and veins.

Propofol has a more potent vasodilator effect on veins than on arteries, and may be associated with inhibition of endothelium-derived relaxing factor and block of voltage-gated influxes of extracellular Ca2+.

Effects of propofol and thiopental in isolated rat aorta and pulmonary artery.

This study was performed to determine if direct arterial dilating actions of propofol contribute to the drug's hypotensive actions. The effects of propofol were compared with those of thiopental on

Propofol Produces Endothelium‐Independent Vasodilation and May Act as a Ca2+Channel Blocker

It is concluded that vasodilation produced by propofol is not endothelium-dependent but is likely due to blockade of voltage-gated influx of extracellular Ca2+.

Vasodilation and Mechanism of Action of Propofol in Porcine Coronary Artery

Propofol possesses vasodilator effect and attenuates the effects of vasoconstrictor agents in porcine coronary artery and an antagonism of calcium channels may be responsible for these effects of propofol.

Influence of contractile agonists on the mechanism of endothelium‐dependent relaxation in rat isolated mesenteric artery

This study demonstrates directly that the relative contribution of nitric oxide (NO) and an NO synthase‐independent repolarization to acetylcholine‐evoked relaxation in rat isolated mesenteric

Modification of Endothelium-Dependent Relaxation by Propofol, Ketamine, and Midazolam

It is concluded that propofol and ketamine suppress endothelium-dependent relaxation, whereas midazolam has no influence, and the suppressive effect of ketamine on endothelial relaxation is mediated by suppression of nitrous oxide (NO) formation, whereas that of prop ofol may be mediated at least partly by suppressionof NO function.

Differential Relaxant Effect of High Concentrations of Intravenous Anesthetics on Endothelin‐Constricted Proximal and Distal Canine Coronary Arteries

It is concluded that thiopental, ketamine, and propofol do not possess a direct effect on the tone of large or small canine coronary arteries at concentrations seen in routine clinical practice.

Cyclic GMP Causes Ca2+ Desensitization in Vascular Smooth Muscle by Activating the Myosin Light Chain Phosphatase*

The results of this study strongly suggest that cGMP indirectly activates light chain phosphatase, the first proposed mechanism for cBromo-cGMP-induced Ca2+ desensitization in vasodilatation.

The contractile responses of isolated dog cerebral and extracerebral arteries to oxybarbiturates and thiobarbiturates.

It is concluded that thiobarbiturates are more potent vasoconstrictors than oxybarbiturating and that the barbiturate produce greater contraction in cerebral arteries than in extracerebral arteries.