The novel serine protease PreR-Co promotes endothelium-independent vasorelaxation in rabbit aortic rings.

@article{PeraldeBruno2003TheNS,
  title={The novel serine protease PreR-Co promotes endothelium-independent vasorelaxation in rabbit aortic rings.},
  author={Mar{\'i}a de los {\'A}ngeles Peral de Bruno and Paula Andrea Vincent and Liliana Romano and D C Guardia and Alfredo Coviello and Eduardo De Vito},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2003},
  volume={284 2},
  pages={
          H704-10
        }
}
The effect of a novel enzyme (PreR-Co) that activates renal prorenin was studied on rabbit aortas with and without endothelium. It was tested 1) in the basal tone of nonstimulated or ANG II-sensitized rings or rings precontracted with norepinephrine (NE), PGF(2alpha), high KCl concentration, and 2) in rings pretreated with enalaprilat, losartan, PD-123319, N(omega)-nitro-l-arginine methyl ester, HOE-140, indomethacin, or serine protease inhibitors (PMSF, aprotinin, or soybean trypsin inhibitor… 

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References

SHOWING 1-10 OF 40 REFERENCES

Role of Endothelium‐Derived Prostanoid in Angiotensin‐Induced Vasoconstriction

The data suggest that a prostanoidmediated and endothelium-dependent mechanism of vasoconstriction contributes to the constrictor effect of angiotensin II in aortic rings of rats in the early phase of aorti coarctation-induced hypertension.

Losartan reduces the vasorelaxant effect of atrial natriuretic peptide on basal tone in aorta.

The data suggest that transient exposure to Ang II induces prolonged, AT1-dependent increases in intracellular free Ca2+ which are antagonized by ANP, similar to the reduction in basal tone evoked by atrial natriuretic peptide.

Identification of epoxyeicosatrienoic acids as endothelium-derived hyperpolarizing factors.

Data support the hypothesis that the EETs are EDHFs, which causes endothelium-dependent relaxations of coronary arteries through its metabolism to epoxyeicosatrienoic acids by cytochrome P450 by boosting the open-state probability of a Ca2+-activated K+ channel in coronary smooth muscle cells.

Angiotensin IV-mediated pulmonary artery vasorelaxation is due to endothelial intracellular calcium release.

  • S. ChenJ. PatelE. Block
  • Biology, Chemistry
    American journal of physiology. Lung cellular and molecular physiology
  • 2000
Results demonstrate that ANG IV-mediated vasodilation of PAs is endothelium dependent and regulated by [Ca(2+)](i) release through receptor-coupled G protein-phospholipase C-PI 3-kinase signaling mechanisms.

The importance of endogenous prostaglandins other than prostacyclin, for the modulation of contractility of some rabbit blood vessels

The contractility of the pulmonary and especially the femoral artery is probably not modulated by PGI2 but rather by PGE2, and observations suggest that in certain blood vessels, prostaglandins other than PGI 2 are important endogenous modulators of contractility.

Relaxation of non-contracted smooth muscle by atrial natriuretic peptide.

The role of the physiological state of the vessel in the reactivity to ANP is demonstrated and a similar vasorelaxant effect of ANP on basal tension could be obtained in the absence of extracellular calcium.

Mechanisms of vasorelaxation induced by eicosapentaenoic acid (20:5n‐3) in WKY rat aorta

Results indicate EPA exerts its endothelium‐independent vasorelaxant effects in WKY rat aortae through production of prostanoids which activate K+ATP channels, and inhibition of Ca2+ mobilization from intracellular pools and influx through the non‐L‐type, but not the L‐ type, Ca2- channel are also possible mechanisms action of EPA's.

Effects of kinins on isolated blood vessels. Role of endothelium.

It was found that the presence of intact endothelium is required only for the relaxation of the dog common carotid artery in response to bradykinin and the inhibition of vascular tone by vasodilators.