Venous endothelium reactivity to Angiotensin II: A study in primary endothelial cultures of rat vena cava and portal vein

Trindade, Marcio Renato; Assunção, Henrique Charlanti Reis; Torres, Tathiany C.; Bertolino, Jéssica Silva; Fernandes, Liliam

doi:10.1016/j.yexcr.2017.11.016

Cited by 3 publications

(5 citation statements)

References 26 publications

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“…Ang II is involved in various cardiovascular diseases, maintaining arterial hypertension by vasoconstrictor mechanisms, stimulating the sympathetic nervous system, increasing the release of aldosterone and increasing the production of superoxide anions, mainly in the endothelium and the adventitia through NADPH oxidase-linked membrane [41,42,43]. Recently, it was demonstrated that the ECs of cava and portal veins show important properties to be activated by Ang II, probably influencing the whole circulatory system [44].…”

Section: Methodsmentioning

confidence: 99%

A Review of the Actions of Endogenous and Exogenous Vasoactive Substances during the Estrous Cycle and Pregnancy in Rats

Jaimes

Vinet

Knox

et al. 2019

Animals

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Vascular endothelium plays a key role in regulating cardiovascular homeostasis by controlling the vascular tone. Variations in sex hormones during the reproductive cycle of females affect the homeostasis of the cardiovascular system. Also, the evidence shows that estrogens show a cardioprotective effect. On this basis, this study describes some vascular responses induced by vasoactive substances during the estrous cycle in rats. We obtained the information available on this topic from the online databases that included scientific articles published in the Web of Science, PubMed, and Scielo. Many investigations have evaluated the vasoactive response of substances such as acetylcholine and norepinephrine during the estrous cycle. In this review, we specifically described the vascular response to vasoactive substances in rats during the estrous cycle, pregnancy, and in ovariectomized rats. In addition, we discussed the existence of different signaling pathways that modulate vascular function. The knowledge of these effects is relevant for the optimization and development of new treatments for some vascular pathologies.

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Section: Methodsmentioning

confidence: 99%

A Review of the Actions of Endogenous and Exogenous Vasoactive Substances during the Estrous Cycle and Pregnancy in Rats

Jaimes

Vinet

Knox

et al. 2019

Animals

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“…However, the specific NO synthase isoform involved in NO synthesis was not addressed in the aforementioned studies. Although both endothelial and neuronal NO synthase isoforms (eNOS and nNOS, respectively) have already been described to be expressed in pulmonary veins of rabbit [ 39 ] and vena cava, portal and pulmonary veins of rats [ 16 , 40 , 41 ], the specific role, and importance of these enzymes to the maintenance of venous tone have not been well elucidated.…”

Section: Venous Endothelium-derived Factorsmentioning

confidence: 99%

“…Increasing concentrations of Ang II induce contraction in isolated inferior vena cava, femoral, superior mesenteric, and portal veins of healthy rats, which is partially counterbalanced by NO since NO synthase inhibition enhances vasoconstriction induced by this peptide [ 44 , 45 ]. Intriguingly, in the primary culture of rat vena cava and portal vein endothelial cells, Ang II increased NO production in the vena cava, but not in the portal vein cells [ 41 ]. This indicates differences between ex vivo and in vitro studies using the same venous vessels.…”

Section: Venous Endothelium-derived Factorsmentioning

confidence: 99%

“…This indicates differences between ex vivo and in vitro studies using the same venous vessels. Endothelial cells from the primary culture of vena cava and portal vein showed, in addition to NO production, a basal production of the COX-derived metabolites, such as prostacyclin (PGI 2 ) and prostaglandin F2α (PGF 2α ), a venous EDRF and EDCF, respectively [ 41 ]. However, the influence of COX-derived metabolites on Ang II-induced contraction is still not a consensus.…”

Section: Venous Endothelium-derived Factorsmentioning

confidence: 99%

“…In isolated vena cava and femoral vein, Ang II-induced venoconstriction was potentiated in the presence of a non-selective COX inhibitor [ 44 ], whereas COX metabolites did not affect the Ang II response in isolated superior mesenteric and portal veins [ 45 ]. Intriguingly, Ang II increased the production of both PGI 2 and PGF 2α in the primary culture of vena cava endothelial cells, and only enhanced the PGF 2α production in the portal vein [ 41 ]. Once again, these results demonstrated that, in addition to NO, the release of COX-derived metabolites also counteracts the venoconstrictor effect of Ang II in a venous bed-dependent manner.…”

Section: Venous Endothelium-derived Factorsmentioning

confidence: 99%

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Venous endothelial function in cardiovascular disease

et al. 2022

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The essential role of the endothelium in vascular homeostasis is associated with the release of endothelium-dependent relaxing and contractile factors (EDRF and EDCF, respectively). Different from arteries, where these factors are widely studied, the vasoactive factors derived from the venous endothelium have been given less attention. There is evidence for a role of the nitric oxide (NO), endothelium-dependent hyperpolarization (EDH) mechanism, and cyclooxygenase (COX)-derived metabolites as EDRFs; while the EDCFs need to be better evaluated since no consensus has been reached about their identity in venous vessels. The imbalance between the synthesis, bioavailability, and/or action of EDRFs and/or EDCFs results in a pathological process known as endothelial dysfunction, which leads to reduced vasodilation and/or increased vasoconstriction. In the venous system, endothelial dysfunction is relevant since reduced venodilation may increase venous tone and decrease venous compliance, thus enhancing mean circulatory filling pressure, which maintains or modify cardiac workload contributing to the etiology of cardiovascular diseases. Interestingly, some alterations in venous function appear at the early stages (or even before) the establishment of these diseases. However, if the venous endothelium dysfunction is involved in these alterations is not yet fully understood and requires further studies. In this sense, this article aims to review the current knowledge on venous endothelial function and dysfunction, and the general state of the venous tone in two important cardiovascular diseases of high incidence and morbimortality worldwide: hypertension and heart failure.

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