Lack of involvement of endothelin‐1 in angiotensin II‐induced contraction of the isolated rat tail artery

Jiang, Yanfen; Triggle, Chris R.

doi:10.1038/sj.bjp.0703674

Cited by 6 publications

(6 citation statements)

References 34 publications

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“…ET-1 mediates vasoconstrictor effects of ANG II in isolated vascular preparations (96, 819). ET A blockade inhibited the vasoconstrictor response to ET-1 in rat mesenteric artery, but not in rat aorta (96) or rat tail artery (341). ET-1 increases the sensitivity of isolated vascular preparations to other vasoconstrictors, and in fact, ET-1 stimulated by ANG II has the same effect to potentiate vasoconstriction (156, 863).…”

Section: Endothelin and Humoral Systemsmentioning

confidence: 98%

Regulation of Blood Pressure and Salt Homeostasis by Endothelin

Kohan

Rossi

Inscho

et al. 2011

Physiological Reviews

367

459

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Endothelin (ET) peptides and their receptors are intimately involved in the physiological control of systemic blood pressure and body Na homeostasis, exerting these effects through alterations in a host of circulating and local factors. Hormonal systems affected by ET include natriuretic peptides, aldosterone, catecholamines, and angiotensin. ET also directly regulates cardiac output, central and peripheral nervous system activity, renal Na and water excretion, systemic vascular resistance, and venous capacitance. ET regulation of these systems is often complex, sometimes involving opposing actions depending on which receptor isoform is activated, which cells are affected, and what other prevailing factors exist. A detailed understanding of this system is important; disordered regulation of the ET system is strongly associated with hypertension and dysregulated extracellular fluid volume homeostasis. In addition, ET receptor antagonists are being increasingly used for the treatment of a variety of diseases; while demonstrating benefit, these agents also have adverse effects on fluid retention that may substantially limit their clinical utility. This review provides a detailed analysis of how the ET system is involved in the control of blood pressure and Na homeostasis, focusing primarily on physiological regulation with some discussion of the role of the ET system in hypertension.

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Section: Endothelin and Humoral Systemsmentioning

confidence: 98%

Regulation of Blood Pressure and Salt Homeostasis by Endothelin

Kohan

Rossi

Inscho

et al. 2011

Physiological Reviews

367

459

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“…These distinct embryonic origin differences also converge in the adult vessels [13]. As noted earlier, the VSMCs of the proximal aorta arise from two distinct embryonic origins: the NC and the somatic mesoderm [14,15]. This juxtaposition of the VSMCs from different embryonic origins in the aorta contributes to the specific ability of the aorta to respond to high local pressure/force loading and various chemical stimulation as well as neuronal-hormonalregulation to meet the physiological requirement of circulation.…”

Section: Origin Of Vsmcsmentioning

confidence: 73%

“…While the embryonic origins of many VSMC populations are known, the exact nature of the VSMC precursor remains elusive. It has been indicated that VSMC progenitors may arise from distinct embryonic sources including the splanchnic mesoderm [18], somatic mesoderm [15,19], neural crest (NC) [14,20], mesothelial [21], and other embryonic cell types [22]. In the aorta, splanchnic mesodermal cells are first recruited and differentiate into VSMCs.…”

Section: Origin Of Vsmcsmentioning

confidence: 99%

“…The rest of the cardiac NC remains in the pharyngeal arch arteries and become the VSMCs of the aortic arch and the arteries of the head and neck [20]. The border that forms between the NC-derived VSMCs of the ascending aortic arch (aAo) and mesoderm-derived VSMCs of the descending aorta (dAo) is maintained throughout development and into adulthood [14,20]. Once cells encircle the aorta and differentiate into VSMCs, they undergo a closely regulated process of layer formation within the media.…”

Section: Origin Of Vsmcsmentioning

confidence: 99%

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Vascular Smooth Muscle Cell

Zhou¹,

Stoll²,

Leimena³

et al. 2018

Muscle Cell and Tissue - Current Status of Research Field

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Vascular smooth muscle cells (VSMCs) are the stromal cells of the vascular wall and are responsible for regulating arterial tone, blood pressure, and blood supply of the tissues. VSMCs display diversity in function and phenotype depending on their location within the arterial tree (large conduit vs. small resistance vessels), their embryologic origin, and their organ-dependent microenvironment. The heterogeneity of VSMCs is regulated by multiple mechanisms including intracellular signaling and changes in the VSMC microenvironment. Genetic disorders and extrinsic stimuli-induced dysfunction in VSMCs are associated with age-related vascular pathogenesis and vascular diseases, and thus are considered as a potential therapeutic target.

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“…22 have reported that verapamil and diltiazem do not inhibit the Ang II‐induced contraction of vascular smooth muscle, indicating that L‐type Ca 2+ channels are not involved in this response. In an experiment using rat tail artery, the Ang II‐ and ET‐1‐induced contraction was found to be insensitive to L‐type Ca 2+ channel antagonist, nifedipine, but blocked by SK, indicating that SK may be useful for the treatment of hypertension in patients insensitive to L‐type calcium channel blocker 23. Bova et al .…”

Section: Discussionmentioning

confidence: 99%

Reduction of blood pressure by store‐operated calcium channel blockers

Elimban

Dhalla

2015

J Cellular Molecular Medi

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The voltage‐operated Ca2+ channels (VOCC), which allow Ca2+ influx from the extracellular space, are inhibited by anti‐hypertensive agents such as verapamil and nifedipine. The Ca2+ entering from outside into the cell triggers Ca2+ release from the sarcoplasmic reticulum (SR) stores. To refill the depleted Ca2+ stores in the SR, another type of Ca2+ channels in the cell membrane, known as store‐operated Ca2+ channels (SOCC), are activated. These SOCCs are verapamil and nifedipine resistant, but are SKF 96465 (SK) and gadolinium (Gd3+) sensitive. Both SK and Gd3+ have been shown to reduce [Ca2+]i in the smooth muscle, but their effects on blood pressure have not been reported. Our results demonstrated that both SK and Gd3+ produced a dose‐dependent reduction in blood pressure in rat. The combination of SK and verapamil produced an additive action in lowering the blood pressure. Furthermore, SK, but not Gd3+ suppressed proliferation of vascular smooth muscle cells in the absence or presence of lysophosphatidic acid (LPA). SK decreased the elevation of [Ca2+]i induced by LPA, endothelin‐1 (ET‐1) and angiotensin II (Ang II), but did not affect the norepinephrine (NE)‐evoked increase in [Ca2+]i. On the other hand, Gd3+ inhibited the LPA and Ang II induced change in [Ca2+]i, but had no effect on the ET‐1 and NE induced increase in [Ca2+]i. The combination of verapamil and SK abolished the LPA‐ or adenosine‐5′‐triphosphate (ATP)‐induced [Ca2+]i augmentation. These results suggest that SOCC inhibitors, like VOCC blocker, may serve as promising drugs for the treatment of hypertension.

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Lack of involvement of endothelin‐1 in angiotensin II‐induced contraction of the isolated rat tail artery

Cited by 6 publications

References 34 publications

Regulation of Blood Pressure and Salt Homeostasis by Endothelin

Regulation of Blood Pressure and Salt Homeostasis by Endothelin

Vascular Smooth Muscle Cell

Reduction of blood pressure by store‐operated calcium channel blockers

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