Perivascular tissue of internal thoracic artery releases potent nitric oxide and prostacyclin-independent anticontractile factor☆

Malinowski, Marcin; Deja, Marek; Gołba, Krzysztof S.; Roleder, Tomasz; Biernat, Jolanta; Woś, Stanisław

doi:10.1016/j.ejcts.2007.11.007

Cited by 79 publications

(66 citation statements)

References 25 publications

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“…2 Second, the vasorelaxing effect of PVATRF and PAME from the aortic PVAT of the WKY was independent of nitric oxide synthesis or the presence of endothelium. This result is consistent with reports by others 2,3,19 in aorta of the SD and in human internal thoracic artery, although this conclusion is not universally supported by others 14,15 in the Wistar rat aortic preparations. The exact reason for the different findings is not known.…”

supporting

confidence: 92%

Role of Perivascular Adipose Tissue–Derived Methyl Palmitate in Vascular Tone Regulation and Pathogenesis of Hypertension

Lee

Chang²,

Chiang³

et al. 2011

Circulation

144

136

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Background-Perivascular adipose tissue (PVAT)-derived relaxing factor (PVATRF) significantly regulates vascular tone. Its chemical nature remains unknown. We determined whether palmitic acid methyl ester (PAME) was the PVATRF and whether its release and/or vasorelaxing activity decreased in hypertension. Methods and Results-Using superfusion bioassay cascade technique, tissue bath myography, and gas chromatography/mass spectrometry, we determined PVATRF and PAME release from aortic PVAT preparations of Wistar Kyoto rats and spontaneously hypertensive rats. The PVAT of Wistar Kyoto rats spontaneously and calcium dependently released PVATRF and PAME. Both induced aortic vasorelaxations, which were inhibited by 4-aminopyridine (2 mmol/L) and tetraethylammonium 5 and 10 mmol/L but were not affected by tetraethylammonium 1 or 3 mmol/L, glibenclamide (3 mol/L), or iberiotoxin (100 nmol/L). Aortic vasorelaxations induced by PVATRF-and PAME-containing Krebs solutions were not affected after heating at 70°C but were equally attenuated after hexane extractions. Culture mediums of differentiated adipocytes, but not those of fibroblasts, contained significant PAME and caused aortic vasorelaxation. The PVAT of spontaneously hypertensive rats released significantly less PVATRF and PAME with an increased release of angiotensin II. In addition, PAME-induced relaxation of spontaneously hypertensive rats aortic smooth muscle diminished drastically, which was ameliorated significantly by losartan. Conclusions-We found that PAME is the PVATRF, causing vasorelaxation by opening voltage-dependent K ϩ channels on smooth muscle cells. Diminished PAME release and its vasorelaxing activity and increased release of angiotensin II in the PVAT suggest a noble role of PVAT in pathogenesis of hypertension. The antihypertensive effect of losartan is attributed partly to its reversing diminished PAME-induced vasorelaxation. (Circulation. 2011;124:1160-1171.) Key Words: angiotensin II Ⅲ fatty acids Ⅲ hypertension Ⅲ potassium ion channels Ⅲ vasomotor tone Ⅲ vasorelaxation Ⅲ losartan T he systemic blood vessels are surrounded by various amounts of perivascular adipose tissue (PVAT). Since the first report by Soltis and Cassis in 1991 that PVAT attenuated contraction of aortic rings to norepinephrine, 1 it has been well accepted that the anticontractile effect of PVAT is due to release of relaxing factor(s) from these adipocytes. 2 The vasodilation induced by PVAT-derived relaxing factor (PVATRF) is independent of the endothelium, cyclooxygenase, or cytochrome P450 pathway. 2,3 The general consensus is that PVATRFinduced vasodilation is due to opening of potassium channels on the smooth muscle cells. [2][3][4][5] The chemical identity of the PVATRF, however, remains unknown. Clinical Perspective on p 1171Our recent studies using superfusion bioassay cascade technique have demonstrated release of an endogenous potent vasodilator, palmitic acid methyl ester (PAME), from the superior cervical ganglion and retina of the rat. 6,7 Because PAME is hydro...

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supporting

confidence: 92%

Role of Perivascular Adipose Tissue–Derived Methyl Palmitate in Vascular Tone Regulation and Pathogenesis of Hypertension

Lee

Chang²,

Chiang³

et al. 2011

Circulation

144

136

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“…3 This vasoregulation occurs in different visceral vascular beds and species, including rats, 1-4,6,7 mice, 10,11 pigs, 8 and humans. 5,12,13 The present study extends those findings to nonvisceral, peripheral skeletal muscle arteries. Both endothelium-independent 1,2,7,13 and endothelium-dependent 7,33 pathways have been suggested to play an important role.…”

Section: Discussionsupporting

confidence: 68%

Role of KCNQ Channels in Skeletal Muscle Arteries and Periadventitial Vascular Dysfunction

et al. 2013

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KCNQ channels have been identified in arterial smooth muscle. However, their role in vasoregulation and chronic vascular diseases remains elusive. We tested the hypothesis that KCNQ channels contribute to periadventitial vasoregulation in peripheral skeletal muscle arteries by perivascular adipose tissue and that they represent novel targets to rescue periadventitial vascular dysfunction. Two models, spontaneously hypertensive rats and New Zealand obese mice, were studied using quantitative polymerase chain reaction, the patch-clamp technique, membrane potential measurements, myography of isolated vessels, and blood pressure telemetry. In rat Gracilis muscle arteries, anticontractile effects of perivascular fat were inhibited by the KCNQ channel blockers XE991 and linopirdine but not by other selective K + channel inhibitors. Accordingly, XE991 and linopirdine blocked noninactivating K + currents in freshly isolated Gracilis artery smooth muscle cells. mRNAs of several KCNQ channel subtypes were detected in those arteries, with KCNQ4 channels being dominant. In spontaneously hypertensive rats, the anticontractile effect of perivascular fat in Gracilis muscle arteries was largely reduced compared with Wistar rats. However, the vasodilator effects of KCNQ channel openers and mRNA expression of KCNQ channels were normal. Furthermore, KCNQ channel openers restored the diminished anticontractile effects of perivascular fat in spontaneously hypertensive rats. Moreover, KCNQ channel openers reduced arterial blood pressure in both models of hypertension independent of ganglionic blockade. Thus, our data suggest that KCNQ channels play a pivotal role in periadventitial vasoregulation of peripheral skeletal muscle arteries, and KCNQ channel opening may be an effective mechanism to improve impaired periadventitial vasoregulation and associated hypertension.

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“…In healthy individuals, PVAT has been demonstrated to exert anti-contractile effects on neighbouring vessels, and this PVAT is less responsive to noradrenaline than naked vessels (Soltis & Cassis 1991). In addition, adventitium-derived relaxing factor (ADRF) experiments have demonstrated PVAT anti-contractility to be due to its function as a paracrine tissue rather than adipose merely obstructing vasoconstrictors (Lohn et al 2002, Gao et al 2005, Malinowski et al 2008, Greenstein et al 2009). …”

Section: Perivascular Adipose Tissuementioning

confidence: 99%

Role of adipokines in cardiovascular disease

Mattu¹,

Randeva²

2012

Journal of Endocrinology

251

203

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The discovery of leptin in 1994 sparked dramatic new interest in the study of white adipose tissue. It is now recognised to be a metabolically active endocrine organ, producing important chemical messengers -adipokines and cytokines (adipocytokines). The search for new adipocytokines or adipokines gained added fervour with the prospect of the reconciliation between cardiovascular diseases (CVDs), obesity and metabolic syndrome. The role these new chemical messengers play in inflammation, satiety, metabolism and cardiac function has paved the way for new research and theories examining the effects they have on (in this case) CVD. Adipokines are involved in a 'good-bad', yin-yang homoeostatic balance whereby there are substantial benefits: cardioprotection, promoting endothelial function, angiogenesis and reducing hypertension, atherosclerosis and inflammation. The flip side may show contrasting, detrimental effects in aggravating these cardiac parameters.

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Perivascular tissue of internal thoracic artery releases potent nitric oxide and prostacyclin-independent anticontractile factor☆

Cited by 79 publications

References 25 publications

Role of Perivascular Adipose Tissue–Derived Methyl Palmitate in Vascular Tone Regulation and Pathogenesis of Hypertension

Role of Perivascular Adipose Tissue–Derived Methyl Palmitate in Vascular Tone Regulation and Pathogenesis of Hypertension

Role of KCNQ Channels in Skeletal Muscle Arteries and Periadventitial Vascular Dysfunction

Role of adipokines in cardiovascular disease

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