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10.14814/phy2.13623 http://scihub22266oqcxt.onion/10.14814/phy2.13623 C5835495!5835495!29504268     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29504268&cmd=llinks): Failed to open stream: HTTP request failed! 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Differential effects of long?term slow?pressor and subpressor angiotensin II on contractile and relaxant reactivity of resistance versus conductance arteries |pdf=|usr=}}{{29504268}} gab.com Text Differential effects of long term slow pressor and subpressor angiotensin II on contractile and relaxant reactivity of resistance versus conductance arteries JO: Physiol Rep http://www.kidney.de/pget.php?&tw=1&pmid=29504268 #FOAvip Vascular reactivity was evaluated in three separate arteries isolated from rats after angiotensin II (Ang II) was infused chronically in two separate experiments, one using a 14?day high, slow?pressor dose known to produce hypertension and the other using a 7?day low, subpressor but hypertensive?sensitizing dose. There were three new findings. First, there was no evidence of altered vascular reactivity in resistance arteries that might otherwise explain the hypertension due to the high Ang II or the hypertensive?sensitizing effect of the low Ang II dose. Second, the high Ang II dose exerted a novel differential effect on arterial contractile responsiveness to the sympathetic neurotransmitter, norepinephrine, depending on the level of sympathetic innervation. It clearly enhanced that responsiveness in the sparsely innervated aorta but not in small mesenteric resistance arteries or the proximal (conductance) portion of the caudal artery, both of which are densely innervated. This suggests that the increased expression of alpha adrenergic receptors after long?term exposure to Ang II as previously reported for aortic smooth muscle, is prevented in densely innervated arteries, likely due to long?term Ang II?mediated increase in sympathetic neural traffic to those vessels. Third, the same high dose of Ang II impaired aortic relaxation in response to the nitric oxide (NO) donor nitroprusside without impairing aortic endothelium?dependent relaxation. NO is the main relaxing substance released by aortic endothelium. Accordingly, it is possible that this dose of Ang II is also associated with enhanced release of and/or enhanced smooth muscle responsiveness to other endothelial relaxing substances in a compensatory capacity. Twit Text FOAVip Differential effects of long term slow pressor and subpressor angiotensin II on contractile and relaxant reactivity of resistance versus conductance arteries ????Physiol Rep http://www.kidney.de/pget.php?&tw=1&pmid=29504268 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29504268 #FOAvip English Wikipedia <ref>{{Cite pmid|29504268}}</ref> Differential effects of long?term slow?pressor and subpressor angiotensin II on contractile and relaxant reactivity of resistance versus conductance arteries #MMPMID29504268 Kopf PG; Phelps LE; Schupbach CD; Johnson AK; Peuler JD Physiol Rep 2018[Mar]; 6 (5): � PMID29504268show ga Vascular reactivity was evaluated in three separate arteries isolated from rats after angiotensin II (Ang II) was infused chronically in two separate experiments, one using a 14?day high, slow?pressor dose known to produce hypertension and the other using a 7?day low, subpressor but hypertensive?sensitizing dose. There were three new findings. First, there was no evidence of altered vascular reactivity in resistance arteries that might otherwise explain the hypertension due to the high Ang II or the hypertensive?sensitizing effect of the low Ang II dose. Second, the high Ang II dose exerted a novel differential effect on arterial contractile responsiveness to the sympathetic neurotransmitter, norepinephrine, depending on the level of sympathetic innervation. It clearly enhanced that responsiveness in the sparsely innervated aorta but not in small mesenteric resistance arteries or the proximal (conductance) portion of the caudal artery, both of which are densely innervated. This suggests that the increased expression of alpha adrenergic receptors after long?term exposure to Ang II as previously reported for aortic smooth muscle, is prevented in densely innervated arteries, likely due to long?term Ang II?mediated increase in sympathetic neural traffic to those vessels. Third, the same high dose of Ang II impaired aortic relaxation in response to the nitric oxide (NO) donor nitroprusside without impairing aortic endothelium?dependent relaxation. NO is the main relaxing substance released by aortic endothelium. Accordingly, it is possible that this dose of Ang II is also associated with enhanced release of and/or enhanced smooth muscle responsiveness to other endothelial relaxing substances in a compensatory capacity. �Differential effects of long?term slow?pressor and subpressor angioten(epmc).pdf DeepDyve Pubget Overpricing