{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T00:14:04Z","timestamp":1790640844875,"version":"4.1.0"},"reference-count":40,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2015,8,3]],"date-time":"2015-08-03T00:00:00Z","timestamp":1438560000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100008890","name":"University of Dundee","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008890","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Clinical Hypertension"],"published-print":{"date-parts":[[2015,11]]},"abstract":"<jats:p>Exaggerated blood pressure (<jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>) response to exercise predicts future hypertension. However, there is considerable lack of understanding regarding the mechanism of how this abnormal response is generated, and how it relates to the future establishment of cardiovascular disease. The authors studied 82 healthy male volunteers without cardiovascular risk factors. The participants were categorized into two age\u2010matched groups depending on their exercise systolic <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content> (Ex<jats:styled-content style=\"fixed-case\">SBP<\/jats:styled-content>) rise after 3\u00a0minutes of exercise using a submaximal step test: exaggerated Ex<jats:styled-content style=\"fixed-case\">SBP<\/jats:styled-content> group (hyper\u2010responders [peak <jats:styled-content style=\"fixed-case\">SBP<\/jats:styled-content> \u2265180\u00a0mm\u00a0Hg]) and low Ex<jats:styled-content style=\"fixed-case\">SBP<\/jats:styled-content> responder group (hypo\u2010responders [peak <jats:styled-content style=\"fixed-case\">SBP<\/jats:styled-content> &lt;180\u00a0mm\u00a0Hg]). Forearm venous occlusion plethysmography and intra\u2010arterial infusions of acetylcholine (<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h), <jats:styled-content style=\"fixed-case\">N<jats:sup>G<\/jats:sup><\/jats:styled-content>\u2010monomethyl\u2010L\u2010arginine (L\u2010<jats:styled-content style=\"fixed-case\">NMMA<\/jats:styled-content>), sodium nitroprusside (<jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>), and norepinephrine (<jats:styled-content style=\"fixed-case\">NE<\/jats:styled-content>) were used to assess vascular reactivity. Proximal aortic compliance was assessed with ultrasound, and neurohormonal blood sampling was performed at rest and during peak exercise. The hyper\u2010responder group exhibited a significantly lower increase in forearm blood flow (<jats:styled-content style=\"fixed-case\">FBF<\/jats:styled-content>) with <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h compared with the hypo\u2010responder group (\u0394<jats:styled-content style=\"fixed-case\">FBF<\/jats:styled-content> 215% [14] vs 332.3% [28], mean [standard error of the mean]; <jats:italic>P<\/jats:italic>&lt;.001), as well as decreased proximal aortic compliance. The vasoconstrictive response to L\u2010<jats:styled-content style=\"fixed-case\">NMMA<\/jats:styled-content> was significantly impaired in the hyper\u2010responder group in comparison to the hypo\u2010responder group (\u0394<jats:styled-content style=\"fixed-case\">FBF<\/jats:styled-content> \u221240.2% [1.6] vs \u221250.2% [2.6]; <jats:italic>P<\/jats:italic>&lt;.05). In contrast, the vascular response to <jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">NE<\/jats:styled-content> were comparable in both groups. Peak exercise plasma angiotensin <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> levels were significantly higher in the hyper\u2010responder group (31 [1] vs 23 [2] pg\/mL, <jats:italic>P<\/jats:italic>=.01). An exaggerated <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content> response to exercise is related to endothelial dysfunction, decreased proximal aortic compliance, and\u00a0increased exercise\u2010related neurohormonal activation, the constellation of which may explain future cardiovascular disease.<\/jats:p>","DOI":"10.1111\/jch.12629","type":"journal-article","created":{"date-parts":[[2015,8,3]],"date-time":"2015-08-03T02:59:49Z","timestamp":1438570789000},"page":"837-844","source":"Crossref","is-referenced-by-count":65,"title":["Exaggerated Exercise Blood Pressure Response and Future Cardiovascular Disease"],"prefix":"10.1111","volume":"17","author":[{"given":"Nikolaos","family":"Tzemos","sequence":"first","affiliation":[{"name":"Institute of Cardiovascular and Medical Sciences British Heart Foundation Glasgow Cardiovascular Research Centre University of Glasgow Glasgow UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pitt 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