{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T19:00:07Z","timestamp":1789412407610,"version":"build-2803163510"},"reference-count":53,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2016,4,9]],"date-time":"2016-04-09T00:00:00Z","timestamp":1460160000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Physiology"],"published-print":{"date-parts":[[2016,5]]},"abstract":"<jats:sec><jats:title>New Findings<\/jats:title><jats:p><jats:list list-type=\"bullet\"><jats:list-item><jats:p>What is the central question of this study?<\/jats:p><jats:p>Does genetic ablation of neurokinin\u20101 receptors alter arterial blood pressure?<\/jats:p><\/jats:list-item><jats:list-item><jats:p>What is the main finding and its importance?<\/jats:p><jats:p><jats:italic>NK1R<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice have increased mean arterial blood pressure, but without a concomitant change in vascular reactivity. This finding suggests that neurokinin\u20101 receptors play a role in the neural regulation of blood pressure.<\/jats:p><\/jats:list-item><\/jats:list><\/jats:p><\/jats:sec><jats:sec><jats:label\/><jats:p>Mice with functional ablation of the neurokinin\u20101 receptor gene,<jats:italic>Tacr1<\/jats:italic>, (<jats:italic>NK1R<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>) express behavioural abnormalities equivalent to those seen in attention deficit hyperactivity disorder (ADHD). An established model of ADHD is the spontaneously hypertensive rat, which exhibits high blood pressure owing to increased central sympathetic drive. In light of the evidence that the neurokinin\u20101 receptor (NK1R) also influences cardiovascular haemodynamics, we have investigated whether<jats:italic>NK1R<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice exhibit raised blood pressure. Cardiovascular parameters were recorded for 24\u00a0h in conscious mice using radiotelemetry. Vascular function was assessed in mesenteric resistance arteries by wire myography. The<jats:italic>NK1R<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice exhibited a higher blood pressure than wild\u2010type animals throughout the 24\u00a0h period. Heart rate and locomotor activity in<jats:italic>NK1R<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice were higher than in wild\u2010type mice during the night period (active phase), consistent with an ADHD\u2010like phenotype, but not during the day. Mesenteric and renal arteries from<jats:italic>NK1R<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice exhibited normal vascular function; the responses to vasoconstrictors (U46619 and phenylephrine) and the endothelium\u2010dependent vasodilator, acetylcholine, were not altered in these animals, suggesting that the NK1R does not regulate vascular tone. Analysis of heart rate variability revealed a higher low\u2010frequency to high\u2010frequency ratio in<jats:italic>NK1R<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice, indicative of increased cardiac sympathetic activity. We propose that the raised blood pressure in<jats:italic>NK1R<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice could be due to a neural mechanism rather than a change in vascular reactivity. Further studies are required to understand this mechanism and to establish whether a subgroup of ADHD patients with polymorphism of the equivalent (<jats:italic>TACR1<\/jats:italic>) gene are affected in a similar way.<\/jats:p><\/jats:sec>","DOI":"10.1113\/ep085347","type":"journal-article","created":{"date-parts":[[2016,2,15]],"date-time":"2016-02-15T05:56:51Z","timestamp":1455515811000},"page":"588-598","source":"Crossref","is-referenced-by-count":9,"title":["Raised arterial blood pressure in neurokinin\u20101 receptor\u2010deficient mice (<i>NK1R<\/i><sup>\u2212\/\u2212<\/sup>): evidence for a neural rather than a vascular mechanism"],"prefix":"10.1113","volume":"101","author":[{"given":"Amie J.","family":"Moyes","sequence":"first","affiliation":[{"name":"The William Harvey Research Institute, Barts and The London School of Medicine and Dentistry Queen Mary University of London London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S. 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