{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T17:09:51Z","timestamp":1781629791712,"version":"3.54.5"},"reference-count":20,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2000,9]]},"abstract":"<jats:p>\n            <jats:italic>Abstract<\/jats:italic>\n            \u2014Altered \u03b2-adrenergic  regulation has been reported in individuals with hypertension. The  variability in vascular responsiveness to \u03b2-agonists, such as  isoproterenol, observed in humans may be explained partially by  \u03b2\n            <jats:sub>2<\/jats:sub>\n            -adrenoceptor polymorphism. Individuals with the  Gln27 form of the receptor may show reduced vascular reactivity  because of downregulation expression of the receptor in the  vasculature. We screened 127 normotensive white subjects, 37 of  whom were homozygous for these alleles. Thirty-two subjects (17  Gln27 and 15 Glu27) agreed to receive brachial artery infusions of  isoproterenol at doses of 1 to 300 ng \u00b7  min\n            <jats:sup>\u2212<\/jats:sup>\n            <jats:sup>1<\/jats:sup>\n            ; forearm blood flow was measured by  using venous occlusion plethysmography. Of these subjects, 25 (12 Glu27  and 13 Gln27) received local doses of isoproterenol (0.3 to 30.0  ng \u00b7 min\n            <jats:sup>\u2212<\/jats:sup>\n            <jats:sup>1<\/jats:sup>\n            ) via a dorsal hand vein  preconstricted with norepinephrine. Compared with subjects  homozygous for the Glu27 allele, subjects with the Gln27  substitution had lower baseline blood flow and, in response to  isoproterenol, had a significantly attenuated increase in forearm blood  flow. This pattern was more marked in veins. We also studied the  relationship between the position 16 polymorphism and vascular  reactivity. Homozygotes for Arg16 had significantly lower basal blood  flow and attenuated increases in forearm blood flow compared with the  Gly16 homozygotes. This was significant in veins but not in arteries.  Thus, \u03b2\n            <jats:sub>2<\/jats:sub>\n            -adrenoceptor genotype determines  vascular responses to isoproterenol in forearm resistance vessels and  in capacitance vessels. Further studies are necessary to establish  whether \u03b2\n            <jats:sub>2<\/jats:sub>\n            -adrenoceptor polymorphisms are important  in the genesis of hypertension.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.36.3.371","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:25:31Z","timestamp":1339460731000},"page":"371-375","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":126,"title":["\u03b2\n            <sub>2<\/sub>\n            -Adrenoceptor Polymorphism Determines Vascular Reactivity in Humans"],"prefix":"10.1161","volume":"36","author":[{"given":"John R.","family":"Cockcroft","sequence":"first","affiliation":[{"name":"From the School of Medical and Surgical Sciences, Division of  Therapeutics, and the Research Centre for Human and Clinical Sciences  (J.P.N.), University of Nottingham Medical School, Queen\u2019s Medical  Centre, Nottingham, UK."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anastasios G.","family":"Gazis","sequence":"additional","affiliation":[{"name":"From the School of Medical and Surgical Sciences, Division of  Therapeutics, and the Research Centre for Human and Clinical Sciences  (J.P.N.), University of Nottingham Medical School, Queen\u2019s Medical  Centre, Nottingham, UK."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Debbie J.","family":"Cross","sequence":"additional","affiliation":[{"name":"From the School of Medical and Surgical Sciences, Division of  Therapeutics, and the Research Centre for Human and Clinical Sciences  (J.P.N.), University of Nottingham Medical School, Queen\u2019s Medical  Centre, Nottingham, UK."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amanda","family":"Wheatley","sequence":"additional","affiliation":[{"name":"From the School of Medical and Surgical Sciences, Division of  Therapeutics, and the Research Centre for Human and Clinical Sciences  (J.P.N.), University of Nottingham Medical School, Queen\u2019s Medical  Centre, Nottingham, UK."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jane","family":"Dewar","sequence":"additional","affiliation":[{"name":"From the School of Medical and Surgical Sciences, Division of  Therapeutics, and the Research Centre for Human and Clinical Sciences  (J.P.N.), University of Nottingham Medical School, Queen\u2019s Medical  Centre, Nottingham, UK."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ian P.","family":"Hall","sequence":"additional","affiliation":[{"name":"From the School of Medical and Surgical Sciences, Division of  Therapeutics, and the Research Centre for Human and Clinical Sciences  (J.P.N.), University of Nottingham Medical School, Queen\u2019s Medical  Centre, Nottingham, UK."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joseph P.","family":"Noon","sequence":"additional","affiliation":[{"name":"From the School of Medical and Surgical Sciences, Division of  Therapeutics, and the Research Centre for Human and Clinical Sciences  (J.P.N.), University of Nottingham Medical School, Queen\u2019s Medical  Centre, Nottingham, UK."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199404143301502"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/hyp.29.6.1273"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-199008000-00001"},{"key":"e_1_3_2_4_2","first-page":"125P","volume":"102","year":"1991","unstructured":"Gray DW, Marshall I. 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Association between essential hypertension in blacks and \u03b22 adrenergic receptor genotype. Hypertension. 1995;26:575. Abstract.","journal-title":"Hypertension"},{"key":"e_1_3_2_17_2","first-page":"430","volume":"1","year":"1992","unstructured":"Chowienczyk PJ, Watts GF, Cockcroft JR, Ritter JM. Impaired endothelium-dependent vasodilation of forearm resistance vessels in hypercholesterolaemia. 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