{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,9,6]],"date-time":"2024-09-06T08:46:15Z","timestamp":1725612375087},"reference-count":39,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[1995,9,15]]},"abstract":"<jats:p>\n            <jats:italic>Background<\/jats:italic>\n            A coronary \u03b1\n            <jats:sub>1<\/jats:sub>\n            -adrenergic constrictor tone exists under conditions associated with increased sympathetic stimulation but not during resting conditions in the normal heart. During renovascular hypertension, elevated circulating angiotensin II may enhance sympathetic stimulation of the heart, even at rest. This study tested the hypothesis that an \u03b1\n            <jats:sub>1<\/jats:sub>\n            -adrenergic constrictor tone imposes limitations on coronary blood flow in resting dogs after development of renovascular hypertension, exacerbates coronary \u03b1-constrictor tone during exercise, and increases coronary vascular adrenergic responsiveness.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Methods and Results<\/jats:italic>\n            Left circumflex blood flow velocity (CFV), aortic pressure (AoP), and heart rate (HR) were examined in five quietly resting dogs during control conditions and after selective \u03b1\n            <jats:sub>1<\/jats:sub>\n            -adrenergic blockade using an intracoronary injection of 0.5 mg prazosin. In the normotensive state, AoP was 87\u00b17 mm Hg (mean\u00b1SD), HR was 105\u00b125 beats per minute, and CFV was 28\u00b16 cm\/s. These parameters were not affected by \u03b1\n            <jats:sub>1<\/jats:sub>\n            -adrenergic blockade. During submaximal exercise, removal of an \u03b1\n            <jats:sub>1<\/jats:sub>\n            -adrenergic constrictor resulted in a 14\u00b14% increase in CFV (\n            <jats:italic>P<\/jats:italic>\n            &lt;.05). Two weeks after development of renovascular hypertension induced by stenosis of the left renal artery, mean AoP was 114\u00b17 mm Hg (\n            <jats:italic>P<\/jats:italic>\n            &lt;.05 versus normotensive state), HR was 111\u00b128 beats per minute, and CFV was 21\u00b18 cm\/s. In contrast to the normotensive state, \u03b1\n            <jats:sub>1<\/jats:sub>\n            -adrenergic blockade caused a 28\u00b16% increase in CFV at rest (\n            <jats:italic>P<\/jats:italic>\n            &lt;.05) and a 27\u00b113% increase in CFV during exercise in the hypertensive state (\n            <jats:italic>P<\/jats:italic>\n            &lt;.05 versus exercise before blockade and versus normotensive state). This resting coronary constrictor tone was associated with enhanced vasoconstrictor responsiveness to norepinephrine and phenylephrine.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Conclusions<\/jats:italic>\n            It appears that renovascular hypertension results in a significant coronary \u03b1\n            <jats:sub>1<\/jats:sub>\n            -adrenergic constrictor tone in the resting dog and an enhanced constrictor tone during exercise.\n          <\/jats:p>","DOI":"10.1161\/01.cir.92.6.1576","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:34:42Z","timestamp":1339461282000},"page":"1576-1581","update-policy":"http:\/\/dx.doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":6,"title":["Coronary \u03b1\n            <sub>1<\/sub>\n            -Constrictor Tone During Renovascular Hypertension"],"prefix":"10.1161","volume":"92","author":[{"given":"Patricia A.","family":"Gwirtz","sequence":"first","affiliation":[{"name":"From the Department of Physiology, University of North Texas Health Science Center at Fort Worth."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1983.63.1.1"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.42.1.201392"},{"key":"e_1_3_2_3_2","first-page":"H645","volume":"250","year":"1986","unstructured":"Nathan HJ, Feigl EO. 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