{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T13:32:59Z","timestamp":1790429579315,"version":"4.1.0"},"reference-count":34,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[1999,10]]},"abstract":"<jats:p>\n            <jats:italic>Abstract<\/jats:italic>\n            \u2014The cardiac abnormalities associated with hypertension include left ventricular hypertrophy and vascular changes. The latter may affect the cardiac microvasculature and predispose to myocardial ischemia. To test the hypothesis that endothelin-1 contributes to changes in the microcirculation of the heart, we studied cardiac microvessels of the deoxycorticosterone acetate\u2013salt (DOCA-salt) model of hypertension in the rat, in which the endothelin system is activated, and the effect of the endothelin-A (ET\n            <jats:sub>A<\/jats:sub>\n            ) subtype\u2013selective endothelin receptor antagonist A-127722. A-127722 (30 mg \u00b7 kg\n            <jats:sup>\u22121<\/jats:sup>\n            \u00b7 d\n            <jats:sup>\u22121<\/jats:sup>\n            ) was administered for 4 weeks. Arterioles (\u226420 \u03bcm in lumen diameter) were identified in the myocardium by use of immunolabeling with an anti\u2013smooth muscle \u03b1-actin antibody, and capillaries with an anti-laminin antibody with nuclear counterstaining by nuclear fast red. Systolic blood pressure was 103\u00b11.6 mm Hg in unilaterally nephrectomized rats (UniNx), 202\u00b13.2 mm Hg in DOCA-salt (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.01 versus UniNx), and 182\u00b13.1 mm Hg in ET\n            <jats:sub>A<\/jats:sub>\n            antagonist\u2013treated DOCA-salt (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.01 versus DOCA-salt or UniNx). Arteriolar and capillary densities were altered significantly in the subendocardial myocardium but not in the subepicardial myocardium of the left ventricle. Arteriolar density per square millimeter was 18.1\u00b11.48 in UniNx, 31.9\u00b13.26 in DOCA-salt (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.01 versus UniNx), and 24.2\u00b11.36 in ET\n            <jats:sub>A<\/jats:sub>\n            antagonist\u2013treated DOCA-salt (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05 versus DOCA-salt or UniNx). Capillary density per square millimeter was 2395\u00b1148 in UniNx, 1576\u00b1107 in DOCA-salt (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.01 versus UniNx), and 1982\u00b131 in ET\n            <jats:sub>A<\/jats:sub>\n            antagonist\u2013treated DOCA-salt (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.01 versus DOCA-salt or UniNx). In conclusion, in DOCA-salt hypertensive rats, subendocardial arteriolar growth and capillary rarefaction were observed in the left ventricular myocardium, and both were partially corrected by ET\n            <jats:sub>A<\/jats:sub>\n            receptor antagonism. This suggests a role for endothelin-1 in cardiac arteriolar growth and capillary rarefaction, which may have pathophysiological implications by contributing to myocardial ischemia in hypertension.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.34.4.795","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:53:46Z","timestamp":1339462426000},"page":"795-801","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":25,"title":["Cardiac Microvasculature in DOCA-Salt Hypertensive Rats"],"prefix":"10.1161","volume":"34","author":[{"given":"Isabelle","family":"Larouche","sequence":"first","affiliation":[{"name":"From the MRC Multidisciplinary Research Group on Hypertension, Clinical Research Institute of Montre\u0301al, Montre\u0301al, Quebec, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ernesto L.","family":"Schiffrin","sequence":"additional","affiliation":[{"name":"From the MRC Multidisciplinary Research Group on Hypertension, Clinical Research Institute of Montre\u0301al, Montre\u0301al, Quebec, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1161\/hyp.25.6.1135"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1990.258.3.C408"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.24.2.183"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.21.3.294"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/0895-7061(95)96213-4"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-2828(95)91263-0"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1996.03530440037034"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198811173192002"},{"key":"e_1_3_2_9_2","doi-asserted-by":"crossref","unstructured":"Li JS Schiffrin EL. 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