{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T10:14:05Z","timestamp":1791195245717,"version":"4.1.0"},"reference-count":50,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2000,11]]},"abstract":"<jats:p>\n            <jats:italic>Abstract<\/jats:italic>\n            \u2014The myogenic response of  skeletal muscle arterioles is enhanced in hypertension because of the  release of endothelin (ET) and prostaglandin H\n            <jats:sub>2<\/jats:sub>\n            (PGH\n            <jats:sub>2<\/jats:sub>\n            )\/thromboxane A\n            <jats:sub>2<\/jats:sub>\n            (TxA\n            <jats:sub>2<\/jats:sub>\n            ) from the endothelium. We  hypothesized that ET and PGH\n            <jats:sub>2<\/jats:sub>\n            \/TxA\n            <jats:sub>2<\/jats:sub>\n            modulate  Ca\n            <jats:sup>2+<\/jats:sup>\n            signaling in arteriolar smooth muscle and thereby  enhance myogenic constriction. Thus, simultaneous changes  in intracellular Ca\n            <jats:sup>2+<\/jats:sup>\n            concentration in smooth muscle  ([Ca\n            <jats:sup>2+<\/jats:sup>\n            ]\n            <jats:sub>i<\/jats:sub>\n            ), measured by fura 2  microfluorometry (expressed as Ca\n            <jats:sup>2+<\/jats:sup>\n            fluorescence  ratio [R\n            <jats:sub>Ca<\/jats:sub>\n            ]), and diameter were obtained as a function of  intraluminal pressure (P\n            <jats:sub>i<\/jats:sub>\n            ) in isolated cannulated gracilis  muscle arterioles (diameter \u2248120 \u03bcm) of normotensive Wistar  rats (WR) and spontaneously hypertensive rats (SHR). In the absence of  extracellular Ca\n            <jats:sup>2+<\/jats:sup>\n            , increases in P\n            <jats:sub>i<\/jats:sub>\n            from 20 to  160 mm Hg increased the passive diameter of arterioles without  changes in R\n            <jats:sub>Ca<\/jats:sub>\n            . In the presence of extracellular  Ca\n            <jats:sup>2+<\/jats:sup>\n            and endothelium, increases in  P\n            <jats:sub>i<\/jats:sub>\n            elicited similar increases in R\n            <jats:sub>Ca<\/jats:sub>\n            (30\u00b17%  for control and 33\u00b18% for SHR at 160 mm Hg) but a significantly  (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05) greater constriction of SHR arterioles  compared with WR arterioles (at 160 mm Hg, 55\u00b14% versus  38\u00b12%, respectively, of passive diameter). In the absence of the  endothelium, P\n            <jats:sub>i<\/jats:sub>\n            -induced changes in the  R\n            <jats:sub>Ca<\/jats:sub>\n            and diameter of SHR and WR arterioles did not differ  significantly. Also, a step increase in P\n            <jats:sub>i<\/jats:sub>\n            (from 80 to  140 mm Hg) elicited a similar increase in R\n            <jats:sub>Ca<\/jats:sub>\n            but  greater constrictions in SHR versus WR arterioles. In the presence of  the TxA\n            <jats:sub>2<\/jats:sub>\n            receptor inhibitor SQ29,548 and the  ET\n            <jats:sub>A<\/jats:sub>\n            receptor inhibitor BQ123, there was no  difference between responses of SHR and WR arterioles. In WR  arterioles, increasing concentrations of KCl elicited a significant  increase in R\n            <jats:sub>Ca<\/jats:sub>\n            (38\u00b17% at 80 mmol\/L) and completely  constricted the arterioles. In contrast, constrictions to ET (52\u00b17%  at 3\u00d710\n            <jats:sup>\u2212<\/jats:sup>\n            <jats:sup>12<\/jats:sup>\n            mol\/L) and the TxA\n            <jats:sub>2<\/jats:sub>\n            agonist U46619 (40\u00b18% at 3\u00d710\n            <jats:sup>\u2212<\/jats:sup>\n            <jats:sup>9<\/jats:sup>\n            mol\/L) were  not accompanied by increases in R\n            <jats:sub>Ca<\/jats:sub>\n            at submaximal  concentrations. Collectively, these findings suggest that in  hypertension, endothelium-derived ET and  PGH\n            <jats:sub>2<\/jats:sub>\n            \/TxA\n            <jats:sub>2<\/jats:sub>\n            increase the Ca\n            <jats:sup>2+<\/jats:sup>\n            sensitivity of the contractile apparatus of arteriolar  smooth muscle; thus, the similar increases in  [Ca\n            <jats:sup>2+<\/jats:sup>\n            ]\n            <jats:sub>i<\/jats:sub>\n            in response to the elevation of  intraluminal pressure elicit greater myogenic constriction.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.36.5.856","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:25:31Z","timestamp":1339460731000},"page":"856-861","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":48,"title":["Endothelin and Prostaglandin H\n            <sub>2<\/sub>\n            \/Thromboxane A\n            <sub>2<\/sub>\n            Enhance Myogenic Constriction in Hypertension by Increasing Ca\n            <sup>2+<\/sup>\n            Sensitivity of Arteriolar Smooth Muscle"],"prefix":"10.1161","volume":"36","author":[{"given":"Zoltan","family":"Ungvari","sequence":"first","affiliation":[{"name":"From the Institute of Pathophysiology (Z.U., A.K.), Semmelweis University  of Medicine, Budapest, Hungary, and the Department of Physiology (Z.U., A.K.),  New York Medical College, Valhalla, NY."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akos","family":"Koller","sequence":"additional","affiliation":[{"name":"From the Institute of Pathophysiology (Z.U., A.K.), Semmelweis University  of Medicine, Budapest, Hungary, and the Department of Physiology (Z.U., A.K.),  New York Medical College, Valhalla, NY."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","first-page":"H1177","volume":"266","year":"1994","unstructured":"Sun D, Kaley G, Koller A. 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