{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,5,23]],"date-time":"2025-05-23T10:52:01Z","timestamp":1747997521783,"version":"3.40.3"},"reference-count":30,"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":[[1996,3]]},"abstract":"<jats:p><jats:italic>Abstract<\/jats:italic>Deoxycorticosterone-salt (DOCA-salt) hypertension is characterized by elevated vasoconstriction to agonists that stimulate G protein\u2013mediated activation of phospholipase C. However, the mechanisms responsible for the augmented responsiveness are unknown. This study tested the hypothesis that this augmented vascular responsiveness is due to elevated content of G\u03b1<jats:sub>q<\/jats:sub>, the G protein \u03b1-subunit that activates phospholipase C. Thoracic aortae from DOCA-salt hypertensive rats (systolic blood pressure 183\u00b17 mm Hg) and normotensive controls (systolic blood pressure 115\u00b12 mm Hg) were homogenized and G protein content determined. Western analysis revealed that G\u03b1<jats:sub>i<\/jats:sub>content was decreased in DOCA compared with control rats (1364\u00b1196 versus 2343\u00b1188 densitometry units,<jats:italic>P<\/jats:italic>\u2264.05) with no differences observed for G\u03b1<jats:sub>q<\/jats:sub>or G\u03b1<jats:sub>s<\/jats:sub>. In addition, contractile responses in denuded femoral artery strips revealed a significant decrease in EC<jats:sub>50<\/jats:sub>values in DOCA arteries to all of the agonists examined: aluminum fluoride (DOCA=1.42, control=2.34 mmol\/L), mastoparan (DOCA=0.51, control=35 \u03bcmol\/L), phenylephrine (DOCA=0.08, control=0.53 \u03bcmol\/L), and serotonin (DOCA=0.014, control=0.04 \u03bcmol\/L, EC<jats:sub>20<\/jats:sub>values). Finally, arteries from DOCA rats contracted with aluminum fluoride had increased sensitivity to G protein antagonists but not to a phospholipase C inhibitor. The enhanced contractile responsiveness in the DOCA arteries may be mediated in part through decreased G\u03b1<jats:sub>i<\/jats:sub>levels. However, it is not caused by increased concentrations of G\u03b1<jats:sub>q<\/jats:sub>in the cell membrane or by increased phospholipase C sensitivity, and the increased constrictor response to G protein stimulators of phospholipase C appears to depend primarily on increased G protein sensitivity.<\/jats:p>","DOI":"10.1161\/01.hyp.27.3.740","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:53:46Z","timestamp":1339462426000},"page":"740-745","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":15,"title":["Increased Responsiveness and Decreased Expression of G Proteins in Deoxycorticosterone Hypertension"],"prefix":"10.1161","volume":"27","author":[{"given":"Nancy L.","family":"Kanagy","sequence":"first","affiliation":[{"name":"From the Department of Physiology, University of New Mexico School of Medicine, Albuquerque (N.L.K.); and the Department of Physiology, University of Michigan, Ann Arbor (R.C.W.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R. Clinton","family":"Webb","sequence":"additional","affiliation":[{"name":"From the Department of Physiology, University of New Mexico School of Medicine, Albuquerque (N.L.K.); and the Department of Physiology, University of Michigan, Ann Arbor (R.C.W.)."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","first-page":"801","volume":"256","year":"1991","unstructured":"Wilson SK. Peripheral alpha-1 and alpha-2 adrenergic receptors in three models of hypertension in rats: an in vitro autoradiography study. J Pharmacol Exp Ther. 1991;256:801-810.","journal-title":"J Pharmacol Exp Ther"},{"key":"e_1_3_2_2_2","first-page":"213","volume":"15","year":"1995","unstructured":"Birnbaumer L, Birnbaumer M. Signal transduction by G proteins: 1994 edition. 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