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Abnormal vascular phosphoinositide hydrolysis in the spontaneously hypertensive rat
Author(s) -
Heagerty A.M.,
Ollerenshaw J.D.,
Swales J.D.
Publication year - 1986
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1986.tb11185.x
Subject(s) - medicine , endocrinology , inositol , hydrolysis , inositol phosphate , phospholipid , blood pressure , basal (medicine) , aorta , chemistry , spontaneously hypertensive rat , phosphatidylinositol , biology , biochemistry , receptor , diabetes mellitus , signal transduction , membrane
1 The production of [ 3 H]‐inositol phosphates was studied in labelled segments of aorta from spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) controls at 5 and 19 weeks, either unstimulated or in the presence of noradrenaline. 2 Basal hydrolysis of inositol phospholipids was significantly enhanced in young SHR ( P < 0.05) compared to controls but this difference was no longer detected at 19 weeks. 3 Noradrenaline increased [ 3 H]‐inositol phosphate accumulation in both SHR and WKY, but maximal hydrolysis was significantly greater in WKY ( P < 0.01), although the ED 50 was similar in both groups of animals. 4 These data demonstrate that phosphatidylinositide hydrolysis is enhanced in the young hypertensive rat at the time blood pressure is rising, but that this activity has declined by the time hypertension has reached an established phase. In addition, α 1 ‐agonist induction of inositol phospholipid hydrolysis differs in the two species of animals, being reduced in genetically mature hypertensive rats.