title: Effect of high potassium diets on the vascular and renal prostaglandin system in stroke-prone spontaneously hypertensive rats.
abstract: High potassium (K) diets are known to have a protective effect on the endothelium and the kidney against hypertensive injury independent of blood pressure change. Vasodepressor prostaglandins (PGs) have been shown to be cytoprotective in various tissues. This study investigated the effect of high K diets on the vascular and renal eicosanoid system in stroke-prone spontaneously hypertensive rats (SHRsp). Eicosanoid production by the aorta and eicosanoid content in the renal cortex were examined in SHRsp rats fed high NaCl diets containing either 0.5% K (normal) or 2.1% K (high). Although the high K diet did not affect the blood pressure, SHRsp on the high K diet had less thickening of the aortic wall than SHRsp on the normal K diet (-15%, p < 0.001). The aortic strip of the high K SHRsp produced less vasodepressor PG than that of the normal K SHRsp when they were incubated in a medium (PGI2 -45%, p < 0.003; PGE2 -34%, p < 0.001). Furthermore, when the aorta was perfused in a chamber at hypertensive pressure, again the high K aorta showed reduced PGI2 production as compared with the normal K aorta (intravascular side -52%, p < 0.01). Eicosanoid content in the renal cortex was not significantly different between the normal K and the high K SHRsp (PGI2 79 vs 87 ng/g dry weight; PGE2 214 vs 233 ng/g dry weight). Thus, the high K diet reduced vascular eicosanoid production but did not alter eicosanoid content in the renal cortex. The reduced vascular eicosanoid production in the high K SHRsp may reflect the reduced necessity for cytoprotective vasodepressor PG against vascular injuries.
authors.affiliation: Department of Medicine, University of Minnesota, Minneapolis, USA.
authors.forename: T
authors.initials: T
authors.lastname: Ishimitsu
authors.forename: L
authors.initials: L
authors.lastname: Tobian
authors.forename: Y
authors.initials: Y
authors.lastname: Uehara
authors.forename: K
authors.initials: K
authors.lastname: Sugimoto
authors.forename: J M
authors.initials: JM
authors.lastname: Lange
mesh_terms: D000284:Administration, Oral; D000818:Animals; D001011:Aorta / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D001012:Aorta, Abdominal / Q000473:pathology; D001013:Aorta, Thoracic / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D002561:Cerebrovascular Disorders / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D004032:Diet; D015232:Dinoprostone / Q000096:biosynthesis; D011464:Epoprostenol / Q000096:biosynthesis; D006973:Hypertension / Q000150:complications / Q000188:drug therapy* / Q000235:genetics / Q000503:physiopathology; D007672:Kidney Cortex / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D009929:Organ Size / Q000187:drug effects; D010477:Perfusion; D011188:Potassium / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D011453:Prostaglandins / Q000378:metabolism*; D051381:Rats; D011918:Rats, Inbred SHR; D013928:Thromboxane A2 / Q000096:biosynthesis
chemical_list: D011453:Prostaglandins; D013928:Thromboxane A2; D011464:Epoprostenol; D015232:Dinoprostone; D011188:Potassium