{"title":"Decreased activity of the sodium-calcium exchanger in tail artery of stroke-prone spontaneously hypertensive rats.","authors":"L E Thompson, G J Rinaldi, D F Bohr","doi":"10.1159/000158810","DOIUrl":null,"url":null,"abstract":"<p><p>The ability of the Na-Ca exchanger to modify vascular relaxation was studied in rings isolated from tail arteries of stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY). The arteries were contracted with norepinephrine (NE) 1 microM and after stabilization they were transferred to a Ca-free physiological salt solution still in presence of NE. The time to 50% relaxation (T-50) in these conditions was significantly greater in SHRSP (78 +/- 7 s) than in WKY (50 +/- 7 s). When the calcium pump was stopped with vanadate (VAN), the Ca uptake by the sarcoplasmic reticulum with ryanodine (RY) and the Na-Ca exchanger with a Na-free PSS, the relaxation was slowed (T-50 increased to 198 +/- 16 s in SHRSP and to 162 +/- 14 s in WKY). Releasing the Na-Ca exchanger only (i.e. still with VAN and RY but with normal Na in the bath) the T-50 for relaxation in Ca-free PSS was, in WKY, nearly as fast as in control conditions (54 +/- 8 s). However, the Na-Ca exchanger in SHRSP was not so effective, and the T-50 for relaxation was slower than in control conditions (122 +/- 10 s). We conclude that the activity of the Na-Ca exchanger is depressed in tail arteries of SHRSP. This abnormality in resistance vessels, would contribute to the enhanced vascular tone present in hypertension.</p>","PeriodicalId":9009,"journal":{"name":"Blood vessels","volume":"27 2-5","pages":"197-201"},"PeriodicalIF":0.0000,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000158810","citationCount":"14","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Blood vessels","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000158810","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 14
Abstract
The ability of the Na-Ca exchanger to modify vascular relaxation was studied in rings isolated from tail arteries of stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY). The arteries were contracted with norepinephrine (NE) 1 microM and after stabilization they were transferred to a Ca-free physiological salt solution still in presence of NE. The time to 50% relaxation (T-50) in these conditions was significantly greater in SHRSP (78 +/- 7 s) than in WKY (50 +/- 7 s). When the calcium pump was stopped with vanadate (VAN), the Ca uptake by the sarcoplasmic reticulum with ryanodine (RY) and the Na-Ca exchanger with a Na-free PSS, the relaxation was slowed (T-50 increased to 198 +/- 16 s in SHRSP and to 162 +/- 14 s in WKY). Releasing the Na-Ca exchanger only (i.e. still with VAN and RY but with normal Na in the bath) the T-50 for relaxation in Ca-free PSS was, in WKY, nearly as fast as in control conditions (54 +/- 8 s). However, the Na-Ca exchanger in SHRSP was not so effective, and the T-50 for relaxation was slower than in control conditions (122 +/- 10 s). We conclude that the activity of the Na-Ca exchanger is depressed in tail arteries of SHRSP. This abnormality in resistance vessels, would contribute to the enhanced vascular tone present in hypertension.