AREGU Mar. 45/3
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چکیده
Fanestil, Darrell D., Duke A. Vaughn, Ronald H. Hyde, and Patricia Blakely. Genetic control of renal thiazide receptor response to dietary NaCl and hypertension. Am. J. Physiol. 276 (Regulatory Integrative Comp. Physiol. 45): R901–R904, 1999.—Excess NaCl increases blood pressure in some strains of animals but not others. An 8% NaCl diet did not change renal thiazide receptor (TZR) density in two salt-resistant normotensive rat strains (Wistar-Kyoto and Sprague-Dawley) [Fanestil, D. D., D. A. Vaughn, and P. Blakely. Am. J. Physiol. 273 (Regulatory Integrative Comp. Physiol. 42): R1241–R1245, 1997]. However, the renal response to salt differs in normal and hypertensive kidneys [Rettig, R., N. Bandelow, O. Patschan, B. Kuttler, B. Frey, and A. Uber. J. Hum. Hypertens. 10: 641–644, 1996]. Therefore, we examined two strains with salt-aggravated hypertension. Renal TZR did not change when Dahl-S (salt sensitive) animals became hypertensive with 8% dietary NaCl. In contrast, renal TZR decreased 34%, whereas blood pressure increased further, in SHR with 8% dietary NaCl. Blood pressure increased after NG-nitro-L-arginine in SHR, but renal TZR did not change, indicating the salt-induced decrease in TZR in SHR cannot be attributed nonspecifically to elevated arterial pressure. We conclude that the renal response to NaCl-induced increases in blood pressure can be genetically modulated independently of the genes that mediate either the primary hypertension or the salt sensitivity of the hypertension. This finding may be of use in future studies directed at identifying genotypes associated with saltdependent hypertension.
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AREGU Mar. 45/3
M. J. P. LENCZOWSKI,1 R.-M. BLUTHÉ,2 J. ROTH,3 G. S. REES,4 D. A. RUSHFORTH,5 A.-M. VAN DAM,1 F. J. H. TILDERS,1 R. DANTZER,2 N. J. ROTHWELL,5 AND G. N. LUHESHI5 1Department of Pharmacology, Faculty of Medicine, Research Institute Neurosciences Vrije Universiteit, Graduate School Neurosciences Amsterdam, 1081 BT Amsterdam, The Netherlands; 2Institut François Magendie, Institut National de la Re...
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Boulton, M., M. Flessner, D. Armstrong, R. Mohamed, J. Hay, and M. Johnston. Contribution of extracranial lymphatics and arachnoid villi to the clearance of a CSF tracer in the rat. Am. J. Physiol. 276 (Regulatory Integrative Comp. Physiol. 45): R818–R823, 1999.—The objective of this study was to determine the relative roles of arachnoid villi and cervical lymphatics in the clearance of a cereb...
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Khan, Janine Y., Rosario A. Rajakumar, Robert A. McKnight, Uday P. Devaskar, and Sherin U. Devaskar. Developmental regulation of genes mediating murine brain glucose uptake. Am. J. Physiol. 276 (Regulatory Integrative Comp. Physiol. 45): R892–R900, 1999.—We examined the molecular mechanisms that mediate the developmental increase in murine whole brain 2-deoxyglucose uptake. Northern and Western...
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McDonald, Roger B., Tana M. Hoban-Higgins, Rodney C. Ruhe, Charles A. Fuller, and Barbara A. Horwitz. Alterations in endogenous circadian rhythm of core temperature in senescent Fischer 344 rats. Am. J. Physiol. 276 (Regulatory Integrative Comp. Physiol. 45): R824–R830, 1999.—We assessed whether alterations in endogenous circadian rhythm of core temperature (CRT) in aging rats are associated wi...
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Rogausch, Heinz, Adriana Del Rey, Jörg Oertel, and Hugo O. Besedovsky. Norepinephrine stimulates lymphoid cell mobilization from the perfused rat spleen via b-adrenergic receptors. Am. J. Physiol. 276 (Regulatory Integrative Comp. Physiol. 45): R724–R730, 1999.—The possibility that norepinephrine (NE) influences lymphoid cell outflow independently of its vasoconstrictor action was investigated ...
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