| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
AJP - Endocrinology and Metabolism, Vol 258, Issue 4 E649-E653, Copyright © 1990 by American Physiological Society
ARTICLES |
E. P. Gomez-Sanchez, M. T. Venkataraman, D. Thwaites and C. Fort
Research Service, J. A. Haley Veterans Administration Hospital, Tampa, Florida.
There is evidence of crucial central nervous system involvement in the pathogenesis of mineralocorticoid-excess salt hypertension, as well as data indicating that corticosterone is the predominant ligand for the type I adrenocorticoid receptor in the brain. Miniosmotic pumps were used to deliver artificial cerebrospinal fluid (CSF), aldosterone (10 ng/h), corticosterone (10 or 20 ng/h), aldosterone (10 ng/h) plus corticosterone [10 ng/h intracerebroventricularly (icv)], or aldosterone (10 ng/h) plus corticosterone (20 ng/h icv). All animals were sensitized to mineralocorticoid hypertension by removing the right kidney and offering saline to drink. Indirect blood pressure by the unheated tail-cuff method and weights were measured twice weekly; 24-h urine volumes were measured once a week. The blood pressures of the four groups did not differ statistically before infusion. The blood pressures of those animals receiving CSF or corticosterone were not significantly elevated after 4-5 wk of intracerebroventricular infusion, whereas the aldosterone group had become significantly elevated within 2 wk. A similar study was done comparing the effects of intracerebroventricular infusion of aldosterone (10 ng/h), aldosterone (10 ng/h) and RU26988 (20 ng/h), and RU26988 (20 ng/h). RU26988, a selective type II receptor agonist, had no effect on the blood pressure, nor did it alter the pressor effect of intracerebroventricular aldosterone. The concomitant infusion of corticosterone antagonized the increase in blood pressure in a dose-dependent manner. Neither steroid nor their combinations produced significant differences in daily urine volume or body weight gain compared with the CSF group.
This article has been cited by other articles:
|
|
 |
|
  Z.-H. Zhang, Y. Yu, Y.-M. Kang, S.-G. Wei, and R. B. Felder Aldosterone acts centrally to increase brain renin-angiotensin system activity and oxidative stress in normal rats Am J Physiol Heart Circ Physiol, February 1, 2008; 294(2): H1067 - H1074. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. A. Scheuer, A. G. Bechtold, and K. A. Vernon Chronic Activation of Dorsal Hindbrain Corticosteroid Receptors Augments the Arterial Pressure Response to Acute Stress Hypertension, January 1, 2007; 49(1): 127 - 133. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. G. Bechtold and D. A. Scheuer Glucocorticoids act in the dorsal hindbrain to modulate baroreflex control of heart rate Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2006; 290(4): R1003 - R1011. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. W. Funder How do central mineralocorticoid receptors modulate blood pressure? Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2005; 288(2): R356 - R357. [Full Text] [PDF]
|
|
|
|
|
|
E. P. Gomez-Sanchez, J. Samuel, G. Vergara, and N. Ahmad Effect of 3{beta}-hydroxysteroid dehydrogenase inhibition by trilostane on blood pressure in the Dahl salt-sensitive rat Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2005; 288(2): R389 - R393. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. A. Scheuer, A. G. Bechtold, S. S. Shank, and S. F. Akana Glucocorticoids act in the dorsal hindbrain to increase arterial pressure Am J Physiol Heart Circ Physiol, January 1, 2004; 286(1): H458 - H467. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. S. Shank and D. A. Scheuer Glucocorticoids reduce responses to AMPA receptor activation and blockade in nucleus tractus solitarius Am J Physiol Heart Circ Physiol, May 1, 2003; 284(5): H1751 - H1761. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Kitagawa, J. Yanagisawa, H. Fuse, S. Ogawa, Y. Yogiashi, A. Okuno, H. Nagasawa, T. Nakajima, T. Matsumoto, and S. Kato Ligand-Selective Potentiation of Rat Mineralocorticoid Receptor Activation Function 1 by a CBP-Containing Histone Acetyltransferase Complex Mol. Cell. Biol., June 1, 2002; 22(11): 3698 - 3706. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. E. Booth, J. P. Johnson, and J. D. Stockand ALDOSTERONE Advan Physiol Educ, March 1, 2002; 26(1): 8 - 20. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Ngarmukos and R. J. Grekin Nontraditional aspects of aldosterone physiology Am J Physiol Endocrinol Metab, December 1, 2001; 281(6): E1122 - E1127. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. M. Rogerson, N. Dimopoulos, P. Sluka, S. Chu, A. J. Curtis, and P. J. Fuller Structural Determinants of Aldosterone Binding Selectivity in the Mineralocorticoid Receptor J. Biol. Chem., December 17, 1999; 274(51): 36305 - 36311. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Sayegh, S. D. Auerbach, X. Li, R. W. Loftus, R. F. Husted, J. B. Stokes, and C. P. Thomas Glucocorticoid Induction of Epithelial Sodium Channel Expression in Lung and Renal Epithelia Occurs via trans-Activation of a Hormone Response Element in the 5'-Flanking Region of the Human Epithelial Sodium Channel alpha Subunit Gene J. Biol. Chem., April 30, 1999; 274(18): 12431 - 12437. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
