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Activation of brain renin-angiotensin-aldosterone system by central sodium in Wistar rats
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| Zeitschriftentitel: | American Journal of Physiology-Heart and Circulatory Physiology |
|---|---|
| Personen und Körperschaften: | , , , , , |
| In: | American Journal of Physiology-Heart and Circulatory Physiology, 291, 2006, 3, S. H1109-H1117 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Physiological Society
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| Schlagwörter: |
| author_facet |
Huang, Bing S. Cheung, Warren J. Wang, Hao Tan, Junhui White, Roselyn A. Leenen, Frans H. H. Huang, Bing S. Cheung, Warren J. Wang, Hao Tan, Junhui White, Roselyn A. Leenen, Frans H. H. |
|---|---|
| author |
Huang, Bing S. Cheung, Warren J. Wang, Hao Tan, Junhui White, Roselyn A. Leenen, Frans H. H. |
| spellingShingle |
Huang, Bing S. Cheung, Warren J. Wang, Hao Tan, Junhui White, Roselyn A. Leenen, Frans H. H. American Journal of Physiology-Heart and Circulatory Physiology Activation of brain renin-angiotensin-aldosterone system by central sodium in Wistar rats Physiology (medical) Cardiology and Cardiovascular Medicine Physiology |
| author_sort |
huang, bing s. |
| spelling |
Huang, Bing S. Cheung, Warren J. Wang, Hao Tan, Junhui White, Roselyn A. Leenen, Frans H. H. 0363-6135 1522-1539 American Physiological Society Physiology (medical) Cardiology and Cardiovascular Medicine Physiology http://dx.doi.org/10.1152/ajpheart.00024.2006 <jats:p> Functional studies indicate that the sympathoexcitatory and pressor responses to an increase in cerebrospinal fluid (CSF) [Na<jats:sup>+</jats:sup>] by central infusion of Na<jats:sup>+</jats:sup>-rich artificial cerebrospinal fluid (aCSF) in Wistar rats are mediated in the brain by mineralocorticoid receptor (MR) activation, ouabain-like compounds (OLC), and AT<jats:sub>1</jats:sub>-receptor stimulation. In the present study, we examined whether increasing CSF [Na<jats:sup>+</jats:sup>] by intracerebroventricular infusion of Na<jats:sup>+</jats:sup>-rich aCSF activates MR and thereby increases OLC and components of the renin-angiotensin system in the brain. Male Wistar rats received via osmotic minipump an intracerebroventricular infusion of aCSF or Na<jats:sup>+</jats:sup>-rich aCSF, in some groups combined with intracerebroventricular infusion of spironolactone (100 ng/h), antibody Fab fragments (to bind OLC), or as control γ-globulins. After 2 wk of infusion, resting blood pressure and heart rate were recorded, OLC and aldosterone content in the hypothalamus were assessed by a specific ELISA or radioimmunoassay, and angiotensin-converting enzyme (ACE) and AT<jats:sub>1</jats:sub>-receptor binding densities in various brain nuclei were measured by autoradiography using <jats:sup>125</jats:sup>I-labeled 351 A and <jats:sup>125</jats:sup>I-labeled ANG II. When compared with intracerebroventricular aCSF, intracerebroventricular Na<jats:sup>+</jats:sup>-rich aCSF increased CSF [Na<jats:sup>+</jats:sup>] by ∼5 mmol/l, mean arterial pressure by ∼20 mmHg, heart rate by ∼65 beats/min, and hypothalamic content of OLC by 50% and of aldosterone by 33%. Intracerebroventricular spironolactone did not affect CSF [Na<jats:sup>+</jats:sup>] but blocked the Na<jats:sup>+</jats:sup>-rich aCSF-induced increases in blood pressure and heart rate and OLC content. Intracerebroventricular Na<jats:sup>+</jats:sup>-rich aCSF increased ACE and AT<jats:sub>1</jats:sub>-receptor-binding densities in several brain nuclei, and Fab fragments blocked these increases. These data indicate that in Wistar rats, a chronic increase in CSF [Na<jats:sup>+</jats:sup>] may increase hypothalamic aldosterone and activate CNS pathways involving MR, and OLC, leading to increases in AT<jats:sub>1</jats:sub>-receptor and ACE densities in brain areas involved in cardiovascular regulation and hypertension. </jats:p> Activation of brain renin-angiotensin-aldosterone system by central sodium in Wistar rats American Journal of Physiology-Heart and Circulatory Physiology |
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American Physiological Society |
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American Journal of Physiology-Heart and Circulatory Physiology |
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| title |
Activation of brain renin-angiotensin-aldosterone system by central sodium in Wistar rats |
| title_unstemmed |
Activation of brain renin-angiotensin-aldosterone system by central sodium in Wistar rats |
| title_full |
Activation of brain renin-angiotensin-aldosterone system by central sodium in Wistar rats |
| title_fullStr |
Activation of brain renin-angiotensin-aldosterone system by central sodium in Wistar rats |
| title_full_unstemmed |
Activation of brain renin-angiotensin-aldosterone system by central sodium in Wistar rats |
| title_short |
Activation of brain renin-angiotensin-aldosterone system by central sodium in Wistar rats |
| title_sort |
activation of brain renin-angiotensin-aldosterone system by central sodium in wistar rats |
| topic |
Physiology (medical) Cardiology and Cardiovascular Medicine Physiology |
| url |
http://dx.doi.org/10.1152/ajpheart.00024.2006 |
| publishDate |
2006 |
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H1109-H1117 |
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<jats:p> Functional studies indicate that the sympathoexcitatory and pressor responses to an increase in cerebrospinal fluid (CSF) [Na<jats:sup>+</jats:sup>] by central infusion of Na<jats:sup>+</jats:sup>-rich artificial cerebrospinal fluid (aCSF) in Wistar rats are mediated in the brain by mineralocorticoid receptor (MR) activation, ouabain-like compounds (OLC), and AT<jats:sub>1</jats:sub>-receptor stimulation. In the present study, we examined whether increasing CSF [Na<jats:sup>+</jats:sup>] by intracerebroventricular infusion of Na<jats:sup>+</jats:sup>-rich aCSF activates MR and thereby increases OLC and components of the renin-angiotensin system in the brain. Male Wistar rats received via osmotic minipump an intracerebroventricular infusion of aCSF or Na<jats:sup>+</jats:sup>-rich aCSF, in some groups combined with intracerebroventricular infusion of spironolactone (100 ng/h), antibody Fab fragments (to bind OLC), or as control γ-globulins. After 2 wk of infusion, resting blood pressure and heart rate were recorded, OLC and aldosterone content in the hypothalamus were assessed by a specific ELISA or radioimmunoassay, and angiotensin-converting enzyme (ACE) and AT<jats:sub>1</jats:sub>-receptor binding densities in various brain nuclei were measured by autoradiography using <jats:sup>125</jats:sup>I-labeled 351 A and <jats:sup>125</jats:sup>I-labeled ANG II. When compared with intracerebroventricular aCSF, intracerebroventricular Na<jats:sup>+</jats:sup>-rich aCSF increased CSF [Na<jats:sup>+</jats:sup>] by ∼5 mmol/l, mean arterial pressure by ∼20 mmHg, heart rate by ∼65 beats/min, and hypothalamic content of OLC by 50% and of aldosterone by 33%. Intracerebroventricular spironolactone did not affect CSF [Na<jats:sup>+</jats:sup>] but blocked the Na<jats:sup>+</jats:sup>-rich aCSF-induced increases in blood pressure and heart rate and OLC content. Intracerebroventricular Na<jats:sup>+</jats:sup>-rich aCSF increased ACE and AT<jats:sub>1</jats:sub>-receptor-binding densities in several brain nuclei, and Fab fragments blocked these increases. These data indicate that in Wistar rats, a chronic increase in CSF [Na<jats:sup>+</jats:sup>] may increase hypothalamic aldosterone and activate CNS pathways involving MR, and OLC, leading to increases in AT<jats:sub>1</jats:sub>-receptor and ACE densities in brain areas involved in cardiovascular regulation and hypertension. </jats:p> |
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| author | Huang, Bing S., Cheung, Warren J., Wang, Hao, Tan, Junhui, White, Roselyn A., Leenen, Frans H. H. |
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| description | <jats:p> Functional studies indicate that the sympathoexcitatory and pressor responses to an increase in cerebrospinal fluid (CSF) [Na<jats:sup>+</jats:sup>] by central infusion of Na<jats:sup>+</jats:sup>-rich artificial cerebrospinal fluid (aCSF) in Wistar rats are mediated in the brain by mineralocorticoid receptor (MR) activation, ouabain-like compounds (OLC), and AT<jats:sub>1</jats:sub>-receptor stimulation. In the present study, we examined whether increasing CSF [Na<jats:sup>+</jats:sup>] by intracerebroventricular infusion of Na<jats:sup>+</jats:sup>-rich aCSF activates MR and thereby increases OLC and components of the renin-angiotensin system in the brain. Male Wistar rats received via osmotic minipump an intracerebroventricular infusion of aCSF or Na<jats:sup>+</jats:sup>-rich aCSF, in some groups combined with intracerebroventricular infusion of spironolactone (100 ng/h), antibody Fab fragments (to bind OLC), or as control γ-globulins. After 2 wk of infusion, resting blood pressure and heart rate were recorded, OLC and aldosterone content in the hypothalamus were assessed by a specific ELISA or radioimmunoassay, and angiotensin-converting enzyme (ACE) and AT<jats:sub>1</jats:sub>-receptor binding densities in various brain nuclei were measured by autoradiography using <jats:sup>125</jats:sup>I-labeled 351 A and <jats:sup>125</jats:sup>I-labeled ANG II. When compared with intracerebroventricular aCSF, intracerebroventricular Na<jats:sup>+</jats:sup>-rich aCSF increased CSF [Na<jats:sup>+</jats:sup>] by ∼5 mmol/l, mean arterial pressure by ∼20 mmHg, heart rate by ∼65 beats/min, and hypothalamic content of OLC by 50% and of aldosterone by 33%. Intracerebroventricular spironolactone did not affect CSF [Na<jats:sup>+</jats:sup>] but blocked the Na<jats:sup>+</jats:sup>-rich aCSF-induced increases in blood pressure and heart rate and OLC content. Intracerebroventricular Na<jats:sup>+</jats:sup>-rich aCSF increased ACE and AT<jats:sub>1</jats:sub>-receptor-binding densities in several brain nuclei, and Fab fragments blocked these increases. These data indicate that in Wistar rats, a chronic increase in CSF [Na<jats:sup>+</jats:sup>] may increase hypothalamic aldosterone and activate CNS pathways involving MR, and OLC, leading to increases in AT<jats:sub>1</jats:sub>-receptor and ACE densities in brain areas involved in cardiovascular regulation and hypertension. </jats:p> |
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| spelling | Huang, Bing S. Cheung, Warren J. Wang, Hao Tan, Junhui White, Roselyn A. Leenen, Frans H. H. 0363-6135 1522-1539 American Physiological Society Physiology (medical) Cardiology and Cardiovascular Medicine Physiology http://dx.doi.org/10.1152/ajpheart.00024.2006 <jats:p> Functional studies indicate that the sympathoexcitatory and pressor responses to an increase in cerebrospinal fluid (CSF) [Na<jats:sup>+</jats:sup>] by central infusion of Na<jats:sup>+</jats:sup>-rich artificial cerebrospinal fluid (aCSF) in Wistar rats are mediated in the brain by mineralocorticoid receptor (MR) activation, ouabain-like compounds (OLC), and AT<jats:sub>1</jats:sub>-receptor stimulation. In the present study, we examined whether increasing CSF [Na<jats:sup>+</jats:sup>] by intracerebroventricular infusion of Na<jats:sup>+</jats:sup>-rich aCSF activates MR and thereby increases OLC and components of the renin-angiotensin system in the brain. Male Wistar rats received via osmotic minipump an intracerebroventricular infusion of aCSF or Na<jats:sup>+</jats:sup>-rich aCSF, in some groups combined with intracerebroventricular infusion of spironolactone (100 ng/h), antibody Fab fragments (to bind OLC), or as control γ-globulins. After 2 wk of infusion, resting blood pressure and heart rate were recorded, OLC and aldosterone content in the hypothalamus were assessed by a specific ELISA or radioimmunoassay, and angiotensin-converting enzyme (ACE) and AT<jats:sub>1</jats:sub>-receptor binding densities in various brain nuclei were measured by autoradiography using <jats:sup>125</jats:sup>I-labeled 351 A and <jats:sup>125</jats:sup>I-labeled ANG II. When compared with intracerebroventricular aCSF, intracerebroventricular Na<jats:sup>+</jats:sup>-rich aCSF increased CSF [Na<jats:sup>+</jats:sup>] by ∼5 mmol/l, mean arterial pressure by ∼20 mmHg, heart rate by ∼65 beats/min, and hypothalamic content of OLC by 50% and of aldosterone by 33%. Intracerebroventricular spironolactone did not affect CSF [Na<jats:sup>+</jats:sup>] but blocked the Na<jats:sup>+</jats:sup>-rich aCSF-induced increases in blood pressure and heart rate and OLC content. Intracerebroventricular Na<jats:sup>+</jats:sup>-rich aCSF increased ACE and AT<jats:sub>1</jats:sub>-receptor-binding densities in several brain nuclei, and Fab fragments blocked these increases. These data indicate that in Wistar rats, a chronic increase in CSF [Na<jats:sup>+</jats:sup>] may increase hypothalamic aldosterone and activate CNS pathways involving MR, and OLC, leading to increases in AT<jats:sub>1</jats:sub>-receptor and ACE densities in brain areas involved in cardiovascular regulation and hypertension. </jats:p> Activation of brain renin-angiotensin-aldosterone system by central sodium in Wistar rats American Journal of Physiology-Heart and Circulatory Physiology |
| spellingShingle | Huang, Bing S., Cheung, Warren J., Wang, Hao, Tan, Junhui, White, Roselyn A., Leenen, Frans H. H., American Journal of Physiology-Heart and Circulatory Physiology, Activation of brain renin-angiotensin-aldosterone system by central sodium in Wistar rats, Physiology (medical), Cardiology and Cardiovascular Medicine, Physiology |
| title | Activation of brain renin-angiotensin-aldosterone system by central sodium in Wistar rats |
| title_full | Activation of brain renin-angiotensin-aldosterone system by central sodium in Wistar rats |
| title_fullStr | Activation of brain renin-angiotensin-aldosterone system by central sodium in Wistar rats |
| title_full_unstemmed | Activation of brain renin-angiotensin-aldosterone system by central sodium in Wistar rats |
| title_short | Activation of brain renin-angiotensin-aldosterone system by central sodium in Wistar rats |
| title_sort | activation of brain renin-angiotensin-aldosterone system by central sodium in wistar rats |
| title_unstemmed | Activation of brain renin-angiotensin-aldosterone system by central sodium in Wistar rats |
| topic | Physiology (medical), Cardiology and Cardiovascular Medicine, Physiology |
| url | http://dx.doi.org/10.1152/ajpheart.00024.2006 |