Intracranial renin alters gustatory neural responses in the nucleus of the solitary tract of rats

2003 ◽  
Vol 284 (4) ◽  
pp. R1108-R1118 ◽  
Author(s):  
R. Tamura ◽  
R. Norgren
Keyword(s):  
Neural Activity ◽  
Renin Angiotensin System ◽  
Intracerebroventricular Injection ◽  
Solitary Tract ◽  
Neural Responses ◽  
Angiotensin System ◽  
Sodium Appetite ◽  
Similar Tendency ◽  
Quinine Hydrochloride ◽  
The Brain

Activation of the renin-angiotensin system in the brain is considered important in the arousal and expression of sodium appetite. To clarify the effects of directly activating this hormonal cascade, taste neurons in the nucleus of the solitary tract of rats were tested with a battery of sapid stimuli after intracerebroventricular injection of renin or its vehicle. The rats were chronically prepared but lightly anesthetized during the recording procedure. Eighty-five taste neurons were tested: 46 after renin injections and 39 after vehicle. Neural activity was counted for 5.0-s periods without stimulation (spontaneous) and during stimulation with water and sapid chemicals. The averaged responses to each of the standard stimuli (0.1 M NaCl, 0.3 M sucrose, 0.01 M citric acid, and 0.01 M quinine hydrochloride) did not differ significantly between the two conditions. When the rats were tested with a concentration range of NaCl, however, after renin the average responses to the hypertonic 0.3 and 1.0 M stimuli were reduced to 74 and 70%, respectively, compared with those after vehicle injections. A similar tendency was evident for the subsample of neurons that responded best to NaCl, but the effect was smaller. These data are consistent with, but not as dramatic as, those reported after dietary-induced sodium appetite.

Repeated sodium depletion affects gustatory neural responses in the nucleus of the solitary tract of rats

1997 ◽  
Vol 273 (4) ◽  
pp. R1381-R1391 ◽  
Author(s):  
Ryoi Tamura ◽  
Ralph Norgren
Keyword(s):  
The Other ◽  
Dietary Sodium ◽  
Gustatory System ◽  
Solitary Tract ◽  
Sodium Restriction ◽  
Neural Responses ◽  
Sodium Depletion ◽  
Sodium Appetite ◽  
The Third ◽  
Quinine Hydrochloride

Furosemide sodium depletions were induced repeatedly to determine the effects on gustatory neural responses in the nucleus of the solitary tract (NST) of chronically prepared, but lightly anesthetized, rats. Sodium-replete and sodium-deplete conditions were alternated four times in each rat. When rats were under depleted conditions, the responses to NaCl were significantly greater than in sodium-replete conditions. This effect was attributable primarily to an increase in the magnitude of response of those neurons that responded better to NaCl than to the other standard stimuli (sucrose, citric acid, and quinine hydrochloride). In addition, the largest change in responsiveness of the NaCl-best neurons occurred during the third and fourth sodium depletions. These results are essentially opposite to those reported for NST neurons when sodium appetite is induced by dietary sodium restriction. This suggests that the coding of intensity in the gustatory system is dependent not only on the animal’s deprivation condition, but also the method through which the deprivation is produced.

scholarly journals Divergent mechanism regulating fluid intake and metabolism by the brain renin-angiotensin system

2012 ◽  
Vol 302 (3) ◽  
pp. R313-R320 ◽  
Author(s):  
Curt D. Sigmund
Keyword(s):  
Blood Pressure ◽  
Fluid Intake ◽  
Renin Angiotensin System ◽  
Metabolic Effects ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Intracellular Form ◽  
Efferent Pathways ◽  
The Brain ◽  
Pituitary Adrenal Axis

The purpose of this review is two-fold. First, I will highlight recent advances in our understanding of the mechanisms regulating angiotensin II (ANG II) synthesis in the brain, focusing on evidence that renin is expressed in the brain and is expressed in two forms: a secreted form, which may catalyze extracellular ANG I generation from glial or neuronal angiotensinogen (AGT), and an intracellular form, which may generate intracellular ANG in neurons that may act as a neurotransmitter. Second, I will discuss recent studies that advance the concept that the renin-angiotensin system (RAS) in the brain not only is a potent regulator of blood pressure and fluid intake but may also regulate metabolism. The efferent pathways regulating the blood pressure/dipsogenic effects and the metabolic effects of elevated central RAS activity appear different, with the former being dependent upon the hypothalamic-pituitary-adrenal axis, and the latter being dependent upon an interaction between the brain and the systemic (or adipose) RAS.

The Brain-Renin-Angiotensin System: Update

1986 ◽  
pp. 123-133 ◽  
Author(s):  
Thomas Unger ◽  
Detlev Ganten ◽  
Gerald Ludwig ◽  
Rudolf E. Lang
Keyword(s):  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Brain

The renin angiotensin system and the brain: New developments

2017 ◽  
Vol 46 ◽  
pp. 1-8 ◽  
Author(s):  
Ehab Farag ◽  
Daniel I. Sessler ◽  
Zeyd Ebrahim ◽  
Andrea Kurz ◽  
Joseph Morgan ◽  
...  
Keyword(s):  
Renin Angiotensin System ◽  
Angiotensin System ◽  
New Developments ◽  
Renin Angiotensin ◽  
The Brain

scholarly journals Bidirectional asymmetry in the neurovisceral communication for the cardiovascular control: New insights

2017 ◽  
Vol 51 (3) ◽  
pp. 157-167 ◽  
Author(s):  
I Prieto ◽  
AB Segarra ◽  
M Martinez-Canamero ◽  
M De Gasparo ◽  
S Zorad ◽  
...  
Keyword(s):  
Essential Role ◽  
Renin Angiotensin System ◽  
Cardiovascular Function ◽  
Cardiovascular Control ◽  
Functional Connection ◽  
Angiotensin System ◽  
Positive Correlations ◽  
Available Information ◽  
The Brain

AbstractThe cardiovascular control involves a bidirectional functional connection between the brain and heart. We hypothesize that this connection could be extended to other organs using endocrine and autonomic nervous systems (ANS) as communication pathways. This implies a neuroendocrine interaction controlling particularly the cardiovascular function where the enzymatic cascade of the renin-angiotensin system (RAS) plays an essential role. It acts not only through its classic endocrine connection but also the ANS. In addition, the brain is functionally, anatomically, and neurochemically asymmetric. Moreover, this asymmetry goes even beyond the brain and it includes both sides of the peripheral nervous and neuroendocrine systems. We revised the available information and analyze the asymmetrical neuroendocrine bidirectional interaction for the cardiovascular control. Negative and positive correlations involving the RAS have been observed between brain, heart, kidney, gut, and plasma in physiologic and pathologic conditions. The central role of the peptides and enzymes of the RAS within this neurovisceral communication, as well as the importance of the asymmetrical distribution of the various RAS components in the pathologies involving this connection, are particularly discussed. In conclusion, there are numerous evidences supporting the existence of a neurovisceral connection with multiorgan involvement that controls, among others, the cardiovascular function. This connection is asymmetrically organized.

Brain renin-angiotensin system and sympathetic hyperactivity in rats after myocardial infarction

1999 ◽  
Vol 276 (5) ◽  
pp. H1608-H1615 ◽  
Author(s):  
Weiguo Zhang ◽  
Bing S. Huang ◽  
Frans H. H. Leenen
Keyword(s):  
Renin Angiotensin System ◽  
Coronary Artery Ligation ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Angiotensin System ◽  
Sympathetic Hyperactivity ◽  
Renin Angiotensin ◽  
Air Jet ◽  
Baroreflex Function ◽  
The Brain

Blockade of brain “ouabain” prevents the sympathetic hyperactivity and impairment of baroreflex function in rats with congestive heart failure (CHF). Because brain “ouabain” may act by activating the brain renin-angiotensin system (RAS), the aim of the present study was to assess whether chronic treatment with the AT1-receptor blocker losartan given centrally normalizes the sympathetic hyperactivity and impairment of baroreflex function in Wistar rats with CHF postmyocardial infarction (MI). After left coronary artery ligation (2 or 6 wk), rats received either intracerebroventricular losartan (1 mg ⋅ kg−1 ⋅ day−1, CHF-Los) or vehicle (CHF-Veh) by osmotic minipumps. To assess possible peripheral effects of intracerebroventricular losartan, one set of CHF rats received the same rate of losartan subcutaneously. Sham-operated rats served as control. After 2 wk of treatment, mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) at rest and in response to air-jet stress and intracerebroventricular injection of the α2-adrenoceptor-agonist guanabenz were measured in conscious animals. Arterial baroreflex function was evaluated by ramp changes in MAP. Compared with sham groups, CHF-Veh groups showed impaired arterial baroreflex control of HR and RSNA, increased sympathoexcitatory and pressor responses to air-jet stress, and increased sympathoinhibitory and hypotensive responses to guanabenz. The latter is consistent with decreased activity in sympathoinhibitory pathways. Chronic intracerebroventricular infusion of losartan largely normalized these abnormalities. In CHF rats, the same rate of infusion of losartan subcutaneously was ineffective. In sham-operated rats, losartan intracerebroventricularly or subcutaneously did not affect sympathetic activity. We conclude that the chronic increase in sympathoexcitation, decrease in sympathoinhibition, and desensitized baroreflex function in CHF all appear to depend on the brain RAS, since this whole pattern of changes can be normalized by chronic central AT1-receptor blockade with losartan.

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