scholarly journals Different neuronal populations of the rat median preoptic nucleus express c-fosduring sleep and in response to hypertonic saline or angiotensin-II

2005 ◽  
Vol 569 (2) ◽  
pp. 587-599 ◽  
Author(s):  
I. Gvilia ◽  
C. Angara ◽  
D. McGinty ◽  
R. Szymusiak
Keyword(s):  
Angiotensin Ii ◽  
Hypertonic Saline ◽  
Preoptic Nucleus ◽  
Median Preoptic Nucleus ◽  
Neuronal Populations

Median preoptic nucleus ablation does not affect angiotensin II-induced hypertension

1986 ◽  
Vol 251 (1) ◽  
pp. H148-H152
Author(s):  
G. D. Fink ◽  
C. A. Bruner ◽  
M. L. Mangiapane
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cardiovascular Responses ◽  
Base Line ◽  
Ang Ii ◽  
Preoptic Nucleus ◽  
Water Excretion ◽  
Median Preoptic Nucleus ◽  
Induced Hypertension

Previous studies implicated the ventral median preoptic nucleus (MNPOv) in cardiovascular responses to circulating and intracerebroventricular angiotensin II (ANG II) and in normal cardiovascular and fluid homoeostasis. In the present experiments, chronically catheterized rats received continuous (24 h/day) intravenous infusions of ANG II (10 ng/min) for 5 days, and changes in mean arterial pressure, heart rate, water intake and urinary electrolyte and water excretion were determined daily. Three groups of rats were compared as follows: 1) sham-operated control rats (n = 12), 2) rats with 20-70% of the MNPOv ablated electrolytically (n = 6), and 3) rats with over 90% of the MNPOv ablated (n = 5). The organum vasculosum of the lamina terminalis was intact in all three groups. Base-line values of all measured variables were identical in the three groups on two control days preceding ANG II infusion and on two recovery days after infusion. During the administration of ANG II for 5 days, mean arterial pressure rose significantly (and similarly) in all three groups of rats; no other variable was significantly affected by ANG II infusion. These results suggest that neural pathways originating in, or passing through, the MNPOv region are not critical in the pathogenesis of ANG II-induced hypertension in the rat.

Thirst and brain angiotensin in cattle

1992 ◽  
Vol 262 (2) ◽  
pp. R204-R210
Author(s):  
J. R. Blair-West ◽  
D. A. Denton ◽  
M. J. McKinley ◽  
R. S. Weisinger
Keyword(s):  
Angiotensin Ii ◽  
Water Intake ◽  
Enzyme Inhibitors ◽  
Converting Enzyme ◽  
Preoptic Nucleus ◽  
Angiotensin I ◽  
Converting Enzyme Inhibitors ◽  
Median Preoptic Nucleus ◽  
Angiotensin I Converting Enzyme ◽  
Reduced Water

Cows that were normally hydrated or deprived of water were given intravenous or intracerebroventricular (icv) infusions of angiotensin I converting-enzyme inhibitors (CEI) or angiotensin II antagonists. Normally hydrated Na-deficient cows increased water intake in a dose-related manner in response to icv infusion of angiotensin I (n = 5). The response to 3 micrograms/h angiotensin I was abolished by concurrent icv infusion of the CEI captopril at 3 mg/h but not by intravenous infusion of captopril at 120 mg/h, which reduced Na appetite (n = 5). The icv infusion of captopril at 12 mg/h did not reduce the water intake of cows that were water restricted for 26.5 h (n = 4) or water restricted and Na deficient (n = 4). The icv infusion of the more lipophilic CEI ramipril at 3 mg/h (n = 7) did not reduce the water intake of normally hydrated or dehydrated cows but reduced the "need-free" intake of Na solution by dehydrated cows. The icv infusion of the nonpeptide antagonist Du Pont 753 at 3 mg/h (n = 7) reduced water intake in dehydrated cows. The results indicate that brain angiotensin may be involved in thirst in cattle. The data suggest that this brain angiotensin II may be formed by a pathway that does not include converting enzyme and that is sited inside the blood brain barrier, possibly in the median preoptic nucleus.

Increased angiotensin II receptors in brain nuclei of DOCA-salt hypertensive rats

1988 ◽  
Vol 255 (3) ◽  
pp. H646-H650 ◽  
Author(s):  
J. S. Gutkind ◽  
M. Kurihara ◽  
J. M. Saavedra
Keyword(s):  
Angiotensin Ii ◽  
Area Postrema ◽  
Experimental Hypertension ◽  
Ang Ii ◽  
Preoptic Nucleus ◽  
Salt Treatment ◽  
Brain Nuclei ◽  
Median Preoptic Nucleus ◽  
Wistar Kyoto

We analyzed angiotensin II (ANG II) receptors by in vitro autoradiography in selective brain nuclei of control, salt-treated (1% NaCl in drinking water), deoxycorticosterone acetate (DOCA)-treated (DOCA pivalate, 25 mg/kg sc weekly), and DOCA-salt-treated (DOCA + salt treatments) uninephrectomized male Wistar-Kyoto rats. After 4 wk of treatment, only the DOCA-salt group developed hypertension. ANG II binding increased in median preoptic nucleus and subfornical organ of salt- and DOCA-treated rats. DOCA-treated rats also showed increased ANG II binding in paraventricular nucleus. DOCA-salt-treated rats showed higher ANG II binding in nucleus of the solitary tract and area postrema, as well as in the areas mentioned before. Although salt and/or DOCA treatments alone increased ANG II receptors in some brain nuclei, after combined DOCA-salt treatment there was significantly higher ANG II binding in all areas, except the median preoptic nucleus. These results suggest that increased ANG II receptors in selected brain areas may play a role in the pathophysiology of mineralocorticoid-salt experimental hypertension.

Comparison of fos-like immunoreactivity induced in rat brain by central injection of angiotensin II and carbachol

1994 ◽  
Vol 267 (3) ◽  
pp. R792-R798 ◽  
Author(s):  
N. E. Rowland ◽  
B. H. Li ◽  
A. K. Rozelle ◽  
G. C. Smith
Keyword(s):  
Angiotensin Ii ◽  
Ang Ii ◽  
Angiotensin Receptor ◽  
Preoptic Nucleus ◽  
Median Preoptic Nucleus ◽  
Immunocytochemical Detection ◽  
Organum Vasculosum Laminae Terminalis ◽  
Hypothalamic Nuclei ◽  
At1 Antagonist ◽  
Intracerebroventricular Injections

Rats were given intracerebroventricular injections of either angiotensin II (ANG II) or the cholinomimetic carbachol. Some rats received cotreatment with ANG II antagonists selective for either angiotensin receptor AT1 (losartan) or AT2 (PD-123319, CGP-42112A). One hour later, the rats were killed and the brains processed for immunocytochemical detection of Fos-like immunoreactivity (FLI). ANG II treatment induced strong FLI in the anterior subfornical organ (SFO), median preoptic nucleus (MnPO), organum vasculosum laminae terminalis (OVLT), and supraoptic and paraventricular hypothalamic nuclei (SON, PVH). The AT1 antagonist abolished FLI in all regions normally stimulated by ANG II. The AT2 antagonist PD-123319 reduced FLI in SON and PVH, but CGP-42112A was less effective. Carbachol induced strong FLI in SON, PVH, and MnPO and only moderate FLI in SFO and OVLT. The AT1 antagonist prevented carbachol-induced FLI in the MnPO only. The distributions of FLI are compared between these central dipsogens and with that previously reported after peripheral infusion of ANG II, and their implications for mapping central thirst pathways are discussed.

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