Ouabain- and central sodium-induced hypertension depend on the ventral anteroventral third ventricle region

1999 ◽  
Vol 276 (1) ◽  
pp. H63-H70 ◽  
Author(s):  
Shereeni J. Veerasingham ◽  
Frans H. H. Leenen
Keyword(s):  
Hypertonic Saline ◽  
Wistar Rats ◽  
Third Ventricle ◽  
Cardiovascular Responses ◽  
Ibotenic Acid ◽  
Air Jet ◽  
Artificial Cerebrospinal Fluid ◽  
Induced Hypertension ◽  
Chronic Infusion

To examine the role of the ventral anteroventral third ventricle (vAV3V) in the hypertension induced by chronic subcutaneous ouabain and intracerebroventricular hypertonic saline, neurons in this area were destroyed by microinjection of an excitotoxin, ibotenic acid. Sham-operated or lesioned Wistar rats were administered ouabain (50 μg/day) or placebo for 3 wk from subcutaneously implanted controlled release pellets or artificial cerebrospinal fluid (CSF) or CSF containing 0.8 mol/l NaCl (5 μl/h) infused intracerebroventricularly for 2 wk. At the end of the experiment, mean arterial pressure (MAP) and heart rate at rest and in response to ganglionic blockade by intravenous hexamethonium (30 mg/kg) were assessed. In rats infused with hypertonic saline, responses to air jet stress were also assessed. Baseline MAP in sham-operated rats receiving intracerebroventricular hypertonic saline or subcutaneous ouabain was significantly higher than in control rats (115 ± 1 vs. 97 ± 3 and 121 ± 3 vs. 103 ± 3 mmHg, respectively). vAV3V lesions abolished the increase in MAP elicited by chronic infusion of hypertonic saline or administration of ouabain. Sham-operated rats treated with hypertonic saline or ouabain exhibited significantly enhanced decreases in MAP to hexamethonium, but lesioned rats did not. Rats infused with hypertonic saline demonstrated enhanced responses to air jet stress that were similar in sham-operated and lesioned rats. These results demonstrate that neurons in the vAV3V are essential for the hypertension induced by intracerebroventricular hypertonic saline and subcutaneous ouabain, possibly by increasing sympathetic tone. Cardiovascular responses to air jet stress appear not to be mediated by the vAV3V.

Mechanisms in the PVN mediating local and central sodium-induced hypertension in Wistar rats

2009 ◽  
Vol 296 (3) ◽  
pp. R618-R630 ◽  
Author(s):  
Alexander Gabor ◽  
Frans H. H. Leenen
Keyword(s):  
Wistar Rats ◽  
Ouabain Binding ◽  
Short Term ◽  
Receptor Stimulation ◽  
Intracerebroventricular Infusion ◽  
Artificial Cerebrospinal Fluid ◽  
Pressor Responses ◽  
Induced Hypertension

Sympathoexcitatory and hypertensive responses to central infusion of Na+-rich artificial cerebrospinal fluid (aCSF) are enhanced by aldosterone and mediated by mineralocorticoid receptors (MRs) and benzamil-blockable Na+ influx, leading to “ouabain” release and ANG II type 1 (AT1) receptor stimulation. The present study evaluated the functional role of these mechanisms in the paraventricular nucleus (PVN). In conscious Wistar rats, Na+-rich aCSF was infused either directly into the PVN or intracerebroventricularly preceded by aldosterone and blockers. Infusion of Na+-rich aCSF in the PVN caused gradual increases in blood pressure (BP) and heart rate (HR). Aldosterone and a subpressor dose of ouabain in the PVN alone did not affect BP and HR but enhanced responses to Na+. Eplerenone, benzamil, and “ouabain”-binding Fab fragments only blocked the enhancement by aldosterone, whereas losartan blocked all responses to Na+-rich aCSF in the PVN. Increases in BP and HR by intracerebroventricular infusion of Na+-rich aCSF were enhanced by aldosterone infused intracerebroventricularly, but not in the PVN. Telmisartan in the PVN again blocked all responses. In contrast, both eplerenone and benzamil in the PVN did not change the pressor responses to intracerebroventricular infusion of aldosterone and Na+-rich aCSF. These findings indicate that AT1 receptors in the PVN mediate the responses to Na+-rich aCSF and their enhancement by aldosterone, both locally in the PVN or in the general CSF. MRs, benzamil-blockable Na+ channels or transporters, and “ouabain” can be functionally active in the PVN, but in Wistar rats appear not to contribute to the pressor responses to short-term increases in CSF [Na+].

Anteroventral third ventricle lesions impair cardiovascular responses to intravenous hypertonic saline infusion

2005 ◽  
Vol 117 (1) ◽  
pp. 9-16 ◽  
Author(s):  
Gustavo Rodrigues Pedrino ◽  
Celisa Tiemi Nakagawa Sera ◽  
Sérgio Luiz Cravo ◽  
Débora Simões de Almeida Colombari
Keyword(s):  
Hypertonic Saline ◽  
Third Ventricle ◽  
Cardiovascular Responses ◽  
Saline Infusion ◽  
Hypertonic Saline Infusion

Neural input modulates osmotically stimulated release of vasopressin into the supraoptic nucleus

1996 ◽  
Vol 270 (5) ◽  
pp. E787-E792 ◽  
Author(s):  
M. Ludwig ◽  
M. F. Callahan ◽  
R. Landgraf ◽  
A. K. Johnson ◽  
M. Morris
Keyword(s):  
Supraoptic Nucleus ◽  
Third Ventricle ◽  
Cardiovascular Responses ◽  
Neural Input ◽  
Artificial Cerebrospinal Fluid ◽  
Extracellular Compartment ◽  
Osmotic Stimulation ◽  
Blood Pressure Responses ◽  
Osmotic Stimuli ◽  
Stimulation Of

The effects of lesioning of the anteroventral third ventricle (AV3V) region on vasopressin (VP) release into the supraoptic nucleus (SON) and blood in response to central and systemic osmotic stimulation were determined. Microdialysis probes were implanted bilaterally within the SON of male urethan-anesthetized rats with sham or AV3V lesions. Osmotic stimuli were administered intraperitoneally (3.5 M NaCl, 600 microliters/100 g body wt) and then via the microdialysis probes (1 M NaCl-artificial cerebrospinal fluid). AV3V lesions attenuated the response to systemic osmotic stimulation. The lesioned rats showed no increase in intranuclear VP release and reduced plasma VP (increase of 42.6 +/- 8.4 vs. 78.0 +/- 16.4 pg/ml) and blood pressure responses (7.1 +/- 2.3 vs. 19.6 +/- 3.2 mmHg) to intraperitoneal NaCl. In contrast, the endocrine and cardiovascular responses to direct osmotic stimulation of the nucleus were as seen in previous studies and seemed to be unaffected by the lesion. These results show that lesion of the AV3V region interrupts neuronal inputs which trigger VP secretion from the posterior pituitary as well as release into the extracellular compartment of the SON.

Role of peripheral and central aromatization in the control of gonadotrophin secretion in the male sheep

1999 ◽  
Vol 11 (5) ◽  
pp. 293 ◽  
Author(s):  
T. P. Sharma ◽  
D. Blache ◽  
M. A. Blackberry ◽  
G. B. Martin
Keyword(s):  
Third Ventricle ◽  
Pulse Frequency ◽  
Major Site ◽  
The Third ◽  
Artificial Cerebrospinal Fluid ◽  
Gonadotrophin Secretion ◽  
Lh Secretion ◽  
Plasma Oestradiol ◽  
Male Sheep

Both testosterone and its aromatized metabolite, oestradiol-17b, are known to act centrally on the secretion of GnRH, but the major site of aromatization is not clear as aromatase activities are found in numerous tissues including brain and testis. Here, we tested the importance of central aromatization of testosterone using a non-steroidal aromatase inhibitor, fadrozole. To distinguish between testicular and non-testicular sites, five intact and five testosterone-infused castrated rams (600 g kg –1 per 24 h for 3 days) were given four injections of fadrozole (i.m; 500 g kg –1 ) at 48, 52, 64 and 68 h relative to the start of testosterone infusion. Control rams (n = 5) received vehicle only. Fadrozole treatment decreased plasma oestradiol-17b concentrations and increased the LH pulse frequency in both intact rams and testosterone-treated castrates, suggesting that non-testicular sites of aromatization are important in the control of pulsatile LH secretion. To test the importance of central aromatization, intact rams (n = 5) were infused into the third ventricle with vehicle (artificial cerebrospinal fluid) or with fadrozole (20 and 200 g kg –1 per day). After two weeks, the same two doses of fadrozole were infused intravenously instead of intracerebrally. Central infusion of fadro-zole did not affect plasma oestradiol concentrations but increased LH pulse frequency. Only the highest dose increased LH pulse frequency when infused intravenously. In conclusion, central aromatization is involved in the control of pulsatile LH secretion in male sheep.

Central V1 AVP receptors are involved in cardiovascular adaptation to hypovolemia in WKY but not in SHR

1996 ◽  
Vol 271 (3) ◽  
pp. H1057-H1064 ◽  
Author(s):  
A. S. Budzikowski ◽  
P. Paczwa ◽  
E. Szczepanska-Sadowska
Keyword(s):  
Cardiovascular Responses ◽  
Receptor Antagonists ◽  
Question Mark ◽  
Spontaneously Hypertensive ◽  
Arterial Bleeding ◽  
Artificial Cerebrospinal Fluid ◽  
Before And After ◽  
Wistar Kyoto ◽  
Lateral Cerebral Ventricle

The present study was designed to determine the role of centrally released arginine vasopressin (AVP) in cardiovascular adaptation to hypotensive hypovolemia in conscious normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). Three groups of experiments were performed on WKY and SHR chronically implanted with lateral cerebral ventricle (LCV) cannulas and with femoral artery catheters. Mean arterial pressure (MAP) and heart rate (HR) were monitored before and after arterial bleeding (1.3% body weight) performed during LCV infusion 1) artificial cerebrospinal fluid (control), 2) V1 AVP-receptor antagonists inverted question mark[d(Et2)Tyr(Me)]DAVP, 5 ng/min inverted question mark, and 3) V2 AVP-receptor antagonists inverted question mark[d(CH2)5-D-Ile2, Ile4, AlaNH2]AVP, 5 ng/min inverted question mark. In control experiments hemorrhage caused similar significant decreases of MAP in both strains and bradycardia in WKY. Blockade of central V1 AVP receptors abolished hemorrhagic bradycardia and significantly reduced hypotension in WKY, with no effect on HR and MAP responses to hypovolemia in SHR. Neither in WKY nor in SHR were the cardiovascular responses to hemorrhage altered by blockade of central V2 receptors. The results suggest that the central V1 AVP system plays a significant role in eliciting hypovolemic bradycardia and hypotension in WKY and that this function is significantly impaired in SHR.

Central ANG II-receptor antagonists impair cardiovascular and vasopressin response to hemorrhage in rats

1995 ◽  
Vol 268 (6) ◽  
pp. R1500-R1506 ◽  
Author(s):  
W. J. Lee ◽  
E. K. Yang ◽  
D. K. Ahn ◽  
Y. Y. Park ◽  
J. S. Park ◽  
...  
Keyword(s):  
Wistar Rats ◽  
Physiological Role ◽  
Ang Ii ◽  
Vasopressin Release ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Artificial Cerebrospinal Fluid ◽  
Wistar Kyoto ◽  
Different Strains

The role of brain angiotensin II (ANG II) in mediating cardiovascular, vasopressin, and renin responses to hemorrhage was assessed in conscious spontaneously hypertensive rats (SHR) and in normotensive Wistar-Kyoto (WKY) and Wistar rats. Intracerebroventricular administration of losartan (10 micrograms) and saralasin (1 microgram.microliter-1.min-1) produced a markedly greater fall in blood pressure and a reduced tachycardia during and after hemorrhage (15 ml/kg) compared with the artificial cerebrospinal fluid control in SHR and Wistar rats but not in WKY rats. Vasopressin release after hemorrhage was also impaired, but renin release was enhanced by intracerebroventricular ANG II antagonists in SHR and Wistar rats but not in WKY rats. Losartan and saralasin produced remarkably similar effects on the cardiovascular, vasopressin, and renin responses to hemorrhage. These data suggest that brain ANG II acting through AT1 receptors plays an important physiological role in mediating rapid cardiovascular regulation and vasopressin release in response to hemorrhage. The relative importance of brain angiotensin system may vary in different strains of rate.

Preoptic recess alpha-adrenoceptors control cardiovascular responses to hyperosmolality

1997 ◽  
Vol 272 (4) ◽  
pp. R1283-R1289 ◽  
Author(s):  
S. L. Bealer
Keyword(s):  
Blood Pressure ◽  
Lateral Ventricle ◽  
Third Ventricle ◽  
Cardiovascular Responses ◽  
Alpha Adrenoceptors ◽  
Diagonal Band ◽  
Arterial Blood ◽  
Artificial Cerebrospinal Fluid ◽  
Alpha2 Adrenoceptor ◽  
Map Data

The roles of alpha-adrenoceptors in the anteroventral third ventricle (AV3V) and diagonal band of Broca (DBB) in cardiovascular responses to peripheral hypertonicity were investigated in conscious rats. Normal artificial cerebrospinal fluid (aCSF) or aCSF containing phentolamine (alpha1- and alpha2-antagonist), yohimbine (alpha2-antagonist), or prazosin (alpha1-antagonist) was perfused through microdialysis probes in the DBB, AV3V, or lateral ventricle during a 30-min infusion of isotonic (0.17 M; 0.1 or 1.7 ml x kg(-1) x min(-1) i.v.) or hypertonic (2.5 M; 0.1 ml x kg(-1) x min(-1) i.v.) NaCl. Hypertonic infusion increased blood pressure [mean arterial blood pressure (MAP); 17 +/- 2 mmHg] and decreased heart rate (HR; 36 +/- 6 beats/min). Both responses were abolished by AV3V administration of phentolamine or yohimbine, whereas prazosin selectively prevented the bradycardia. Phentolamine in the DBB or lateral ventricle did not alter either response. Stimulation of AV3V alpha1-adrenoceptors (phenylephrine) decreased HR and MAP, whereas alpha2-adrenoceptor stimulation (clonidine) produced bradycardia but increased MAP. Data suggest that alpha-adrenoceptors in the AV3V, but not the DBB, regulate cardiovascular responses to hyperosmolality.

Role of vasopressin in cardiovascular responses to acute and chronic hyperosmolality

1992 ◽  
Vol 262 (1) ◽  
pp. R25-R32 ◽  
Author(s):  
R. D. Russ ◽  
B. L. Brizzee ◽  
B. R. Walker
Keyword(s):  
Hypertonic Saline ◽  
Water Deprivation ◽  
Peripheral Resistance ◽  
Plasma Osmolality ◽  
Cardiovascular Responses ◽  
Saline Infusion ◽  
Minor Role ◽  
Arterial Blood ◽  
Hypertonic Saline Infusion

Experiments were performed in conscious chronically instrumented rats to determine the role of arginine vasopressin (AVP) in the cardiovascular adjustments to acute and chronic increases in plasma osmolality. Animals were implanted with pulsed Doppler flow probes and arterial and venous catheters for the determination of cardiac output, mean arterial blood pressure (MABP), and heart rate and for the calculation of total peripheral resistance and baroreflex sensitivity (BRS). Before and after raising plasma osmolality by either 48-h water deprivation or acute hypertonic saline infusion, specific V1- or V2-vasopressinergic receptor antagonists or vehicle were administered to the animals, and the cardiovascular responses were noted. MABP was significantly elevated in water-deprived animals. These animals also exhibited significantly increased BRS, which was further increased by administration of the V1-receptor antagonist. Animals subjected to acute hypertonic saline infusion also demonstrated increased MABP, although the infusion, unlike water deprivation, did not affect BRS. We observed no significant effects on any other variable measured. We conclude that AVP plays a relatively minor role in the cardiovascular adjustments to acute and chronic hyperosmolality.

Role of vasopressin, catecholamines, and plasma volume in hypertonic saline-induced hypertension

1981 ◽  
Vol 240 (6) ◽  
pp. H827-H831 ◽  
Author(s):  
P. Hatzinikolaou ◽  
H. Gavras ◽  
H. R. Brunner ◽  
I. Gavras
Keyword(s):  
Blood Pressure ◽  
Hypertonic Saline ◽  
Plasma Volume ◽  
Residual Pressure ◽  
Volume Changes ◽  
Beta Adrenoceptor ◽  
Induced Hypertension ◽  
Fluid Load ◽  
Blood Pressures

Elevation of blood pressure induced by an acute sodium and fluid load in the anephric state has been attributed to intravascular fluid volume expansion. The present experiments were designed to study the role of vasopressin and catecholamines in this type of hypertension. Normotensive anephric rats, adrenergically intact or pretreated with alpha- and beta-adrenoceptor blockade, and deoxycorticosterone (DOC)-salt-treated anephric rats, intact or pretreated with alpha- and beta-adrenoceptor blockade, received an infusion of 2 ml containing 3 meq NaCl, followed by intravenous administration of an analogue antagonist of the vasopressor effect of arginine-vasopressin (AVP). Pressure increments induced by hypertonic saline were abolished by an AVP antagonist partly in the adrenergically intact animals (leaving a small residual pressure elevation) and completely in adrenergically blocked animals, which had a larger AVP component. Volumes expansion did not necessarily accompany increase in blood pressure after saline infusion. In fact some DOC-salt-treated animals with the highest blood pressures and norepinephrine levels exhibited contraction of plasma volume. Increments in blood pressure were negatively correlated with plasma volume changes (r = -0.687, P less than 0.05) in these animals and positively with norepinephrine levels in all adrenergically intact animals (r = 0.818, P less than 0.001). It is concluded that the hypertensive response elicited by acute hypertonic saline load is due to vasoconstriction mediated partly by vasopressin and partly by the sympathetic system, which may in some way attenuate the effect of vasopressin.

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