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.

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.

Evidence for a central role for vasopressin in cardiovascular regulation

1983 ◽  
Vol 244 (6) ◽  
pp. H852-H859 ◽  
Author(s):  
K. H. Berecek ◽  
R. L. Webb ◽  
M. J. Brody
Keyword(s):  
Vascular Resistance ◽  
Third Ventricle ◽  
Cardiovascular Responses ◽  
Cardiovascular Regulation ◽  
Brattleboro Rats ◽  
Vascular Responses ◽  
The Third ◽  
Neuronal Systems ◽  
Mesenteric Vascular Resistance ◽  
Stimulation Of

Central vasopressin (VP) may modulate the functional activity of specific neuronal systems involved in cardiovascular regulation. To test this hypothesis we compared cardiovascular (CV) responses to electrical stimulation of the anteroventral region of the third ventricle (AV3V) in Brattleboro rats homozygous for diabetes insipidus (DI), in heterozygous DI rats (DI-HZ) and in normal Long-Evans rats (LE). We also studied the effects of peripheral and intracerebroventricular (ivt) treatment of DI rats with VP and treatment of LE rats with an antipressor blocker of VP on cardiovascular responses to AV3V stimulation. Stimulation of the AV3V region in anesthetized LE rats produced a frequency-dependent increase in renal (RVR) and mesenteric vascular resistance (MVR), a decrease in hindquarter vascular resistance (HQVR), and a decrease in arterial pressure (AP) and heart rate (HR). DI and DI-HZ rats showed significantly greater decreases in AP and HR and lesser changes in RVR, MVR, and HQVR. The deficiency in vasoconstriction in DI rats appeared to be centrally mediated inasmuch as vascular responses to peripherally administered phenylephrine and nerve stimulation were comparable in LE and DI rats. Treatment of DI rats with VP peripherally improved CV responses to AV3V stimulation. An even greater improvement in CV responses to AV3V stimulation was obtained when DI were given ivt infusion of VP. Finally, following intravenous administration of an antipressor VP blocker LE rats showed a greater decrease in AP and HR and lesser resistance changes in response to AV3V stimulation. Our data suggest that cardiovascular responses elicited from stimulation of the AV3V region may depend, in part, on a central vasopressin mechanism.

Similarity of cardiovascular responses to exercise and to diencephalic stimulation

1960 ◽  
Vol 198 (6) ◽  
pp. 1139-1142 ◽  
Author(s):  
Orville A. Smith ◽  
Robert F. Rushmer ◽  
Earl P. Lasher
Keyword(s):  
Heart Rate ◽  
Third Ventricle ◽  
Left Ventricular Pressure ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
The Third ◽  
Stimulating Electrodes ◽  
Stimulation Of

Devices to measure left ventricular pressure, diameter and heart rate in animals with closed chests were placed on the hearts of dogs. After recovery from this operation the dogs were trained to exercise on a treadmill and the cardiovascular responses to this exercise were recorded. Stimulating electrodes were then stereotaxically placed in the diencephalon. In some dogs the electrodes were chronically implanted, and the stimulation was carried out after recovery from this second operation. In other animals stimulation was carried out immediately while they were under chloralose anesthesia. Stimulation of the H1 and H2 fields of Forel and the periventricular gray of the third ventricle resulted in cardiovascular responses similar to those which result from exercise.

Osmotic stimulation of the supraoptic nucleus: central and peripheral vasopressin release and blood pressure

1994 ◽  
Vol 266 (3) ◽  
pp. E351-E356 ◽  
Author(s):  
M. Ludwig ◽  
T. Horn ◽  
M. F. Callahan ◽  
A. Grosche ◽  
M. Morris ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Supraoptic Nucleus ◽  
Pressor Response ◽  
Extracellular Fluid ◽  
Brain Regions ◽  
Vasopressin Release ◽  
Peptide Release ◽  
Osmotic Stimulation ◽  
Stimulation Of

Experiments were performed to determine the effect of direct osmotic stimulation of the supraoptic nucleus (SON) on central and peripheral vasopressin (AVP) release and arterial pressure. A microdialysis method was used to deliver hyperosmotic NaCl, mannitol or urea bilaterally into the SON and to sample SON extracellular fluid and blood. Simultaneous brain and blood microdialysis showed that hyperosmotic NaCl increased central and peripheral AVP release and increased mean arterial pressure (MAP). The pressor response was not blocked by intravenous injection of a V1-receptor antagonist, D(CH2)5Tyr(Me)AVP, suggesting that circulating AVP was not involved in that response. Hyperosmotic mannitol or urea caused an increase in central peptide release, but failed to affect MAP or peripheral AVP release. The results suggest that central AVP release within the SON may be due to osmoreceptor stimulation while the peripheral effects on AVP release and MAP are specific for sodium. The results also demonstrate the utility of brain and blood microdialysis for the delivery of stimuli into specific brain regions with simultaneous monitoring of central and peripheral peptide release.

The Supraoptic Nucleus of the Hypothalamus Modulates Autonomic, Neuroendocrine, and Behavioral Responses to Acute Restraint Stress in Rats

2019 ◽  
Vol 110 (1-2) ◽  
pp. 10-22 ◽  
Author(s):  
Silvana Lopes-Azevedo ◽  
Eduardo Albino Trindade Fortaleza ◽  
Cristiane Busnardo ◽  
América Augusto Scopinho ◽  
Melina Matthiesen ◽  
...  
Keyword(s):  
Plasma Levels ◽  
Restraint Stress ◽  
Supraoptic Nucleus ◽  
Behavioral Responses ◽  
Cardiovascular Responses ◽  
Temperature Plasma ◽  
Acute Restraint Stress ◽  
Artificial Cerebrospinal Fluid ◽  
Male Wistar Rats ◽  
Neuroendocrine Responses

Aims: Acute restraint stress (RS) has been reported to cause neuronal activation in the supraoptic nucleus of the hypothalamus (SON). The aim of the study was to evaluate the role of SON on autonomic (mean arterial pressure [MAP], heart rate [HR], and tail temperature), neuroendocrine (corticosterone, oxytocin, and vasopressin plasma levels), and behavioral responses to RS. Methods: Guide cannulas were implanted bilaterally in the SON of male Wistar rats for microinjection of the unspecific synaptic blocker cobalt chloride (CoCl2, 1 mM) or vehicle (artificial cerebrospinal fluid, 100 nL). A catheter was introduced into the femoral artery for MAP and HR recording. Rats were subjected to RS, and it was studied the effect of microinjection of CoCl2 or vehicle into the SON on pressor and tachycardic responses, drop in tail temperature, plasma oxytocin, vasopressin, and corticosterone levels, and anxiogenic-like effect induced by RS. Results: SON pretreatment with CoCl2 reduced the RS-induced MAP and HR increase, without affecting the RS-evoked tail temperature decrease. Microinjection of CoCl2 into areas surrounding the SON did not affect RS-induced increase in MAP and HR, reinforcing the idea that SON influences RS-evoked cardiovascular responses. Also, SON pretreatment with CoCl2 reduced RS-induced increase in corticosterone and oxytocin, without affecting vasopressin plasma levels, suggesting its involvement in RS-induced neuroendocrine responses. Finally, the CoCl2 microinjection into SON inhibited the RS-caused delayed anxiogenic-like effect. Conclusion: The results indicate that SON is an important component of the neural pathway that controls autonomic, neuroendocrine, and behavioral responses induced by RS.

Supraoptic neurones in Brattleboro rats respond normally to changes in plasma osmotic pressure

1985 ◽  
Vol 105 (1) ◽  
pp. 87-90 ◽  
Author(s):  
R. E. J. Dyball ◽  
G. Leng
Keyword(s):  
Water Balance ◽  
Supraoptic Nucleus ◽  
Tap Water ◽  
Discharge Rate ◽  
Urine Volume ◽  
Plasma Osmolality ◽  
Brattleboro Rats ◽  
Osmotic Stimulation ◽  
Noradrenergic Innervation ◽  
Osmotic Stimuli

ABSTRACT Brattleboro rats homozygous for hypothalamic diabetes insipidus (DI rats) were anaesthetized with urethane. Extracellular recordings were made from antidromically identified neurones of the supraoptic nucleus. About half (77 out of 153) of the neurones recorded in DI rats showed phasic patterns of discharge activity similar to those which are characteristic of vasopressin-secreting neurones in normal rats during hyperosmotic stimulation. Significantly fewer neurones showed phasic activity in DI rats which had been pretreated with vasopressin tannate at a dose which significantly reduced urine volume, water intake and plasma osmolality. Acute systemic hyperosmotic stimulation, induced by an i.p. injection of 1 ml 1·5 m-NaCl, increased the discharge rate of each of 14 neurones from DI rats by 1–5 spikes/s. Hypo-osmotic stimulation, induced by an intragastric injection of 10 ml tap water, reduced the discharge rate of each of four neurones from DI rats by 50% or more. We conclude that supraoptic neurones in DI rats respond normally to acute systemic osmotic stimuli despite the total absence of vasopressin in these rats and despite their chronically disturbed water balance. This implies that the osmoreceptor mechanism which drives the supraoptic nucleus does not adapt substantially during prolonged disturbance of water balance and functions outside the normal physiological range of plasma osmolality, and that the reported alteration of noradrenergic innervation of the neurones in DI rats does not affect their osmotic responsiveness. J. Endocr. (1985) 105, 87–90

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.

Crosstalk in the magnocellular system during osmotic stimulation of one supraoptic nucleus

1994 ◽  
Vol 33 (6) ◽  
pp. 645-654 ◽  
Author(s):  
Joan Y. Summy-Long ◽  
Inga Neumann ◽  
Mary Lee Terrell ◽  
Ellen Koehler ◽  
Shelley Gestl ◽  
...  
Keyword(s):  
Supraoptic Nucleus ◽  
Magnocellular System ◽  
Osmotic Stimulation ◽  
Stimulation Of

Central injection of physostigmine attenuates exercise-induced pressor response in conscious cats

1997 ◽  
Vol 273 (1) ◽  
pp. R393-R399 ◽  
Author(s):  
A. Ally ◽  
G. A. Hand ◽  
J. H. Mitchell
Keyword(s):  
Muscarinic Receptors ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Voluntary Exercise ◽  
Intracerebroventricular Administration ◽  
Static Exercise ◽  
Artificial Cerebrospinal Fluid ◽  
Central Muscarinic Receptors ◽  
Exercise Induced ◽  
Stimulation Of

The effects of intracerebroventricular administration of physostigmine, a cholinesterase inhibitor, on the cardiovascular responses evoked by static voluntary exercise were investigated using conscious cats. Four cats were trained to press a bar (200-650 g) with one forelimb for at least 20 s. The changes in mean arterial pressure (MAP), heart rate (HR), and developed force during the first five trials in 30 min by each individual cat were averaged, and a mean of the four values was then calculated. After the cats exercised for 30 min, either artificial cerebrospinal fluid (CSF) or physostigmine (5 micrograms) was administered intracerebroventricularly. Before physostigmine, exercise trials by the cats increased MAP and HR by 17 +/- 3 mmHg and 42 +/- 4 beats/min, respectively. Administration of physostigmine did not alter the resting MAP and HR but attenuated the MAP and HR responses to exercise (5-30 min postphysostigmine: MAP = 8 +/- 3 mmHg, HR = 25 +/- 7 beats/min; 30-60 min postphysostigmine: MAP = 4 +/- 3 mmHg, HR = 19 +/- 8 beats/min). Intracerebroventricular administration of CSF had no effect on the cardiovascular responses to static exercise. Pretreatment with the muscarinic antagonist, atropine (25 micrograms icv), blocked the attenuating effects of subsequent intracerebroventricular administration of physostigmine. These results demonstrate that stimulation of central muscarinic receptors attenuates the cardiovascular responses to static exercise by conscious cats. In addition, the present study suggests that there is no tonic effect of central muscarinic receptors on the cardiovascular responses to voluntary exercise.

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