Inhibitory mechanism of the nucleus of the solitary tract involved in the control of cardiovascular, dipsogenic, hormonal, and renal responses to hyperosmolality

2013 ◽  
Vol 304 (7) ◽  
pp. R531-R542 ◽  
Author(s):  
Graziela T. Blanch ◽  
André H. Freiria-Oliveira ◽  
David Murphy ◽  
Renata F. Paulin ◽  
José Antunes-Rodrigues ◽  
...  
Keyword(s):  
Water Intake ◽  
Pressor Response ◽  
Plasma Osmolality ◽  
Visceral Afferents ◽  
Solitary Tract ◽  
Plasma Vasopressin ◽  
Inhibitory Mechanisms ◽  
Acute Increase ◽  
Renal Responses ◽  
Vasopressinergic Neurons

The nucleus of the solitary tract (NTS) is the primary site of visceral afferents to the central nervous system. In the present study, we investigated the effects of lesions in the commissural portion of the NTS (commNTS) on the activity of vasopressinergic neurons in the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei, plasma vasopressin, arterial pressure, water intake, and sodium excretion in rats with plasma hyperosmolality produced by intragastric 2 M NaCl (2 ml/rat). Male Holtzman rats with 15–20 days of sham or electrolytic lesion (1 mA; 10 s) of the commNTS were used. CommNTS lesions enhanced a 2 M NaCl intragastrically induced increase in the number of vasopressinergic neurons expressing c-Fos in the PVN (28 ± 1, vs. sham: 22 ± 2 c-Fos/AVP cells) and SON (26 ± 4, vs. sham: 11 ± 1 c-Fos/AVP cells), plasma vasopressin levels (21 ± 8, vs. sham: 6.6 ± 1.3 pg/ml), pressor responses (25 ± 7 mmHg, vs. sham: 7 ± 2 mmHg), water intake (17.5 ± 0.8, vs. sham: 11.2 ± 1.8 ml/2 h), and natriuresis (4.9 ± 0.8, vs. sham: 1.4 ± 0.3 meq/1 h). The pretreatment with vasopressin antagonist abolished the pressor response to intragastric 2 M NaCl in commNTS-lesioned rats (8 ± 2.4 mmHg at 10 min), suggesting that this response is dependent on vasopressin secretion. The results suggest that inhibitory mechanisms dependent on commNTS act to limit or counterbalance behavioral, hormonal, cardiovascular, and renal responses to an acute increase in plasma osmolality.

scholarly journals Catecholaminergic neurons in the comissural region of the nucleus of the solitary tract modulate hyperosmolality-induced responses

2015 ◽  
Vol 309 (9) ◽  
pp. R1082-R1091 ◽  
Author(s):  
Andre H. Freiria-Oliveira ◽  
Graziela T. Blanch ◽  
Gustavo R. Pedrino ◽  
Sergio L. Cravo ◽  
David Murphy ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Water Intake ◽  
Pressor Response ◽  
Plasma Osmolality ◽  
Solitary Tract ◽  
Inhibitory Mechanisms ◽  
Body Fluid Homeostasis ◽  
Pressure Water ◽  
Acute Increase ◽  
Renal Responses

Noradrenergic A2 neurons of the nucleus of the solitary tract (NTS) have been suggested to contribute to body fluid homeostasis and cardiovascular regulation. In the present study, we investigated the effects of lesions of A2 neurons of the commissural NTS (cNTS) on the c-Fos expression in neurons of the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei, arterial pressure, water intake, and urinary excretion in rats with plasma hyperosmolality produced by intragastric 2 M NaCl (2 ml/rat). Male Holtzman rats (280–320 g) received an injection of anti-dopamine-β-hydroxylase-saporin (12.6 ng/60 nl; cNTS/A2-lesion, n = 28) or immunoglobulin G (IgG)-saporin (12.6 ng/60 nl; sham, n = 24) into the cNTS. The cNTS/A2 lesions increased the number of neurons expressing c-Fos in the magnocellular PVN in rats treated with hypertonic NaCl (90 ± 13, vs. sham: 47 ± 20; n = 4), without changing the number of neurons expressing c-Fos in the parvocellular PVN or in the SON. Contrary to sham rats, intragastric 2 M NaCl also increased arterial pressure in cNTS/A2-lesioned rats (16 ± 3, vs. sham: 2 ± 2 mmHg 60 min after the intragastric load; n = 9), an effect blocked by the pretreatment with the vasopressin antagonist Manning compound (0 ± 3 mmHg; n = 10). In addition, cNTS/A2 lesions enhanced hyperosmolality-induced water intake (10.5 ± 1.4, vs. sham: 7.7 ± 0.8 ml/60 min; n = 8–10), without changing renal responses to hyperosmolality. The results suggest that inhibitory mechanisms dependent on cNTS/A2 neurons reduce water intake and vasopressin-dependent pressor response to an acute increase in plasma osmolality.

Effect of ovariectomy and treatment with ovarian steroids on vasopressin release and fluid balance in the rat

1990 ◽  
Vol 124 (2) ◽  
pp. 277-284 ◽  
Author(s):  
K. Peysner ◽  
M. L. Forsling
Keyword(s):  
Water Intake ◽  
Fluid Balance ◽  
Plasma Concentrations ◽  
Plasma Osmolality ◽  
Control Group ◽  
Oestrogen Treatment ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Progesterone Treatment ◽  
Food And Water Intake

ABSTRACT Plasma vasopressin concentrations have previously been shown to vary during the oestrous cycle of the rat, being highest on the morning of pro-oestrus and lowest on dioestrus day 1. To determine the effect of gonadal steroids on vasopressin secretion and fluid balance, mature rats were ovariectomized and given oestrogen, progesterone or vehicle alone s.c. for periods of up to 16 days. Plasma vasopressin concentrations fell after ovariectomy and this was reflected in an increase in 24-h urine volume. The normal increase in plasma vasopressin concentrations seen over daylight hours was also suppressed. The change in vasopressin concentrations observed on steroid treatment depended upon both the dose and the duration. High doses of oestrogen were associated with a fall in plasma vasopressin, probably as a result of fluid retention. Thus, of an initial group of rats given silicone elastomer implants containing 50, 500 or 1000 μg oestradiol in oil, plasma vasopressin concentrations were reduced after 7 days treatment with 1000 μg oestradiol implants in association with reduced plasma sodium concentrations. Daily s.c. injections of 100 μg oestradiol benzoate/100 g body weight produced an immediate small increase in plasma vasopressin concentrations, but by 14 days the plasma concentrations of 0·7 ± 0·16 pmol/l (mean ± s.e.m.) had fallen significantly and were less than those in the vehicle-treated group (1·2± 0·26 pmol/l). However, after treatment for 14 days with implants containing only 50 μg oestradiol, plasma vasopressin concentations were higher compared with the group receiving vehicle alone, despite the fact that the plasma osmolality was lower in the latter group, suggesting a long term resetting of the osmoreceptors. Progesterone treatment with two implants containing 17·5 mg progesterone in oil was associated with an initial suppression of plasma vasopressin concentrations, but 16 days after the implant the plasma concentrations were higher than in the control group. Neither oestrogen nor progesterone restored the vasopressin concentrations to those seen in the intact animal. Oestrogen treatment resulted in a reduction in food and water intake, whereas progesterone treatment produced an initial increase in food and water intake, and a fall in plasma osmolality which could account for the reduced plasma vasopressin. This was followed by an increase in urine flow over days 6 to 15. Thus ovariectomy had a marked effect on circulating vasopressin concentrations, probably as a result of complex changes since administration of either oestrogen or progesterone in doses giving normal circulating concentrations had little effect. Journal of Endocrinology (1990) 124, 277–284

Fluid volume and osmoregulation in humans after a week of head-down bed rest

2001 ◽  
Vol 281 (1) ◽  
pp. R310-R317 ◽  
Author(s):  
Morten Heiberg Bestle ◽  
Peter Norsk ◽  
Peter Bie
Keyword(s):  
Excretion Rate ◽  
Sodium Intake ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Bed Rest ◽  
Ang Ii ◽  
Plasma Vasopressin ◽  
Saline Loading ◽  
Body Fluid Homeostasis ◽  
Renal Responses

Body fluid homeostasis was investigated during chronic bed rest (BR) and compared with that of acute supine conditions. The hypothesis was tested that 6° head-down BR leads to hypovolemia, which activates antinatriuretic mechanisms so that the renal responses to standardized saline loading are attenuated. Isotonic (20 ml/kg body wt) and hypertonic (2.5%, 7.2 ml/kg body wt) infusions were performed in eight subjects over 20 min following 7 and 10 days, respectively, of BR during constant sodium intake (200 meq/day). BR decreased body weight (83.0 ± 4.8 to 81.8 ± 4.4 kg) and increased plasma osmolality (285.9 ± 0.6 to 288.5 ± 0.9 mosmol/kgH2O, P < 0.05). Plasma ANG II doubled (4.2 ± 1.2 to 8.8 ± 1.8 pg/ml), whereas other endocrine variables decreased: plasma atrial natriuretic peptide (42 ± 3 to 24 ± 3 pg/ml), urinary urodilatin excretion rate (4.5 ± 0.3 to 3.2 ± 0.1 pg/min), and plasma vasopressin (1.7 ± 0.3 to 0.8 ± 0.2 pg/ml, P < 0.05). During BR, the natriuretic response to the isotonic saline infusion was augmented (39 ± 8 vs. 18 ± 6 meq sodium/350 min), whereas the response to hypertonic saline was unaltered (32 ± 8 vs. 29 ± 5 meq/350 min, P< 0.05). In conclusion, BR elicits antinatriuretic endocrine signals, but it does not attenuate the renal natriuretic response to saline stimuli in men; on the contrary, the response to isotonic saline is augmented.

Lateral parabrachial serotonergic mechanisms: angiotensin-induced pressor and drinking responses

1995 ◽  
Vol 269 (5) ◽  
pp. R1044-R1049 ◽  
Author(s):  
J. V. Menani ◽  
A. K. Johnson
Keyword(s):  
Water Intake ◽  
Lateral Ventricle ◽  
Pressor Response ◽  
Ang Ii ◽  
Receptor Ligands ◽  
Inhibitory Mechanisms ◽  
Lateral Parabrachial Nucleus ◽  
Left Lateral Ventricle ◽  
Pressor Responses ◽  
Serotonergic Receptor

This study investigated the effects of bilateral injections of serotonergic receptor ligands into the lateral parabrachial nucleus (LPBN) on the pressor and dipsogenic responses induced by intracerebroventricular (i.c.v.) injection of angiotensin II (ANG II). Rats with stainless steel cannulas implanted bilaterally into the LPBN and into the left lateral ventricle were used to study i.c.v. ANG II-induced water intake and pressor responses. Pretreatment with the serotonergic 5-HT1/5-HT2 receptor antagonist methysergide (1-8 micrograms/200 nl) bilaterally injected into the LPBN increased the water intake induced by i.c.v. ANG II (50 ng/microliters) administered via the lateral ventricle, but pretreatment with methysergide (4 micrograms/200 nl) did not change the pressor response produced by i.c.v. ANG II. After bilateral injection of either serotonin (5-HT, 5 micrograms/200 nl) or the serotonergic 5-HT2a/5-HT2c receptor agonist (+/-)-2,5-dimetoxy-4-iodoamphetamine hydrochloride (DOI; 0.5-10 micrograms/200 nl) into the LPBN, the water intake induced by ANG II was significantly reduced. These results are consistent with Other observations indicating that the LPBN is associated with inhibitory mechanisms controlling water intake induced by ANG II treatment and suggest that serotonergic pathways may be involved in this effect.

scholarly journals Gastrointestinal and renal responses to variable water intake in whitebellied sunbirds and New Holland honeyeaters

2013 ◽  
Vol 216 (9) ◽  
pp. 1537-1545 ◽  
Author(s):  
C. Purchase ◽  
K. R. Napier ◽  
S. W. Nicolson ◽  
T. J. McWhorter ◽  
P. A. Fleming
Keyword(s):  
Water Intake ◽  
Renal Responses ◽  
Variable Water

scholarly journals Urine and Plasma Osmolality in Patients with Autosomal Dominant Polycystic Kidney Disease: Reliable Indicators of Vasopressin Activity and Disease Prognosis?

2015 ◽  
Vol 41 (3) ◽  
pp. 248-256 ◽  
Author(s):  
Niek F. Casteleijn ◽  
Debbie Zittema ◽  
Stephan J.L. Bakker ◽  
Wendy E. Boertien ◽  
Carlo A. Gaillard ◽  
...  
Keyword(s):  
Water Intake ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Kidney Volume ◽  
Polycystic Kidney ◽  
Estimated Gfr ◽  
Total Kidney Volume ◽  
Autosomal Dominant Polycystic Kidney ◽  
Crude Analysis

Background: Vasopressin plays an essential role in osmoregulation, but has deleterious effects in patients with ADPKD. Increased water intake to suppress vasopressin activity has been suggested as a potential renoprotective strategy. This study investigated whether urine and plasma osmolality can be used as reflection of vasopressin activity in ADPKD patients. Methods: We measured urine and plasma osmolality, plasma copeptin concentration, total kidney volume (TKV, by MRI) and GFR (125I-iothalamate). In addition, change in estimated GFR (eGFR) during follow-up was assessed. Results: Ninety-four patients with ADPKD were included (56 males, age 40 ± 10, mGFR 77 ± 32 ml/min/1.73 m2, TKV 1.55 (0.99-2.40) l. Urine osmolality, plasma osmolality and copeptin concentration were 420 ± 195, 289 ± 7 mOsmol/l and 7.3 (3.2-14.6) pmol/l, respectively. Plasma osmolality was associated with copeptin concentration (R = 0.54, p < 0.001), whereas urine osmolality was not (p = 0.4). In addition, urine osmolality was not associated with TKV (p = 0.3), in contrast to plasma osmolality (R = 0.52, p < 0.001) and copeptin concentration (R = 0.61, p < 0.001). Fifty-five patients were followed for 2.8 ± 0.8 years. Baseline plasma and urine osmolality were not associated with change in eGFR (p = 0.6 and p = 0.3, respectively), whereas baseline copeptin concentration did show an association with change in eGFR, in a crude analysis (St. β = -0.41, p = 0.003) and also after adjustment for age, sex and TKV (St. β = -0.23, p = 0.05). Conclusions: These data suggest that neither urine nor plasma osmolality are valid measures to identify ADPKD patients that may benefit from increasing water intake. Copeptin appears a better alternative for this purpose.

Relationship between plasma osmolality and plasma vasopressin in human subjects

1980 ◽  
Vol 238 (4) ◽  
pp. E313-E317 ◽  
Author(s):  
M. Hammer ◽  
J. Ladefoged ◽  
K. Olgaard
Keyword(s):  
Linear Models ◽  
Human Subjects ◽  
Plasma Osmolality ◽  
Metabolic Clearance ◽  
Parabolic Model ◽  
Pronounced Increase ◽  
Plasma Vasopressin ◽  
Log Linear ◽  
The Relationship ◽  
Best Fit

The relationship between plasma osmolality (pOsm) and plasma vasopressin (pAVP) was studied in 13 human subjects during dehydration. The fit of linear, log-linear, parabolic, and exponential models was tested. For all of the data, the nonlinear models had the best fit. However, when individual differences in either gain or threshold were allowed for, the linear models were better than log-linear models. Finally, analyses were made with individual data points. Linear models had the best fit in half of the subjects, whereas for the others the parabolic model gave the best fit. For those subjects investigated in the low range of the osmoregulatory curve, a linear relationship was found, whereas, for those having the most pronounced increase in pOsm, the most significant improvement was found with the parabolic model. This finding indicates that the relationship is not stable during dehydration in the whole range and that hypovolemia probably can influence the secretion rate and/or metabolic clearance rate and thereby the relationship.

Role of lateral hypothalamus on fluid, electrolyte, and cardiovascular responses to activation of the MSA

1994 ◽  
Vol 266 (2) ◽  
pp. R496-R502 ◽  
Author(s):  
A. S. Haibara ◽  
W. A. Saad ◽  
J. V. Menani ◽  
L. A. Camargo ◽  
A. Renzi
Keyword(s):  
Water Intake ◽  
Lateral Hypothalamus ◽  
Cardiovascular Responses ◽  
Electrolytic Lesion ◽  
Opioid Agonist ◽  
Inhibitory Mechanisms ◽  
Pressor Responses ◽  
Medial Septal Area ◽  
Opiate Agonist

In this study we investigated the influence of electrolytic lesion or of opioid agonist injections into the lateral hypothalamus (LH) on the dipsogenic, natriuretic, kaliuretic, antidiuretic, pressor, and bradycardiac effects of cholinergic stimulation of the medial septal area (MSA) in rats. Sham- and LH-lesioned male Holtzman rats received a stainless steel cannula implanted into the LH. Other groups of rats had cannulas implanted simultaneously into the MSA and LH. Carbachol (2 nmol) injection into the MSA induced water intake, pressor, and bradycardic responses. LH lesion reduced all of these effects (1-3 and 15-18 days). Previous injection of synthetic opiate agonist, FK-33824 (100 ng), into the LH reduced the water intake, natriuresis, kaliuresis, and pressor responses induced by carbachol injected into the MSA. These data show that both electrolytic lesion or injection of an opiate agonist in the LH reduces the fluid-electrolyte and cardiovascular responses to cholinergic activation of the MSA. The involvement of LH with central excitatory and inhibitory mechanisms related to fluid-electrolytic and cardiovascular control is suggested.

Osmoregulation of thirst and vasopressin during normal menstrual cycle

1988 ◽  
Vol 254 (4) ◽  
pp. R641-R647 ◽  
Author(s):  
T. J. Vokes ◽  
N. M. Weiss ◽  
J. Schreiber ◽  
M. B. Gaskill ◽  
G. L. Robertson
Keyword(s):  
Menstrual Cycle ◽  
Luteal Phase ◽  
Plasma Osmolality ◽  
Free Water ◽  
Urine Osmolality ◽  
Free Water Clearance ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Normal Menstrual Cycle ◽  
Basal Plasma

Changes in osmoregulation during normal menstrual cycle were examined in 15 healthy women. In 10 women, studied repetitively during two consecutive menstrual cycles, basal plasma osmolality, sodium, and urea decreased by 4 mosmol/kg, 2 meq/l, and 0.5 mM, respectively (all P less than 0.02) from the follicular to luteal phase. Plasma vasopressin, protein, hematocrit, mean arterial pressure, and body weight did not change. In five other women, diluting capacity and osmotic control of thirst and vasopressin release were assessed in follicular, ovulatory, and luteal phases. Responses of thirst and/or plasma vasopressin, urine osmolality, osmolal and free water clearance to water loading, and infusion of hypertonic saline were normal and similar in the three phases. However, the plasma osmolality at which plasma vasopressin and urine osmolality were maximally suppressed as well as calculated osmotic thresholds for thirst and vasopressin release were lower by 5 mosmol/kg in the luteal than in the follicular phase. This lowering of osmotic thresholds for thirst and vasopressin release, which occurs in the luteal phase, is qualitatively similar to that observed in pregnancy and should be taken into account when studying water balance and regulation of vasopressin secretion in healthy cycling women.

scholarly journals The unsilent majority–TRPV1 drives “spontaneous” transmission of unmyelinated primary afferents within cardiorespiratory NTS

2012 ◽  
Vol 303 (12) ◽  
pp. R1207-R1216 ◽  
Author(s):  
Michael C. Andresen ◽  
Mackenzie E. Hofmann ◽  
Jessica A. Fawley
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Visceral Afferents ◽  
Transient Receptor Potential Vanilloid ◽  
Control Mechanisms ◽  
Solitary Tract ◽  
Organ Systems ◽  
Asynchronous Release ◽  
Transient Receptor ◽  
Afferent Terminals

Cranial primary afferent sensory neurons figure importantly in homeostatic control of visceral organ systems. Of the two broad classes of visceral afferents, the role of unmyelinated or C-type class remains poorly understood. This review contrasts key aspects of peripheral discharge properties of C-fiber afferents and their glutamate transmission mechanisms within the solitary tract nucleus (NTS). During normal prevailing conditions, most information arrives at the NTS through myelinated A-type nerves. However, most of visceral afferent axons (75–90%) in NTS are unmyelinated, C-type axons. Centrally, C-type solitary tract (ST) afferent terminals have presynaptic transient receptor potential vanilloid type 1 (TRPV1) receptors. Capsaicin activation of TRPV1 blocks phasic or synchronous release of glutamate but facilitates release of glutamate from a separate pool of vesicles. This TRPV1-operated pool of vesicles is active at normal temperatures and is responsible for actively driving a 10-fold higher release of glutamate at TRPV1 compared with TRPV1− terminals even in the absence of afferent action potentials. This novel TRPV1 mechanism is responsible for an additional asynchronous release of glutamate that is not present in myelinated terminals. The NTS is rich with presynaptic G protein-coupled receptors, and the implications of TRPV1-operated glutamate offer unique targets for signaling in C-type sensory afferent terminals from neuropeptides, inflammatory mediators, lipid metabolites, cytokines, and cannabinoids. From a homeostatic view, this combination could have broad implications for integration in chronic pathological disturbances in which the numeric dominance of C-type endings and TRPV1 would broadly disturb multisystem control mechanisms.

Sign in / Sign up

Export Citation Format

Share Document