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.

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.

Role of vasopressin and sympathetic nervous system during hypertonic NaCl infusion in conscious dog

1985 ◽  
Vol 248 (5) ◽  
pp. H652-H657 ◽  
Author(s):  
E. M. Hasser ◽  
J. R. Haywood ◽  
V. S. Bishop
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Plasma Osmolality ◽  
Ganglionic Blockade ◽  
Osmotic Stimulus ◽  
Sympathetic Nervous ◽  
Subsequent Administration

The contribution of arginine vasopressin (AVP) and the sympathetic nervous system to the pressor response elicited by hypertonic NaCl infusion was investigated in conscious dogs with intact carotid sinus baroreceptors or in dogs subjected to chronic sinoaortic baroreceptor denervation (SAD). Infusion of 6% NaCl at 0.05 ml X kg-1 X min-1 for 60 min increased plasma osmolality an average of 12 +/- 2 mosmol/kg in both intact and SAD dogs. Arterial pressure increased 6 +/- 2 mmHg in intact animals and was normalized by subsequent administration of a specific vascular AVP antagonist. Pretreatment with the AVP antagonist did not alter resting arterial pressure but prevented the increase due to the osmotic stimulus. Pretreatment with ganglionic blockade reduced resting arterial pressure (-17 +/- 2 mmHg). Subsequent infusion of hypertonic NaCl elevated arterial pressure (21 +/- 7 mmHg) to a significantly greater level than that observed with the autonomic nervous system intact. In SAD dogs, the osmotic stimulus increased arterial pressure (16 +/- 1 mmHg) to a significantly greater extent than in intact animals. Subsequent administration of AVP antagonist normalized arterial pressure, and pretreatment with the antagonist prevented any pressor response. Pretreatment with ganglionic blockade did not alter the pressor response (15 +/- 2 mmHg) to hypertonic NaCl. Data suggest that the increase in arterial pressure due to an osmotic stimulus is due to AVP release and does not require a functional sympathetic nervous system. The response is normally buffered by arterial baroreflexes, presumably due to sympathetic withdrawal.

Effect of short-term administration of vasopressin on arterial pressure and norepinephrine turnover in Long–Evans rats

1987 ◽  
Vol 65 (10) ◽  
pp. 2142-2146 ◽  
Author(s):  
R. L. Kline ◽  
K.-Y. Chow ◽  
P. F. Mercer
Keyword(s):  
Arterial Pressure ◽  
Water Intake ◽  
Urine Output ◽  
Plasma Osmolality ◽  
Chronic Administration ◽  
Urine Osmolality ◽  
Cardiovascular Reflexes ◽  
High Dose ◽  
Normal Fluid ◽  
Long Evans

Vasopressin (AVP) in acute experiments has been shown to influence cardiovascular reflexes, but the effect of a more prolonged administration of AVP on the sympathetic nervous system has not been investigated. Long–Evans rats were treated for 7 days with AVP (Pitressin tannate in oil, with single daily doses of 100 or 500 mU∙100 g−1, s.c.) to determine whether AVP alters norepinephrine (NE) turnover in kidney, intestine, or skeletal muscle. Control rats were given equal doses of peanut oil daily. NE turnover was determined by measuring the decline in tissue levels of NE for 8 h after inhibition of tyrosine hydroxylase with α-methyl-p-tyrosine (300 mg∙kg−1, i.p. every 4 h). Measurements of water intake, urine output, and urine osmolality showed that chronic administration of the high dose, but not the low dose, of AVP produced maintained increases in urine osmolality and decreases in water intake and urine output. Body weight, plasma osmolality, plasma electrolytes, and hematocrit were not significantly altered by AVP treatment, but mean arterial pressure was elevated significantly (control, 105 ± 3 mmHg versus AVP, 119 ± 4 mmHg, p < 0.05) (1 mmHg = 133.3 Pa) in the high dose group. Plasma renin activity was decreased slightly, but significantly in rats treated with the high dose of AVP. Compared with results in control animals, there were no statistically significant changes in NE turnover after chronic administration of either the low or the high dose of AVP. The results indicate that administration of AVP for 7 days to rats in normal fluid balance does not result in a decrease in NE turnover in peripheral organs.

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.

Pressor response to chemoreflex activation before and after microinjection of glycine into the NTS of awake rats

2003 ◽  
Vol 284 (4) ◽  
pp. R1000-R1009 ◽  
Author(s):  
Franklin F. Pimentel ◽  
Leni G. H. Bonagamba ◽  
Benedito H. Machado
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Receptor Antagonist ◽  
Pressor Response ◽  
Glycine Receptor ◽  
Potassium Cyanide ◽  
Solitary Tract ◽  
Before And After ◽  
Nitroprusside Infusion ◽  
Awake Rats

Microinjection of glycine into the rostral (bilateral) and caudal (midline) commissural nucleus of the solitary tract (NTS) using three guide cannulas implanted in the direction of these sites produced an increase in mean arterial pressure (MAP) and abolished the pressor response to chemoreflex activation [potassium cyanide ( n = 7)]. Strychnine, a glycine receptor antagonist, attenuated the increase in MAP, and in this new experimental condition ( n = 5) the pressor response to chemoreflex activation was not altered. Considering that the effect of glycine on the attenuation of the pressor response to chemoreflex activation could be secondary to the increase in baseline MAP, in a third group of rats ( n = 5) sodium nitroprusside infusion (intravenous) after microinjections of glycine into the NTS normalizes MAP. In this case, the pressor response to chemoreflex activation was similar to the control. These data show that glycine when microinjected bilaterally into the lateral commissural NTS as well as into the medial commissural NTS plays no major inhibitory role in the processing of the neurotransmission of the sympathoexcitatory component of the chemoreflex.

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.

Regional pulmonary blood flow during 96 hours of hypoxia in conscious sheep

1986 ◽  
Vol 61 (6) ◽  
pp. 2136-2143 ◽  
Author(s):  
D. C. Curran-Everett ◽  
K. McAndrews ◽  
J. A. Krasney
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Superior Vena ◽  
Acute Hypoxia ◽  
Vena Cava ◽  
Normobaric Hypoxia ◽  
Pulmonary Arterial

The effects of acute hypoxia on regional pulmonary perfusion have been studied previously in anesthetized, artificially ventilated sheep (J. Appl. Physiol. 56: 338–342, 1984). That study indicated that a rise in pulmonary arterial pressure was associated with a shift of pulmonary blood flow toward dorsal (nondependent) areas of the lung. This study examined the relationship between the pulmonary arterial pressor response and regional pulmonary blood flow in five conscious, standing ewes during 96 h of normobaric hypoxia. The sheep were made hypoxic by N2 dilution in an environmental chamber [arterial O2 tension (PaO2) = 37–42 Torr, arterial CO2 tension (PaCO2) = 25–30 Torr]. Regional pulmonary blood flow was calculated by injecting 15-micron radiolabeled microspheres into the superior vena cava during normoxia and at 24-h intervals of hypoxia. Pulmonary arterial pressure increased from 12 Torr during normoxia to 19–22 Torr throughout hypoxia (alpha less than 0.049). Pulmonary blood flow, expressed as %QCO or ml X min-1 X g-1, did not shift among dorsal and ventral regions during hypoxia (alpha greater than 0.25); nor were there interlobar shifts of blood flow (alpha greater than 0.10). These data suggest that conscious, standing sheep do not demonstrate a shift in pulmonary blood flow during 96 h of normobaric hypoxia even though pulmonary arterial pressure rises 7–10 Torr. We question whether global hypoxic pulmonary vasoconstriction is, by itself, beneficial to the sheep.

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 Developmental Changes in Hemodynamic Responses and Cardiovagal Modulation during Isometric Handgrip Exercise

2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
Styliani Goulopoulou ◽  
Bo Fernhall ◽  
Jill A. Kanaley
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Isometric Contraction ◽  
Pressor Response ◽  
Reflex Response ◽  
Group Differences ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Isometric Handgrip Exercise ◽  
Pressor Reflex

The purpose of this study was to examine differences in pressor response and cardiovagal modulation during isometric handgrip exercise (IHG) between children and adults. Beat-to-beat heart rate (HR) and blood pressure were measured in 23 prepubertal children and 23 adults at baseline and during IHG. Cardiovagal modulation was quantified by analysis of HR variability. Mean arterial pressure responses to IHG were greater in adults compared to children (P<.05) whereas there were no group differences in HR responses (P>.05). Children had a greater reduction in cardiovagal modulation in response to IHG compared to adults (P<.05). Changes in mean arterial pressure during IHG were correlated with baseline cardiovagal modulation and force produced during isometric contraction (P<.05). In conclusion, differences in pressor reflex response between children and adults cannot be solely explained by differences in autonomic modulation and appear to be associated with factors contributing to the force produced during isometric contraction.

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.

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