The influence of vasopressin on oxytocin-induced changes in urine flow in the male rat

1982 ◽  
Vol 100 (2) ◽  
pp. 216-220 ◽  
Author(s):  
Mary L. Forshing ◽  
M.J. Brimble ◽  
R. J. Balment
Keyword(s):  
Urine Flow ◽  
Male Rat ◽  
Water Excretion ◽  
Plasma Vasopressin ◽  
Renal Receptor ◽  
Diuretic Response ◽  
Long Evans ◽  
Induced Changes ◽  
Renal Water Excretion

Abstract. Oxytocin administration in rats infused with hypotonic saline is associated with a saliuresis and altered renal water excretion. The role of vasopressin in determining the pattern of oxytocin-induced changes in urine flow was investigated in Long Evans and vasopressin-deficient Brattleboro rats, which exhibit contrasting diuretic and antidiuretic responses to oxytocin. Ethanol anaesthesia and water loading in Long Evans suppressed plasma vasopressin levels and was associated with an antidiuretic response to oxytocin. Vasopressin administration in the Brattleboro rat reversed the oxytocin-induced antidiuresis normally observed in vasopressin dificiency. These results taken with previous observations, have been interpreted as indicative that oxytocin acts as a weak agonist at the renal vasopressin receptor. When plasma vasopressin is suppressed or absent oxytocin acts as a weak antidiuretic agent, but in the presence of higher vasopressin levels a diuretic response to oxytocin is seen which follows displacement of vasopressin, the more potent antidiuretic agent, from the renal receptor.

Elevation of Plasma Vasopressin in Spontaneous Migraine

Cephalalgia ◽  
1991 ◽  
Vol 11 (6) ◽  
pp. 249-250 ◽  
Author(s):  
KK Hampton ◽  
A Esack ◽  
RC Peatfield ◽  
PJ Grant
Keyword(s):  
Blood Flow ◽  
Acute Attack ◽  
Peripheral Blood Flow ◽  
Posterior Pituitary ◽  
Water Excretion ◽  
Paired Samples ◽  
Plasma Vasopressin ◽  
Antidiuretic Effect ◽  
Renal Water Excretion

Vasopressin is a vasoactive hormone secreted from the posterior pituitary. At low concentration its role is in regulating renal water excretion, but at higher concentrations it has a number of extrarenal actions, including effects on blood flow. To investigate the role of vasopressin in spontaneous migraine, paired samples were collected from 14 subjects (a) during an acute attack of spontaneous migraine, and (b) when symptom-free for at least seven days. During an attack, vasopressin was consistently raised (median (range) 3.5 (1.2–9.6) pg/ml v 0.5 (0.5–1.1) pg/ml, p < 0.001). The highest vasopressin concentration occurred in the only patient who vomited. The results suggest vasopressin rises during an attack of spontaneous migraine, and this may, in part, be related to emesis. In the majority, vasopressin levels only rose sufficiently to have some renal antidiuretic effect, although in some these levels could have been sufficient to cause alteration in peripheral blood flow. Release of vasopressin may be responsible for the facial pallor and antidiuresis observed in migraine.

Activation of histamine H3 receptors inhibits renal noradrenergic neurotransmission in anesthetized dogs

2001 ◽  
Vol 280 (5) ◽  
pp. R1450-R1456 ◽  
Author(s):  
Tomoyuki Yamasaki ◽  
Isao Tamai ◽  
Yasuo Matsumura
Keyword(s):  
Receptor Antagonist ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Urinary Sodium ◽  
Renal Nerve ◽  
Anesthetized Dogs ◽  
Induced Changes ◽  
Antidiuretic Action

To investigate the possible involvement of histamine H3 receptors in renal noradrenergic neurotransmission, effects of (R)alpha-methylhistamine (R-HA), a selective H3-receptor agonist, and thioperamide (Thiop), a selective H3-receptor antagonist, on renal nerve stimulation (RNS)-induced changes in renal function and norepinephrine (NE) overflow in anesthetized dogs were examined. RNS (0.5–2.0 Hz) produced significant decreases in urine flow and urinary sodium excretion and increases in NE overflow rate (NEOR), without affecting renal hemodynamics. When R-HA (1 μg · kg−1 · min−1) was infused intravenously, mean arterial pressure and heart rate were significantly decreased, and there was a tendency to reduce basal values of urine flow and urinary sodium excretion. During R-HA infusion, RNS-induced antidiuretic action and increases in NEOR were markedly attenuated. Thiop infusion (5 μg · kg−1 · min−1) did not affect basal hemodynamic and excretory parameters. Thiop infusion caused RNS-induced antidiuretic action and increases in NEOR similar to the basal condition. When R-HA was administered concomitantly with Thiop infusion, R-HA failed to attenuate the RNS-induced antidiuretic action and increases in NEOR. However, in the presence of pyrilamine (a selective H1-receptor antagonist) or cimetidine (a selective H2-receptor antagonist) infusion, R-HA attenuated the RNS-induced actions, similarly to the case without these antagonists. Thus functional histamine H3 receptors, possibly located on renal noradrenergic nerve endings, may play the role of inhibitory modulators of renal noradrenergic neurotransmission.

Protective role of Lycopene against Aroclor 1254-induced changes on GLUT4 in the skeletal muscles of adult male rat

2012 ◽  
Vol 36 (3) ◽  
pp. 320-328 ◽  
Author(s):  
Anne Augustine Williams ◽  
Jayaraman Selvaraj ◽  
Chinnapaiyan Srinivasan ◽  
Sampath Sathish ◽  
Parsanathan Rajesh ◽  
...  
Keyword(s):  
Adult Male ◽  
Skeletal Muscles ◽  
Protective Role ◽  
Male Rat ◽  
Aroclor 1254 ◽  
Adult Male Rat ◽  
Induced Changes

Mechanism of cold diuresis in the rat

1983 ◽  
Vol 244 (2) ◽  
pp. F210-F216 ◽  
Author(s):  
M. L. Morgan ◽  
R. J. Anderson ◽  
M. A. Ellis ◽  
T. Berl
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Hemodynamic Parameters ◽  
Water Excretion ◽  
Urinary Osmolality ◽  
6 Hydroxydopamine ◽  
Renal Water Excretion

The effect of cold exposure (CE) on renal water excretion has not been clearly delineated. Conscious rats were exposed to decreased ambient temperature (15 degrees C). Forty-five minutes of CE resulted in reversible increases in urine flow and decreases in urine osmolality. The diuresis was not due to a diminished response to vasopressin (VP), as the antidiuresis associated with 500 microU of Pitressin given to water-diuresing rats was comparable at 15 and 30 degrees C. To determine whether the diuresis was due to intrarenal factors, glomerular filtration rate, renal blood flow, sodium excretion, and osmolar clearances were measured and found to be equivalent during control and cold conditions. To determine whether the observed diuresis was due to suppression of endogenous VP, VP-free Brattleboro rats undergoing a constant VP infusion were cold exposed. In these rats, CE was not associated with a change in either urine flow or urinary osmolality. This antidiuretic hormone-mediated mechanism was corroborated by a decrease in immunoassayable VP levels. To determine the mechanism whereby CE suppresses endogenous VP, plasma osmolality and hemodynamic parameters were measured. Although CE was not associated with a change in plasma osmolality, it did result in a significant increase in both mean arterial pressure and cardiac index. Pretreatment of rats with 6-hydroxydopamine prevented both the increase in mean arterial pressure and cold diuresis. We conclude that the diuresis observed upon exposure to 15 degrees C results from nonosmotic suppression of endogenous VP, as a consequence of the increase in mean arterial pressure.

scholarly journals Cooperative role of ETA and ETB receptors in mediating the diuretic response to intramedullary hyperosmotic NaCl infusion

2010 ◽  
Vol 299 (6) ◽  
pp. F1424-F1432 ◽  
Author(s):  
Erika I. Boesen ◽  
David M. Pollock
Keyword(s):  
Renal Medulla ◽  
Baseline Period ◽  
Urine Flow ◽  
Receptor Blockade ◽  
Endothelin Receptor ◽  
High Salt Diet ◽  
Salt Diet ◽  
Urine Production ◽  
Diuretic Response

Acute intramedullary infusion of hyperosmotic NaCl, used to simulate a high-salt diet-induced increase of medullary osmolality, increases urine production and endothelin release from the kidney. To determine whether endothelin mediates this diuretic and natriuretic response, urine flow and Na+ excretion rate were measured during acute intramedullary infusion of hyperosmotic NaCl in anesthetized rats, with or without endothelin receptor antagonism. Isosmotic NaCl was infused into the left renal medulla during an equilibration period and 30-min baseline period, followed by hyperosmotic NaCl for two additional 30-min periods. Hyperosmotic NaCl infusion significantly increased urine flow of vehicle-treated rats (from 5.9 ± 0.9 to 11.1 ± 1.8 μl/min). Systemic ETB receptor blockade enhanced this effect (A-192621; from 7.7 ± 1.1 to 18.7 ± 2.9 μl/min; P < 0.05), ETA receptor blockade (ABT-627) had no significant effect alone, but the diuresis was markedly attenuated by combined ABT-627 and A-192621 administration (from 4.4 ± 0.7 to 5.4 ± 0.9 μl/min). Mean arterial pressures overall were not significantly different between groups. Surprisingly, the natriuretic response to hyperosmotic NaCl infusion was not significantly altered by systemic endothelin receptor blockade, and furthermore, intramedullary ETB receptor blockade enhanced the diuretic and natriuretic response to hyperosmotic NaCl infusion. ETA receptor blockade significantly attenuated both the diuretic and natriuretic responses to hyperosmotic NaCl infusion in ETB receptor-deficient sl/sl rats. These results demonstrate an important role of endothelin in mediating diuretic responses to intramedullary infusion of hyperosmotic NaCl. Moreover, these data suggest ETA and ETB receptors are both required for the full diuretic and natriuretic actions of endothelin.

scholarly journals Role of prostaglandins in the regulation of renal water excretion

1981 ◽  
Vol 19 (6) ◽  
pp. 851-859 ◽  
Author(s):  
Herbert J. Kramer ◽  
Kilian Glänzer ◽  
Rainer Düsing
Keyword(s):  
Water Excretion ◽  
Renal Water Excretion

scholarly journals Role of plasma vasopressin in the impairment of water excretion in nephrotic syndrome

1984 ◽  
Vol 25 (2) ◽  
pp. 422-429 ◽  
Author(s):  
Mario Usberti ◽  
Stefano Federico ◽  
Sergio Meccariello ◽  
Bruno Cianciaruso ◽  
Mario Balletta ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Water Excretion ◽  
Plasma Vasopressin

Antagonists of the antidiuretic activity of vasopressin

1988 ◽  
Vol 254 (2) ◽  
pp. F165-F177 ◽  
Author(s):  
L. B. Kinter ◽  
W. F. Huffman ◽  
F. L. Stassen
Keyword(s):  
Water Excretion ◽  
Water Handling ◽  
Water Salt ◽  
Renal Responses ◽  
Renal Water Excretion ◽  
Adh Activity ◽  
Stimulation Of

Competitive antagonists of the antidiuretic (ADH) activity of vasopressin were first described some six years ago. When studied in vitro, ADH antagonists displace vasopressin from specific renal binding sites and antagonize, in a competitive fashion, vasopressin stimulation of adenylate cyclase and transepithelial water, salt, and urea fluxes. When studied in vivo, the ADH antagonists increase renal water excretion and antagonize, in a competitive fashion, the ADH activity of vasopressin. Marked species heterogeneity is apparent with ADH antagonists in vivo, and inconsistencies between in vitro and in vivo findings within the same species are reported. Other renal responses associated with administration of ADH antagonists include changes in renal hemodynamics and renal salt and urea excretion. The effects on salt excretion appear to be limited to those species in which vasopressin stimulation of epithelial salt reabsorption has been demonstrated. In summary, the role of vasopressin as the principal factor regulating renal water handling is supported by experience with ADH receptor antagonists. However, that experience also indicates the emerging significance of autocoids, and other synergistic factors, to affect ADH receptor/effector mechanisms and to modulate renal ADH responses.

scholarly journals Diuretic effect of hypoxia, hypocapnia, and hyperpnea in humans: relation to hormones and O2 chemosensitivity

2000 ◽  
Vol 88 (2) ◽  
pp. 599-610 ◽  
Author(s):  
Wulf Hildebrandt ◽  
Andy Ottenbacher ◽  
Markus Schuster ◽  
Erik R. Swenson ◽  
Peter Bärtsch
Keyword(s):  
Random Order ◽  
Systemic Blood Pressure ◽  
Urine Flow ◽  
Hypoxic Ventilatory Response ◽  
Venous Compliance ◽  
Double Blind ◽  
Diuretic Response ◽  
Male Subjects ◽  
Sodium Clearance

We studied the contributions of hypoxemia, hypocapnia, and hyperpnea to the acute hypoxic diuretic response (HDR) in humans and evaluated the role of peripheral O2 chemosensitivity and renal hormones in HDR. Thirteen healthy male subjects (age 19–38 yr) were examined after sodium equilibration (intake: 120 mmol/day) during 90 min of normoxia (NO), poikilocapnic hypoxia (PH), and isocapnic hypoxia (IH) ( days 1–3, random order, double blind), as well as normoxic voluntary hyperpnea (HP; day 4), matching ventilation during IH. O2 saturation during PH and IH was kept equal to a mean level measured between 30 and 90 min of breathing 12% O2 in a pretest. Urine flow during PH and IH (1.81 ± 0.92 and 1.94 ± 1.03 ml/min, respectively) but not during HP (1.64 ± 0.96 ml/min) significantly exceeded that during NO (control, 1.38 ± 0.71 ml/min). Urine flow increases vs. each test day's baseline were significant with PH, IH, and HP. Differences in glomerular filtration rate, fractional sodium clearance, urodilatin, systemic blood pressure, or leg venous compliance were excluded as factors of HDR. However, slight increases in plasma and urinary endothelin-1 and epinephrine with PH and IH could play a role. In conclusion, the early HDR in humans is mainly due to hypoxia and hypocapnia. It occurs without natriuresis and is unrelated to O2 chemosensitivity (hypoxic ventilatory response).

Renal medullary interstitial infusion of diltiazem alters sodium and water excretion in rats

1992 ◽  
Vol 263 (5) ◽  
pp. R1064-R1070 ◽  
Author(s):  
S. Lu ◽  
R. J. Roman ◽  
D. L. Mattson ◽  
A. W. Cowley
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Urine Flow ◽  
Water Excretion ◽  
Doppler Flowmetry ◽  
Blood Flows ◽  
Electromagnetic Flow Probe ◽  
Interstitial Infusion

The role of renal papillary blood flow in regulation of fluid and electrolyte excretion was examined. The effects of an acute infusion of diltiazem (5 micrograms.kg-1 x min-1) into the renal medullary interstitium on papillary blood flow and sodium and water excretion were studied. Changes of renal blood flow were measured using an electromagnetic flow probe. Cortical and papillary blood flows were measured using laser-Doppler flowmetry. Renal and cortical blood flows were unchanged during medullary interstitial infusion of diltiazem, but papillary blood flow increased 26% (P < 0.05) and remained elevated for 1 h after diltiazem infusion was discontinued. Glomerular filtration rate (GFR) of the infused kidney increased by 21% from a control of 1.0 +/- 0.1 ml.min-1 x g-1 during infusion of diltiazem (P < 0.05), but it returned to control after diltiazem infusion was stopped. Urine flow and sodium excretion increased by 70% (P < 0.05), and fractional sodium excretion rose from 1.5 +/- 0.2 to 2.4 +/- 0.3% of the filtered load during the hour after diltiazem infusion. Renal blood flow, cortical and papillary blood flow, GFR, urine flow, and sodium excretion in the 0.9% sodium chloride vehicle-infused kidney were not significantly altered during the experiment. Intravenous infusion of the same dose of diltiazem (5 micrograms.kg-1 x min-1) increased GFR by 22%, but had no effect on urine flow and sodium excretion. These results indicate that renal medullary interstitial infusion of diltiazem selectively increased renal papillary blood flow, which was associated with an increase of sodium and water excretion.

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