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).

scholarly journals Brain dopamine response in human opioid addiction

2008 ◽  
Vol 193 (1) ◽  
pp. 65-72 ◽  
Author(s):  
Mark R.C. Daglish ◽  
Tim M. Williams ◽  
Sue J. Wilson ◽  
Lindsay G. Taylor ◽  
Chin B. Eap ◽  
...  
Keyword(s):  
Dopamine Release ◽  
Subjective Experience ◽  
Methadone Maintenance ◽  
Random Order ◽  
Rat Striatum ◽  
Dopamine System ◽  
Double Blind ◽  
Brain Scans ◽  
Positron Emission

BackgroundDrugs of dependence cause dopamine release in the rat striatum. Human neuroimaging studies have shown an increase in dopamine in the equivalent region in response to stimulants and other drugsAimsWe tested whether opioids provoke dopamine release and its relationship to the subjective experienceMethodIn two combined studies 14 heroin addicts on methadone maintenance treatment underwent two positron emission tomography brain scans of the dopamine system using [11C]-raclopride following an injection of placebo and either 50 mg intravenous diamorphine or 10 mg subcutaneous hydromorphone in a double-blind, random order designResultsBoth opioids produced marked subjective and physiological effects, but no measurable change in [11C]-raclopride bindingConclusionsThe absence of a dopamine response to opioid agonists contrasts with that found with stimulant drugs and suggests dopamine may not play the same role in addiction to opioids. This questions the role of dopamine in the subjective experience of heroin in opioid addicts

Respiratory load compensation. I. Role of the cerebrum

1993 ◽  
Vol 74 (2) ◽  
pp. 853-858 ◽  
Author(s):  
F. Xu ◽  
R. F. Taylor ◽  
T. McLarney ◽  
L. Y. Lee ◽  
D. T. Frazier
Keyword(s):  
Blood Gases ◽  
Random Order ◽  
Systemic Blood Pressure ◽  
Respiratory Pattern ◽  
Load Compensation ◽  
Arterial Blood ◽  
Before And After ◽  
Resistive Loads ◽  
Adult Cats

This study examines the extent to which the cerebrum and other suprapontine structures modulate the respiratory response to added mechanical resistive loads to breathing. Nine adult cats were anesthetized with thiopental sodium, tracheotomized, and instrumented with diaphragm electromyographic (EMGdi) recording electrodes. Two levels of resistive loads and tracheal occlusion were applied at the onset of inspiration in random order before and after decerebration. The integrated signal of the EMGdi (integral of EMGdi) was used to detect changes in respiratory timing and as an index of respiratory motor drive. The results showed that, compared with intact cats, decerebration did not significantly change baseline values for peak integral of EMGdi, respiratory timing, systemic blood pressure, or arterial blood gases. Although the percent changes in the peak integral of EMGdi elicited by the added loads were still significantly greater than those elicited by unloaded control breaths after decerebration, the magnitude of the responses was significantly attenuated at all load levels compared with the intact preparation. It is concluded that the cerebrum and/or other suprapontine structures provide information that is facilitatory to the respiratory pattern generator with little effect on timing.

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.

Sustained venoconstriction in man supplemented with CO2 at high altitude

1976 ◽  
Vol 40 (1) ◽  
pp. 96-100 ◽  
Author(s):  
J. C. Cruz ◽  
R. F. Grover ◽  
J. T. Reeves ◽  
J. T. Maher ◽  
A. Cymerman ◽  
...  
Keyword(s):  
Blood Pressure ◽  
High Altitude ◽  
Systemic Blood Pressure ◽  
Group Differences ◽  
Venous Compliance ◽  
Systemic Blood ◽  
Urinary Catecholamines ◽  
Arterial Ph ◽  
Flow Group ◽  
Male Subjects

Venoconstriction occurs at high altitude. This study sought to determine whether hypoxia or hypocapnia is the cause of the venoconstriction. Five male subjects were exposed to 4,000–4,400 m (PB 440–465 mmHg) with supplemental 3.77 +/- 0.02% CO2 in a hypobaric chamber for 4 days. Similar alveolar O2 tensions were obtained in four control subjects exposed to 3,500–4,100 m (PB 455–492 mmHg) without CO2. A water-filled plethysmograph was used to determine forearm flow and venous compliance. Systemic blood pressure was measured with the cuff procedure. Catecholamines were measured in 24-h urine collections. Venous compliance fell at high altitude in both groups and was less (P less than 0.01) than control values. Forearm flow and resistance were unaltered at altitude in the group with CO2 supplementation while forearm flow decreased and resistance increased in the hypocapnic group at 72 h of exposure. Urinary catecholamines increased in the group with CO2 and remained unaltered in the hypocapnic group. It is concluded that hypoxia is responsible for decreasing venous compliance, and hypocapnia for increasing resistance and decreasing flow. Group differences observed in urinary catecholamines may be explained by differences in arterial pH.

Effect of aminophylline on plasma [K+] and hypoxic ventilatory response during mild exercise in men

1994 ◽  
Vol 77 (4) ◽  
pp. 1763-1768 ◽  
Author(s):  
T. Igarashi ◽  
M. Nishimura ◽  
Y. Akiyama ◽  
M. Yamamoto ◽  
K. Miyamoto ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Hypoxic Ventilatory Response ◽  
Double Blind ◽  
Endogenous Adenosine ◽  
Adenosine Uptake ◽  
Body Activity ◽  
K Concentration ◽  
End Tidal ◽  
Arterial O2 Saturation

To examine the role of endogenous adenosine on the hypoxic ventilatory response (HVR) enhanced during exercise, we measured HVR at rest and during mild exercise (12.5 W) in nine healthy men in a supine position after pretreatment with aminophylline (5 mg/kg), an adenosine receptor blocker, or dipyridamole (0.6 mg/kg), an adenosine uptake blocker, by using a 3-day double-blind placebo-controlled design. Although HVR was enhanced during exercise on all occasions, HVR with aminophylline [0.42 +/- 0.07 (SE) l.min-1.%fall-1 of arterial O2 saturation] was significantly lower than that with placebo (0.64 +/- 0.13 l.min-1.%fall-1) or dipyridamole (0.64 +/– 0.08 l.min-1.%fall-1) during exercise (P < 0.05 for both) at similar end-tidal PCO2 on the 3 days but not at rest. We then examined the changes in plasma K+ concentration ([K+]) and catecholamines, the other possible endogenous potentiators of the carotid body activity. The exercise- and hypoxia-induced increases in plasma [K+] were significantly lower with aminophylline (0.23 +/- 0.09 meq/l) than with the placebo (0.51 +/- 0.10 meq/l) or dypyridamole (0.58 +/- 0.13 meq/l) (P < 0.05 for both). We therefore conclude that aminophylline attenuates the enhancement of HVR during mild exercise and that this might be due to its attenuating effect on exercise- and hypoxia-associated increases in plasma [K+] rather than due to its antagonizing effect on endogenous adenosine.

scholarly journals Acute effects of pharmacological modifications of fatty acid metabolism on human satiety

2008 ◽  
Vol 101 (12) ◽  
pp. 1867-1877 ◽  
Author(s):  
Blandine Gatta ◽  
Christine Zuberbuehler ◽  
Myrtha Arnold ◽  
Roberte Aubert ◽  
Wolfgang Langhans ◽  
...  
Keyword(s):  
Energy Intake ◽  
Plasma Concentrations ◽  
Eating Behaviour ◽  
Random Order ◽  
Normal Weight ◽  
Mean Differences ◽  
Plasma Leptin ◽  
Desire To Eat ◽  
Male Subjects

The role of NEFA in eating behaviour is still poorly known. Our objective was to examine whether etomoxir (ETO), an inhibitor of NEFA oxidation, or ( − )-hydroxycitrate (HCA), an inhibitor of lipogenesis which may indirectly stimulate NEFA oxidation, alters satiety. Post-lunch satiety was measured in eight normal-weight male subjects who were deprived of time cues and received on three occasions either ETO (320 mg), HCA (2 g) or placebo (PLA) in random order. Between lunch and dinner, blood was withdrawn continuously and collected every 10 min for measures of plasma concentrations of glucose, insulin, lactate, TAG, NEFA, β-hydroxybutyrate (BHB), leptin and ghrelin. Results showed that HCA began to decrease hunger and desire to eat compared to PLA and ETO 210 min after lunch and increased satiety duration compared to PLA by 70 (se23) min (P < 0·05), but did not modify energy intake at dinner. ETO did not affect any variable of satiety. HCA increased NEFA concentrations during the pre-dinner period, whereas ETO increased and decreased plasma concentrations of NEFA and BHB, respectively. Mean differences in plasma NEFA concentrations between HCA and PLA were predictive of the differences in satiety duration between treatments (r20·71,P < 0·01). Among treatments, plasma leptin concentration at dinner onset was the only blood variable correlated with energy intake at this meal (r− 0·75,P < 0·0005). In healthy, normal-weight men, acute HCA increased the intensity and duration of satiety possibly via increased NEFA disposal for oxidation.

scholarly journals ACTH Infusion Impairs Baroreflex Sensitivity—Implications for Cardiovascular Hypoglycemia-Associated Autonomic Failure

2020 ◽  
Vol 105 (7) ◽  
pp. 2345-2353
Author(s):  
Janet H Leung ◽  
Omar F Bayomy ◽  
Istvan Bonyhay ◽  
Johanna Celli ◽  
Jeffrey White ◽  
...  
Keyword(s):  
Outcome Measures ◽  
Baroreflex Sensitivity ◽  
Autonomic Failure ◽  
Random Order ◽  
Double Blind ◽  
Clinical Research Center ◽  
Early Afternoon ◽  
Treatment Analysis ◽  
Placebo Infusion

Abstract Context Hypoglycemia attenuates cardiovascular homeostatic autonomic control. This attenuation, known as the cardiovascular component of hypoglycemia-associated autonomic failure (HAAF), is characterized most notably by decreased baroreflex sensitivity (BRS) that begins during hypoglycemia and persists until at least the next day, despite return to euglycemia. Understanding the mechanisms underlying this reduction in BRS is important because BRS attenuation is associated with increased morbidity and mortality. Objective The objective of this work is to investigate the role of the adrenocorticotropin (ACTH)-adrenal axis in decreasing BRS. We tested the hypothesis that infusion of ACTH 1–24 (cosyntropin), as compared to placebo, would acutely suppress BRS, and that this decrease in BRS would be present the next day. Design A double-blind, placebo-controlled, random-order, cross-over study was conducted. Setting This study took place in a clinical research center. Participants Participants included healthy men and women. Interventions Interventions included an intravenous infusion of cosyntropin (70 μg/hour for 2.5 hours in the morning and again in the early afternoon) vs normal saline placebo. Main Outcome Measures Outcome measures included BRS during and 16 hours after cosyntropin vs placebo infusions. Results Cosyntropin infusion attenuated BRS (mm Hg/ms) as compared to placebo (baseline 17.8 ± 1.38 vs 17.0 ± 2.07; during 14.4 ± 1.43 vs 17.3 ± 1.65; and next day 14.8 ± 1.42 vs 18.9 ± 2.04; P &lt; .05, time by treatment, analysis of variance). BRS was decreased during the final 30 minutes of the morning cosyntropin infusion as compared to baseline (P &lt; .01) and remained suppressed the next day (16 hours after afternoon infusion) (P &lt; .025). Placebo infusion did not significantly change BRS. Corrected QT interval was not affected. Conclusions ACTH attenuates BRS, raising the possibility that hypoglycemia-induced increases in ACTH may contribute to the cardiovascular component of HAAF.

Role of endogenous adenosine in hypoxic ventilatory response in humans: a study with dipyridamole

1994 ◽  
Vol 76 (1) ◽  
pp. 196-203 ◽  
Author(s):  
M. Yamamoto ◽  
M. Nishimura ◽  
S. Kobayashi ◽  
Y. Akiyama ◽  
K. Miyamoto ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Crossover Fashion ◽  
Hypoxic Ventilatory Response ◽  
Double Blind ◽  
Adenosine Receptor Antagonist ◽  
Endogenous Adenosine ◽  
Progressive Hypoxia ◽  
Sustained Hypoxia

To examine the role of endogenous adenosine in hypoxic ventilatory response, we measured, in nine normal young adults, ventilatory responses to isocapnic progressive hypoxia and subsequent sustained hypoxia [arterial O2 saturation (SaO2); 80%, 20 min] with and without pretreatment with dipyridamole in a double-blind crossover fashion. Dipyridamole, an adenosine uptake blocker, was expected to enhance the effect of endogenous adenosine. Pretreatment with dipyridamole (0.5 mg/kg) significantly augmented the slope of the ventilatory response to isocapnic progressive hypoxia from 0.35 +/- 0.13 (SE) to 0.70 +/- 0.25 l.min-1.%fall of SaO2(-1) (P < 0.01), although there were no significant changes in resting ventilation. On the other hand, minute ventilation, when expressed as a percentage of peak ventilation, declined to 68.4 +/- 4.3% with dipyridamole at the 9–11th min of sustained hypoxia, which was significantly lower than the 90.2 +/- 8.3% with a placebo (P < 0.05), and finally reached 56.1 +/- 7.2% with dipyridamole and 78.7 +/- 9.2% with the placebo (P < 0.1) at the 18–20th min of sustained hypoxia. In an attempt to more specifically examine the role of adenosine, aminophylline (5 mg/kg), an adenosine receptor antagonist, was injected before pretreatment with dipyridamole in four subjects. Aminophylline infusion abolished or at least attenuated the effect of dipyridamole in all four subjects. These data suggest that endogenous adenosine has a modulatory role in hypoxic ventilatory response in adult humans.

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.

scholarly journals Exercise-induced GH secretion is enhanced by the oral ingestion of melatonin in healthy adult male subjects

1999 ◽  
Vol 141 (1) ◽  
pp. 22-26 ◽  
Author(s):  
DR Meeking ◽  
JD Wallace ◽  
RC Cuneo ◽  
M Forsling ◽  
DL Russell-Jones
Keyword(s):  
Initial Period ◽  
Area Under The Curve ◽  
Random Order ◽  
Controlled Study ◽  
Double Blind ◽  
Post Exercise ◽  
Gh Secretion ◽  
Exercise Induced ◽  
Male Subjects ◽  
Peak Increase

There is evidence that melatonin may play a role in modulating pituitary secretion, although the mechanisms are unclear. We examined the effects of a single dose of oral melatonin (5mg) on exercise-induced GH secretion. In a randomised, double-blind, placebo-controlled study, seven healthy male subjects undertook an initial period of graded bicycle ergometric exercise to determine maximum workload and oxygen uptake (VO(2max)). Subjects were subsequently studied on two further occasions, receiving either melatonin or placebo in random order at the onset of each study (-60min). At 0 min a period of bicycle exercise was performed for 8 min at a workload corresponding to 70% of that achieved at VO(2max). Serum GH and IGF-binding protein-1 (IGFBP-1) concentration was measured at 15-min intervals from the onset of the study until 120 min post-exercise. Blood was also sampled for the measurement of plasma glucose, insulin, non-esterified fatty acids, IGFBP-3, melatonin and vasopressin concentration. There was an exercise-induced increase in GH concentration following melatonin which was greater compared with placebo as assessed by both area under the curve (P<0.01) and peak increase in GH levels (P<0.01). The peak increase in IGFBP-1 levels post-exercise was also significantly greater following melatonin compared with placebo (P<0. 01) but did not quite reach levels of significance as measured by area under the curve (P=0.07). Since exercise-induced GH secretion is thought to be mediated predominantly through a hypothalamic pathway, it seems likely that melatonin facilitates GH secretion at a hypothalamic level.

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