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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using the isolated rat kidney perfused with an artificial medium containing glucose as the sole fuel, we studied the renal handling of immunoreactive arginine vasopressin (AVP) and determined the effect of various factors on the ability of the kidney to remove AVP. In control kidneys perfused with AVP at concentrations below 116 muU/ml, the organ clearance of AVP (OC(AVP)) was 1,145+/-47 (SE) mul/min, whereas glomerular filtration rate (GFR) averaged 515+/-37 mul/min. Filtration could thus account for up to 45% of the OC(AVP), the balance presumably being cleared from the peritubular circulation. Of the AVP filtered, only 38% could be recovered in the urine (urinary clearance AVP averaged 205+/-12 mul/min) suggesting that the balance was taken up by the tubular epithelium and degraded. Fractional excretion of filtered AVP rose significantly in the presence of anoxia and cold (10 degrees C) to 49 and 59%, respectively, but was not affected by ouabain or high levels of AVP (458+/-58 muU/ml). The OC(AVP) was not significantly altered by the absence of glucose in the perfusate, anoxia, or ureteral ligation, maneuvers that were associated with significant reductions in GFR. In these and the control experiments, there was a significant inverse correlation between GFR and peritubular clearance emphasizing the importance of the latter (r = -0.749; P < 0.001). Cold, ouabain, and high concentrations of AVP reduced the clearance of AVP by the kidneys. On the basis of these studies we conclude that the kidney clears AVP from the circulation via two pathways, glomerular clearance and peritubular clearance. This exposes both the luminal and contraluminal surfaces of the tubular cells to the hormone, allowing these cells to remove AVP from the filtrate and the peritubular compartment. Noteworthy is the observation that under several conditions when GFR falls reducing the glomerular clearance of AVP, peritubular clearance increases and the total clearance of AVP by the kidney remains constant.
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PMID:The handling of immunoreactive vasopressin by the isolated perfused rat kidney. 76 48

Investigators have described changes in pituitary corticotropes that correlate with changes in the physiological state of the animal. The stellate subtype degranulated and enlarged initially after adrenalectomy. This was followed by repopulation of the granules during the first 3 weeks after surgery with larger granules. There was also an increase in the percentage of corticotropes. More recent studies have shown that chronic stimulation with corticotropin-releasing hormone (CRH) produces some of the same changes; however, the magnitude differs because of corticosterone feedback. Corticotropes are heterogeneous in size, shape, storage patterns, and secretory responses. Specific changes are evident within a short time after stimulation as well. Their average cellular area increases within 1-2 h of stimulation by CRH in vitro or cold stress in vivo. Whereas many corticotropes acutely stimulated by cold or a novel environment are better granulated, others are depleted of granules. Cold stress for 30 min also stimulates an increase in the percentage of immunoreactive corticotropes and cells that bind CRH or arginine vasopressin (AVP). Secretagogues like CRH or epidermal growth factor (EGF) act in vitro to increase percentages of cells that store adrenocorticotropin (ACTH) or express mRNA for pro-opiomelanocortin. AVP or angiotensin II (A-II), or their activated second messengers, also increase percentages of cells that bind CRH and store ACTH. Inhibition of ACTH secretion by ion channel blockers or corticosterone has potent inhibitory effects on percentages of CRH-bound cells. AVP binding is not affected. Some of the inhibitory states reduce the average area of corticotropes. However, about 30% of the cells remain unaffected by these inhibitors. The rapid changes in cell percentages with the different treatments have led workers to postulate the existence of reserve cells that may be sensitive to certain levels of types of stimuli. Several candidate reserve cells are proposed. One group of cells that store ACTH with gonadotropins may function in the proestrous female to stimulate adrenal progesterone. Another multihormonal cell may function during cold stress to release both ACTH and thyroid-stimulating hormone (TSH) under the influence of AVP. There may be subpopulations of corticotropes that act in synchrony with other cell populations. They may be awaiting the proper type or combination of secretagogues to support the pituitary-adrenal and other axes.
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PMID:Structure-function correlates in the corticotropes of the anterior pituitary. 133 2

1. The effects of a single oral dose (100 mg) of flosequinan on systemic and regional (forearm, splanchnic and renal) vascular responses to simulated orthostatic stress (lower body negative pressure, LBNP) were investigated in nine healthy male volunteers, in a double-blind, placebo-controlled crossover study. 2. Forty-five minutes after its administration and before LBNP, flosequinan induced a significant decrease in total peripheral and in forearm vascular resistances without any concomitant change in arterial pressure, in heart rate and in the investigated biological parameters (plasma catecholamines, arginine vasopressin and renin activity). 3. After flosequinan and placebo, LBNP induced similar decreases in central venous pressure at all levels of LBNP (-10, -20 and -40 mm Hg) and in pulse pressure at LBNP -40 mm Hg. LBNP-induced increase in forearm vascular resistance was significantly more marked after flosequinan than after placebo at all levels of LBNP, and this was also true for splanchnic vascular resistance but at LBNP -40 mm Hg only. However, inasmuch as the basal values of these two parameters before LBNP were lower after flosequinan than after placebo, their final values after LBNP -40 mm Hg were similar. Finally, LBNP-induced changes in renal vascular resistance, glomerular filtration rate and filtration fraction as well as in plasma catecholamines, arginine vasopressin and renin activity were similar after flosequinan and placebo at all levels of LBNP. 4. Flosequinan affected neither reflex control of heart rate (phenylephrine test) nor non-specific vasoconstrictor responses (cold pressor test). (ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Flosequinan does not affect systemic and regional vascular responses to simulated orthostatic stress in healthy volunteers. 138 45

The influence of moderate cold exposure on the hormonal responses of atrial natriuretic factor (ANF), arginine vasopressin (AVP), catecholamines, and plasma renin activity (PRA) after exhaustive exercise was studied in 9 young and 10 middle-aged subjects. Exercise tests were randomly performed in temperate (30 degrees C) and cold (10 degrees C) environments. Heart rate, oxygen consumption, and peripheral arterial blood pressure were measured at regular intervals. Blood samples were collected before and immediately after exercise at 30 or 10 degrees C. Plasma sodium and potassium concentrations as well as hemoglobin and hematocrit were measured, and the change in plasma volume was calculated. At rest and during exercise, oxygen consumption was similar during exposure to both temperate and cold temperatures. During submaximal exercise intensities, the rise in heart rate was blunted while the increase in systolic blood pressure was significantly greater at 10 than at 30 degrees C. The increases in plasma sodium and potassium concentrations after exhaustion were similar between environments, as was the decrease in plasma volume. In both groups, all plasma hormones were significantly elevated postexercise, with the AVP response similar at 10 and 30 degrees C. However, the norepinephrine and ANF responses were significantly greater while the PRA response was significantly reduced at 10 degrees C. In the middle-aged subjects the epinephrine response to exercise was higher at 10 than at 30 degrees C. The greater ANF and reduced PRA responses to exercise in the cold may have resulted from central hemodynamic changes caused by cold-induced cutaneous vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hormonal responses to exercise during moderate cold exposure in young vs. middle-age subjects. 144 5

The involvement of arginine vasopressin (AVP) has been investigated in cold water swim (CWS) stress-induced antinociception (SIA) and CWS-induced hypothermia. The antinociceptive action of AVP (0.5 micrograms, i.c.v.) pre-CWS was antagonized by d(CH2)5Tyr(Me)AVP (0.5 micrograms, i.c.v.) but not by naloxone (5 micrograms, i.c.v.). CWS produced SIA on the hot-plate which was initially naloxone-insensitive. Neither AVP nor its antagonist had any significant effect on CWS SIA. AVP-induced increase in body temperature, during recovery from CWS-induced hypothermia, was significantly (P < 0.001) reduced in the presence of its antagonist. These findings suggest that the antinociceptive and thermoregulatory actions of AVP may be mediated via V1-receptors.
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PMID:Antinociceptive and thermoregulatory actions of vasopressin are sensitive to a V1-receptor antagonist. 147 Mar 6

Acute cold stress is a consistent stimulus to ACTH secretion in rats yet inhibits arginine vasopressin (AVP) in both rats and humans. We have studied the interrelationships of AVP, corticotrophin-releasing factor, and atrial natriuretic factor (ANF) in the hypothalamo-pituitary-adrenal response to acute cold stress in normal humans. Six healthy male volunteers deprived of food and fluid for 6 h, and minimally clothed, were studied in the early afternoon. After a 30-min period at 22 C, subjects were exposed to cold stress (4 C for 30 min), followed by a 30-min equilibration period at 22 C. By the end of the period of cold exposure there was a fall in plasma volume of 7.8 +/- 1.4% (mean +/- SEM), a significant increase in both systolic blood pressure (P = 0.0001) and in plasma norepinephrine level (P = 0.0001), but no change in plasma epinephrine or in plasma ANF. Plasma AVP levels fell significantly (P less than 0.01) to reach a nadir at 5-10 min after cold exposure before returning to baseline levels. A significant fall in plasma cortisol levels occurred during the first 15 min of the baseline period and remained stable thereafter. No significant changes in plasma corticotrophin-releasing factor or ACTH occurred. These results suggest that cold inhibition of AVP release, presumably via afferent baroreceptor pathways, may act to reduce the response of the corticotrophs to a potentially noxious stimulus. Inhibition of AVP and/or ACTH during acute cold exposure are not dependent upon an increase in plasma ANF.
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PMID:Vasopressin, corticotrophin-releasing factor, and pituitary adrenal responses to acute cold stress in normal humans. 151 64

It has been reported that after 40 minutes of stimulation of the medullary reticular formation (MORF), widespread significant increase by 1.4% to 2.8% in brain water content occurs in white matter of the injured hemisphere. Recent studies indicate that centrally released arginine vasopressin (AVP) influences water permeability of the brain in both normal and pathological conditions. The present study was carried out to clarify the effect of electrical stimulation of MORF on centrally released AVP. The cats were divided into three groups. In group A (16 cats), electrical stimulation of MORF (1msec, 5V, 50Hz) was carried out for 80 minutes in normal cats. In group B (11 cats), stimulation was started 17 hours after cold injury under the same conditions and carried out for 80 minutes. In group C (10 cats), angiotensin II was administered to elevate blood pressure to the same degree as during MORF stimulation 17 hours after cold injury. AVP concentrations in the cerebrospinal fluid (CSF), plasma and brain tissue of the injured and non-injured white matter were measured by radioimmunoassay. Plasma osmolality was also determined by the freezing point depression method. Normal values (mean +/- S. D.) of CSF and plasma AVP were 4.0 +/- 2.2 and 9.9 +/- 3.6 pg/ml respectively. Plasma AVP and osmolality did not show significant changes before and at the end of experiments in all groups. There were no significant changes in CSF AVP by induced hypertension for 80 minutes (Group C). Stimulation of the medullary reticular formation resulted in significant and progressive increase in CSF AVP in normal and injured brain (Group A, B).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes in centrally released arginine vasopressin by stimulation of the medullary reticular formation]. 156 84

The experimental evidence for the antipyretic action of arginine vasopressin (AVP) in guinea-pigs can be summarized as follows: The febrile response to a bacterial pyrogen can be reduced by a microinfusions of exogenous AVP into the ventral septal area of the limbic system. Immunohistochemical studies indicate increased activity of AVP terminals in the ventral septal area (VSA) and in parvocellular AVP neurones of the hypothalamic paraventricular nucleus (PVN) in several stressful situations accompanied by reduced febrile responses (late stage of pregnancy, immobilization, cold adaptation, osmotic stimulation). Also the peripheral and/or central release of AVP measured in some of these situations is increased. Electrical stimulation of the PVN suppresses fever, this suppression can, at least partly, be cancelled by simultaneous intraseptal application of the vasopressinergic V1 receptor antagonist. The documented AVP pathways from the PVN to the septum receive noradrenergic afferents from the lower brainstem. Chronic destruction of these afferents by microinjections of 6-hydroxydopamine (6-OHDA) significantly reduced the fever responses to pyrogen application, while microinfusion of noradrenaline (NA) enhances the fever reaction.
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PMID:Evidence for antipyretic vasopressinergic pathways and their modulation by noradrenergic afferents. 161 Jul 78

We assessed the effects of cold and isolation stress on arginine vasopressin (AVP) mRNA in the paraventricular (PVN) and supraoptic (SON) nuclei of the hypothalamus. Vasopressin mRNA levels were determined by in situ hybridization histochemistry at the cellular level. In posterior magnocellular neurons of the PVN isolation stress for 7 or 14 days increased vasopressin mRNA levels 28 and 29%, respectively, compared to group-housed controls. No significant alterations in vasopressin gene expression were observed in the SON after 7 or 14 days of isolation stress. Scattered magnocellular AVP mRNA-expressing cells of the medial parvocellular PVN showed increases of 19 and 34% after 7 and 14 days of isolation, respectively. We also studied the effect of cold or combined cold and isolation stress on vasopressin gene expression in the PVN and SON. Cold stress for 3 h daily for 4 consecutive days increased AVP mRNA levels in the posterior magnocellular PVN by 15%. Cold-isolated animals showed an increase of 21%. No significant effect on AVP mRNA levels in the SON was observed. In contrast to the posterior magnocellular PVN, cold or cold-isolation stress increased AVP mRNA in magnocellular neurons of the medial parvocellular region of the PVN by 25 and 43%, respectively, relative to control rats. These results suggest that psychological and metabolic stress may be added to the list of stressors that activate the hypothalamo-neurohypophysial system.
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PMID:Genomic effects of cold and isolation stress on magnocellular vasopressin mRNA-containing cells in the hypothalamus of the rat. 202 10

Cold stress stimulates the release of both ACTH and TSH from the pituitary. More striking changes in ACTH content have been seen in the intermediate lobe after cold stress. Therefore, this study was designed to test responses of individual anterior lobe corticotropes to cold exposure. Male rats were exposed to either 30 min of cold (+3-5 C), 30 min of a novel, temperate environment (+24 C) or were unstressed (+24 C). Pituitaries were fixed and embedded in preparation for immunolabeling for ACTH or TSH-beta at the light (semithin sections) and electron microscopic levels. The semithin sections were used to measure areas of corticotropes and thyrotropes with Bioquant image analysis equipment. Separate groups of pituitaries were dissociated and the cells were cultured for 2 or 15 h. Then the cells were stimulated for 5-10 min with biotinylated analogs of corticotropin-releasing hormone (bio-CRH) or arginine vasopressin (bio-AVP) to detect the target cells cytochemically. A third group of dissociated cells were fixed for immunolabeling for ACTH, 16K fragment of pro-opiomelanocortin, beta-endorphin, or TSH-beta. Cold exposure resulted in a 1-4-fold increase in the levels of serum ACTH over that of unstressed rats. This was correlated with a 40% increase in the percentage of cells that contained 16K fragment and a 30-40% increase in percentages of cells storing ACTH or beta-endorphin. Cold stress also increased the percentage of cells that bound bio-CRH or bio-AVP by 45%. Analyses of semithin sections showed that areas of corticotropes increased by 21% following cold stress. The number of rows of immunolabeled (ACTH) secretion granules also increased in corticotropes from cold-stressed rats. Exposure to a novel environment for 30 min resulted in no significant increase in serum ACTH over that of unstressed rats. There was, however, a 20% increase in percentages of cells that stored 16K fragment, beta-endorphin, or target cells that bound bio-CRH. However, the corticotropes were not significantly larger. Many of the cells exhibited reduced numbers of immunolabeled secretory granules. Other corticotropes resembled those from cold-stressed rats. When TSH cells were studied, their percentages increased from 8 +/- 3% to 15.8 +/- 4% and their areas increased by 22% following exposure to cold. After exposure to a novel environment, percentages of cells that stored TSH-beta increased to 11 +/- 2%, however, no changes in areas of TSH cells were measured. These studies demonstrated that the anterior lobe corticotrope is clearly activated by exposure to both cold and novel environment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cytochemical studies of responses of corticotropes and thyrotropes to cold and novel environment stress. 216 13


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