Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper reviews experimental findings which support the concept that vasopressin (VP) and the process of urine concentration may be involved in the progression of chronic renal failure (CRF). The influence of dietary protein intake on the progression of CRF may also involve VP and the operation of the concentrating process. VP receptors have been identified in glomeruli and VP is able to constrict mesangial cells as does angiotensin II. Acute VP infusion increases the glomerular transcapillary hydraulic pressure difference, and chronic VP infusion increases GFR. In rats with CRF (induced by 5/6 nephrectomy), VP levels were found elevated. In rats with 5/6 nephrectomy, we increased experimentally water intake in order to decrease circulating VP levels, urine concentration, and free water reabsorption. Several indices of progression of CRF, including proteinuria, hypertension and glomerulosclerosis, were significantly reduced, thus suggesting a contribution of VP in progression. Lowering protein intake in CRF could be beneficial because proteins, but not carbohydrates or lipids, produce metabolic end products (mainly urea, ammonia, protons, etc.) that are excreted by the kidney, and concentrated in the urine. In healthy subjects (man or rat), high protein (HP) intake favors urine concentration and causes changes in kidney function and morphology very similar to those induced by chronic VP infusion or water restriction. These changes involve an increase in transport activity of the thick ascending limb (where the initial active step of the concentrating process takes place) and may affect filtration rate and/or glomerular hemodynamics secondarily, by decreasing salt concentration at the macula densa and depressing tubuloglomerular feedback.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Possible involvement of vasopressin and urine concentrating process in the progression of chronic renal failure. 270

It has not yet been clarified whether prilocaine-induced methemoglobinemia is a problem in patients with chronic anemia. We therefore performed supraclavicular brachial blockade for upper limb surgery (6 mg/kg prilocaine 2% + 0.1 IU vasopressin/ml) in ten female patients with chronic renal failure (mean Hb 8.19%) requiring hemodialysis. Before the blockade, a catheter was inserted into the opposite internal jugular vein and blood samples were drawn before and 10, 15, 20, 30, 45, 60, 90, 120 and 180 min after injection. Plasma prilocaine concentrations and methemoglobin levels were within the ranges measured by other authors in healthy patients. There was no correlation between plasma prilocaine levels and methemoglobinemia. We therefore consider prilocaine to be a safe local anesthetic in patients with renal failure and chronic anemia.
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PMID:[Supraclavicular plexus blockade using prilocaine in patients with chronic anemia]. 271 Sep 68

The effect of lactation on stress-induced hormone responses and changes in hypothalamic mRNA was assessed in female rats. In control animals the stimulus of ip hypertonic saline resulted in increased plasma levels of corticosterone, oxytocin, and vasopressin and hypothalamic content of CRF and enkephalin mRNA. In lactating females, however, the corticosterone response to this stress failed to reach significance, the plasma oxytocin response was markedly reduced, and the vasopressin response was unaffected. Lactation also resulted in an abolition of the CRF and enkephalin mRNA responses to stress. In contrast, the hypothalamic CRF response to adrenalectomy was unaffected by lactation status. Removal of the pups from their mothers resulted in a return of CRF and enkephalin mRNA responses to stress within 2 days. Lactation is associated with a selective inhibition of normal hypothalamic stress responses.
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PMID:Lactation inhibits stress-mediated secretion of corticosterone and oxytocin and hypothalamic accumulation of corticotropin-releasing factor and enkephalin messenger ribonucleic acids. 278 27

Favourable results with the use of inhibitors of the angiotension I-converting enzyme in the therapy not only of high-renin but also normo-renin and low-renin hypertension revived interest in research in the area of the renin-angiotensin (RAS) system. The use of classical radioimmunological, radiohistochemical receptor studies as well as of recent methods of molecular biology and pathology revealed that for the regulation of blood pressure and the extracellular volume and pathogenesis of hypertension not only RAS components in systemic blood are important but also local tissue RAS with an autocrine and paracrine action at the site of its origin. Cerebral RAS participates in the central cardiovascular regulation, in the control of the salt and water intake, the secretion of antidiuretic hormone and ACTH. In the cardiovascular apparatus RAS is responsible not only for vasoconstriction but it acts also as a growth factor promoting the development of cardiac and vascular hypertrophy. In the kidneys RAS decides on the blood flow, its distribution, glomerular filtration. Its excessive stimulation may contribute in arterial hypertension, diabetic nephropathy and in residual nephrons during chronic renal failure, to the change from functional hyperfiltration to irreversible structural damage of the nephron. Inhibitors of the converting enzyme not only reduce the peripheral vascular resistance in arterial hypertension but influence also the tissue production of angiotensin II and thus the regression of cardiovascular hypertrophy and progression of renal damage.
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PMID:[Renaissance of the renin-angiotensin system in the pathogenesis and therapy of arterial hypertension]. 280 32

We examined the effect of neurohypophysectomy with and without vasopressin replacement on the ACTH response to hypotension and ovine CRF infusion and on the adrenocortical response to ACTH and angiotensin II infusion in conscious dogs. Nitroprusside hypotension (decrease in mean arterial pressure of 25 mm Hg) in the intact state resulted in large increases in plasma arginine vasopressin (pAVP; from 2.6 +/- 0.3 to 296 +/- 63 pg/ml) and ACTH (from 35 +/- 6 to 395 +/- 92 pg/ml). Neurohypophysectomy resulted in greatly attenuated pAVP (8.4 +/- 1.6 pg/ml) and ACTH (80 +/- 10 pg/ml) responses to hypotension which were not normalized by physiological low dose vasopressin replacement (6-18 pg/kg.min continuously, iv, for 2 weeks). However, acute administration of vasopressin (4-6 ng/kg.min) simultaneously with hypotension in the neurohypophysectomized (neurohypox) dog, which produced pAVP levels equivalent to the hypotensive response to intact dogs, almost completely normalized the ACTH response to hypotension (to 248 +/- 74 pg/ml). The ACTH response to 20 ng/kg.min ovine CRF, iv (from 43 +/- 8 to 268 +/- 77 pg/ml), was not attenuated by neurohypophysectomy. The cortisol responses to infusion of 0.5 and 2 ng/kg.min ACTH-(1-24), iv, were essentially normal in neurohypox dogs. However, the ACTH and aldosterone responses to 5 ng/kg.min angiotensin II infusion iv were attenuated in neurohypox dogs off AVP replacement. Histological examination revealed normal adrenal glands and anterior pituitaries in neurohypox dogs. Immunocytochemical staining for vasopressin and neurophysin revealed normal cell bodies in the paraventricular and supraoptic nuclei of the hypothalami from neurohypox dogs. However, median eminence staining for AVP and neurophysin was greatly diminished in neurohypox dogs. In summary, neurohypophysectomy 1) attenuated the ACTH response to hypotension and angiotensin II, but not to CRF, and 2) attenuated the aldosterone response to high dose angiotensin II. Furthermore, the deficit in ACTH secretion was almost completely normalized by increasing plasma AVP levels to those observed in the intact dogs. We conclude that an action of circulating pAVP increases ACTH secretion by a direct effect at the pituitary and by activating afferent input to the hypothalamus.
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PMID:Control of adrenocorticotropin secretion and adrenocortical sensitivity in neurohypophysectomized conscious dogs: effects of acute and chronic vasopressin replacement. 283 Oct 29

Control of ACTH secretion in the pituitary in the absence of target cells for CRF, the most potent ACTH secretagogue, was studied in dissociated bovine anterior pituitary cells treated with a potent selective cytotoxin. The cytotoxin is a conjugate of the CRF analog [Nle21,38, Arg36]rat (r) CRF and the plant toxin gelonin. Dissociated bovine anterior pituitary cells were pretreated with vehicle, 2 nM ovine CRF, 2 nM cytotoxic conjugate, or unconjugated [Nle21,38,Arg36]rCRF and gelonin in amounts equivalent to that of 2 nM cytotoxic conjugate for 12 h, then extensively washed and cultured for 3 days before acute secretion experiments. Unstimulated ACTH secretion was similar in all groups. ACTH secretion in response to CRF was attenuated by pretreatment with the cytotoxic conjugate; CRF (2.5 nM)-stimulated secretion was 7.0, 6.3, and 2.8 times the unstimulated rate in cells pretreated with vehicle, 2 nM CRF, or 2 nM cytotoxic conjugate, respectively. Likewise, the ACTH secretory response to a cAMP analog was attenuated by pretreatment with the conjugate; 8-bromo-cAMP (10 mM)-stimulated secretion was 6.8, 7.1, and 3.3 times the unstimulated rate in cells pretreated with vehicle, CRF, or conjugate, respectively. In contrast, the ACTH responses to vasopressin (VP) or oxytocin (OR) remained intact. VP stimulated the ACTH secretion rate by 4.2, 4.0, and 3.5 times, respectively, in the three groups. OT stimulated the ACTH secretion rate by 2.7, 2.6, and 2.3 times in the three groups. Pretreatment with the conjugate attenuated the response to CRF and VP in combination by the same amount as it attenuated the response to CRF alone. The ACTH secretory responses in cells pretreated with unconjugated [Nle21,38,Arg36]rCRF and gelonin were not different from responses in cells pretreated with vehicle. These results suggest that there is a separate mechanism or cell type for OT- and VP-stimulated ACTH secretion distinct from that responsible for the action of CRF on pituitary cells.
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PMID:Dissociation of the adrenocorticotropin secretory responses to corticotropin-releasing factor (CRF) and vasopressin or oxytocin by using a specific cytotoxic analog of CRF. 283 Oct 39

The hypothalamo-pituitary-adrenal axis is controlled by complex regulatory mechanisms. Numerous factors such as CRF, vasopressin, oxytocin, angiotensin II and conceivably other hormones--all controlled by various substances acting on central locations--stimulate the release of the stress hormone ACTH. On the other hand, glucocorticoids inhibit the secretion of ACTH by acting at the hypothalamic and/or pituitary level. The release of ACTH is therefore the final outcome of the interactions between the hypothalamus, the adrenal gland and possibly other organs. The multimolecular nature of the factors responsible for the control of the pituitary-adrenal axis is an attractive hypothesis because of the great variety of stress stimuli. The various factors could have specific roles in various stress situations. They provide a highly sensitive mechanism regulating very finely the stress hormone in response to a whole variety of endogenous and exogenous stimuli. Depending on the type of stress, they may therefore singly or in combination affect the amount and duration of ACTH and steroid secretion. The released glucocorticoids may then produce their numerous effects on inflammatory and immunological processes, carbohydrate metabolism, shock and water balance. It has been postulated that these effects may be important in order to prevent host responses from over-reacting to stress and threatening homeostasis. However, proof of the necessity of the glucocorticoid hypersecretion in response to stress remains elusive.
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PMID:Stress and the pituitary-adrenal axis. 283 73

A 71-year-old man was referred to Tokai University Hospital because of cold intolerance, slow speech and slowing down of his intellectual and motor activities. Free thyroxine index, and free T-4 and T-3 levels were low (1.4, 0.7 ng/dl and 0.4 ng/ml, respectively) with normal TSH (2.5 microIU/ml). A skull X-ray showed enlargement of the sella turcica and his CT scan revealed an intrasellar mass. LH, FSH, ACTH and PRL did not rise in response to the intravenous administration of LH-RH and insulin. A diagnosis of pan-hypopituitarism due to a pituitary tumor was established. The release of ACTH and cortisol was restored under stimulation of CRF or lysine vasopressin. TSH responded to TRH in a delayed manner. The pituitary tumor was removed by a transsphenoidal operation and diagnosed histologically as craniopharyngioma. Our hospital has experienced nine cases of craniopharyngioma in the last 10 years but the present case was the only intrasellar craniopharyngioma.
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PMID:A case of intrasellar craniopharyngioma. 283 33

About one third of patients receiving dialysis for end stage renal failure have chronic fluid overload despite advice to restrict their oral fluid intake. To investigate the potential of an angiotensin converting enzyme inhibitor in reducing the urge to drink and consequent gain in weight, a double blind, placebo controlled crossover trial of enalapril was conducted in 25 patients receiving dialysis who had fluid overload. The trial comprised a baseline period of four weeks; two periods of treatment, each of four weeks, during which patients received either placebo or enalapril 5 mg twice each week; and a follow up period of four weeks. Five patients withdrew from the trial, one because of an adverse drug reaction to enalapril. A range of biochemical and behavioural variables was measured during the baseline period, at the completion of periods 1 and 2, and during follow up. These variables included gain in weight between dialysis sessions; blood pressure; plasma concentrations of sodium, angiotensin II, and vasopressin; plasma renin and angiotensin converting enzyme activities; osmolality; and estimations of thirst, intake of fluid, and control of drinking. Enalapril caused a significant reduction in gain in weight between dialysis sessions, thirst, and oral intake of fluid in parallel with significantly increased renin activity, significantly decreased angiotensin converting enzyme activity, and decreased concentrations of angiotensin II. Gain in weight and angiotensin converting enzyme activity returned to baseline values once patients stopped taking enalapril. These results suggest that enalapril may act on the renin-angiotensin system and reduce intake of fluid by inhibiting angiotensin converting enzyme.
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PMID:Controlled trial of enalapril in patients with chronic fluid overload undergoing dialysis. 283

The regulation of pituitary and brain CRF receptors and corticotroph responses during stress were studied in rats subjected to prolonged immobilization. Plasma ACTH levels showed the characteristic biphasic changes, with a rapid 23-fold increase in 15 min, followed by a decrease to about twice the basal levels after 6-h immobilization. In contrast, plasma corticosterone levels were markedly elevated throughout the duration of the stress. Pituitary CRF receptor content, measured by binding of [125I]Tyr-ovine CRF to pituitary membrane-rich fractions, was unchanged after 2.5 h, but was reduced by 28 +/- 2.7% (+/- SE) and 47.6 +/- 1.1% after 18 and 48 h of immobilization, respectively. These results were confirmed by autoradiography in slide-mounted frozen pituitary sections. In contrast, no changes in CRF receptor content were observed in brain areas, including olfactory bulb, frontoparietal cortex, hippocampus, amygdala, and lateral septum. A concomitant decrease in immunoreactive (ir) CRF content in the median eminence of rats immobilized for 48 h is consistent with the hypothesis that increased release of CRF into the portal circulation occurs during chronic stress. Despite pituitary CRF receptor loss and reduced in vitro responses to CRF, the increases in plasma ACTH and corticosterone in vivo after ether exposure or CRF injection were greater and more prolonged in rats immobilized for 48 h than in nonimmobilized controls. The decrease in pituitary CRF receptors was accompanied by decreased CRF-stimulated cAMP and ACTH release in cultured pituitary cells from 48-h restrained rats. However, concomitant incubation of cells with CRF and vasopressin restored cAMP and ACTH responses to control levels, suggesting that the simultaneous release of both regulators from the hypothalamus determines the plasma ACTH level. These findings indicate that the decrease in plasma ACTH during the adaptation phase to stress is accompanied by decreases in pituitary CRF receptors. However, the enhanced pituitary response to a superimposed stress or CRF injection implies that the decrease in plasma ACTH levels during prolonged stress may be due to adaptive changes at the central level. These findings emphasize the importance of the integrated actions of CRF and other regulators in the control of the pituitary adrenal-axis during stress.
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PMID:Corticotropin-releasing factor receptors and pituitary adrenal responses during immobilization stress. 283 59


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