Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1332347 (ADH)
 2,230 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

These studies further define the mechanisms by which insulin stimulates Na transport in the toad bladder. Serosal but not mucosal addition of insulin, 100-1,000 mU/ml, stimulated short-circuit current (SCC) by 25-50%. The initial rise in SCC occurred at 5 min and the peak response at 15-25 min. Doses of insulin greater than 250 mU/ml increased SCC values for up to 3 h. Actinomycin D did not block the early rise in SCC produced by insulin, but it blocked the delayed effects. Insulin increased SCC in substrate-depleted bladders, although the increase in SCC was less (P less than 0.01) than in nonsubstrate-depleted bladders. Pyruvate addition to substrate-depleted bladders restored to normal the rise in SCC observed after insulin. Simultaneous addition of ADH and insulin led to an increase in SCC that was greater than the sum of the responses observed when each hormone was added independently. Synergistic effects on SCC were also obtained with cyclic AMP and insulin. Insulin did not increase cyclic AMP levels in toad bladder epithelial cells. It is suggested that insulin stimulates active Na transport by two mechanisms: 1) a rapid phase, which may involve unmasking of pump sites within the membrane, and 2) a delayed effect which seems to require protein synthesis. The synergism of which seems to require protein synthesis. The synergism of insulin with ADH or cyclic AMP may reflect a facilitative effect of insulin on ADH or cyclic AMP-sensitive pump sites or, alternatively, the uncovering of latent pump sites that then may be available to stimulation by ADH or cyclic AMP.
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PMID:Effects of insulin, ADH, and cyclic AMP on sodium transport in the toad bladder. 19 86

Rats with hereditary hypothalamic diabetes insipidus, devoid of endogenous ADH, exhibited a prompt antidiuresis when injected subcutaneously or intraarterially with ovine prolactin. The antidiuresis was accompanied by a decrease in free water clearance and an increase in urine osmolality without a change in osmolal clearance or creatinine excretion. Measurement of PAH and insulin clearances indicated that prolactin had no effect on renal plasma flow or glomerular filtration rate. Prolactin injection caused a transient decrease in urinary sodium excretion, but proximal tubular sodium reabsorption, estimated by lissamine green transit time, was unaffected. The antidiuretic effect of prolactin could not be attributed to ADH contamination of the ovine prolactin preparation. Kidney cyclic AMP content was increased significantly 5 min after injection of prolactin. Thus, prolactin has an antidiuretic effect similar to that which occurs as a result of ADH action on the kidney and does not require either the release or the presence of ADH in order to cause the antidiuresis. Further, the impaired water excretion cannot be attributed to an increase in proximal tubular sodium reabsorption or to alteration of renal hemodynamics. It is suggested that prolactin has a direct ADH-like action on the kidney resulting in antidiuresis.
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PMID:Antidiuretic action of prolactin in the rat with diabetes insipidus. 19 85

A case of pseudohypoparathyroidism has been investigated. Indirect evidence allows to eliminate a defect of renal 1 alpha-hydroxylase as the determining factor of this condition. Similarly, the increased size of the mean surface area of the cross-section of periosteocytic lacunae, as determined on decalcified sections of bone obtained by transiliac biopsy, shows the osteocytes to be sensitive to the endogenous PTH, discarding cAMP response to PTH in bone as a prerequisite for PTH action on bone. The authors conclude from these data and from previous experiments that the defect of parathyroid function in this condition probably relates to the existence of an abnormal PTH molecule and/or metabolism and/or interaction with the receptors sites. The endocrine function was studied as well. Prediabetes was demonstrated, as well as primary latent hypothyroidism (TRH test). Prolactin release could not be stimulated by TRH, levodopa, metoclopramide, chlorpromazine and insulin hypoglycemia. The latter produced a normal release of ACTH (as ascertained by plasma cortisol levels) and GH, and possibly a sluggish response of glucagon and gastrin. There was a deficiency of urinary concentration upon restriction of fluid intake. This was only partially corrected by ADH administration.
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PMID:[Physio-pathology of pseudohypoparathyroidism (author's transl)]. 22 97

The experiments were performed in vitro using the frog skin preparations and Ussing method. The effect of methoxyflurane was investigated in 18 sections and that of diethyl ether in 16 sections. Both the anaesthetics were found to affect the frog skin preparation in qualitatively similar way. They both demonstrated a two-phase character of action. Decrease in active sodium transport is preceeded by a transient increase in bioelectric indices of the membrane. The effect was reversible after removing of the drugs from the medium. In order to determine the mechanism of action of the two anaesthetics they were given in combination with ADH and insulin. It was found that the mechanism of action of both the drugs is not analogical to any of the hormones examined, at least, as far as the first phase of action is concerned.
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PMID:The comparative evaluation of methoxyflurane and diethyl ether action upon an active sodium transport across isolated frog skin preparation. 108 43

1. In this study we found that insulin mixed with m-cresol, normally used as pharmaceutical preparation, shows an earlier and larger stimulating effect on transepithelial sodium transport than insulin alone. 2. The action displayed by the m-cresol seems to be specific for insulin because m-cresol mixed with ADH, a hormone known to stimulate sodium transport, failed to show the potentiation seen for insulin. 3. It is proposed that m-cresol could facilitate the interaction with its receptor by modifying the insulin molecule. 4. This finding could be of biological and pharmacological importance.
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PMID:Potentiation by m-cresol on transepithelial sodium transport across frog skin induced by insulin. 136 10

A 46-year-old man, presenting with headache, nausea, and lassitude, was diagnosed as having diabetes mellitus and hyponatremia, and admitted to Tohoku University Hospital. Insulin treatment improved the hyperglycemia but aggravated hyponatremia, which was proved to be elicited by the inappropriate secretion of antidiuretic hormone (SIADH). An acute water load failed to suppress ADH release in the supine posture but slightly increased plasma atrial natriuretic peptide (ANP). On the other hand, plasma ADH markedly increased in response to an upright posture, accompanied by a fall in blood pressure and a rise in heart rate. After treatment with droxidopa "a sympathomimetic drug", ambulatory blood pressure gradually increased and hyponatremia disappeared. However, blood pressure and ADH responses to upright posture were not improved by treatment with the drug. Moreover, plasma ADH was still not sufficiently suppressed by acute water loading in the supine position, but plasma ANP markedly increased, thereby resulting in urinary dilution and natriuresis. These results suggest that exaggerated ADH release (SIADH) was brought about by the baroreceptor reflex stimulated by the postural hypotension, and also by the impaired osmoregulation associated with diabetic neuropathy, and that droxidopa improved cardiovascular function and increased ANP release with resultant urinary dilution and natriuresis in spite of slightly increased ADH release.
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PMID:A case of syndrome of inappropriate secretion of antidiuretic hormone associated with diabetes mellitus. 179 39

After burn trauma, a very marked endocrine response occurs. Almost all the known hormones take part in it. Their response influences very much the postburn metabolic changes and participates in the integration of the body's response with the nervous and immune systems. In this review, mainly the changes in various hormone levels are described, as well as the possible role of the acute phase response after burn trauma, and the communications between the endocrine and immune systems, the cells of the latter are able to respond to various hormonal stimuli and to secrete various hormones themselves. Some of the hormones are very sensitive indicators of the burn stress, e.g., the T3 levels (very low), testosterone in males (very low), dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S) (very low), ADH, catecholamines, renin and angiotensin II, cortisol (high), 17-beta-estradiol in males (usually elevated). Other hormones are usually elevated, but not always (ACTH, aldosterone, prolactin, glucagon, immunoreactive insulin, beta-endorphin, rT3, 11-beta-hydroxyandrostenedione), but there are hormones that are unually low (T4, FSH, androstenedione, progesterone--the latter especially in females). Calcitonin, parathyroid hormone, growth hormone are sometimes elevated, as well as LH (measured with RIA methods). TSH is usually normal, the biologically measured LH was reported to be low. The levels of the sensitive indicators of burn stress may be used to evaluate the effect of treatment: if the burn patient is properly treated, the indicators may become earlier normal.
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PMID:Endocrine changes after burn trauma--a review. 251 73

The heart is the major source of atrial natriuretic peptides (ANP). A propeptide is stored in atrial myocytes. In normal humans, atrial distension secondary to volume overload and/or increased atrial pressures are thought to stimulate the secretion of biologically active alpha-ANP (ANF-[99-126], 28 amino residues) into the circulation. Plasma immunoreactive ANP (irANP) rises in response to acute sodium-volume loading, the central shift of volume produced by lying down or by immersion, acute increases in blood pressure (BP), dynamic exercise, or the administration of glucocorticoids or mineralocorticoids. Plasma irANP also rises with aging. Synthetic alpha-ANP infused acutely i.v. can lower BP, reduce plasma volume by an extravascular shift, cause baroreflex-mediated sympathetic activation, directly inhibit adrenal steroidogenesis and lower plasma aldosterone and cortisol, directly inhibit renal renin release, elevate plasma insulin; diuresis, free water clearance and natriuresis increase already in response to low alpha-ANP doses that raise plasma irANP within the physiological-pathological range. It follows that in addition to direct influences on cardiovascular and renal function, the ANP system may comprise a cardio-adrenal feedback mechanism and perhaps also modulate insulin and the release of ADH. The major although yet unproven physiological role of the ANP system may be the protection of the heart against volume and/or pressure overload. The pathophysiological, diagnostic and therapeutic aspects of elevated plasma irANP values, ANP measurements, or administration of synthetic ANP, respectively, in various diseases are currently under intense study and of great potential interest.
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PMID:Atrial natriuretic peptide in man. 252 24

The endocrine (plasma renin activity, insulin and ADH) and hemodynamic responses (heart rate and mean arterial pressure) to isoprenaline infusion were examined in conscious deoxycorticosterone-salt hypertensive rats (DS) and compared with uninephrectomized-salt control rats (US). A dose-related rise in plasma renin activity and plasma insulin values was found in US rats, while no change in either parameter was observed in DS rats after 30 min of isoprenaline infusion. ADH was not increased in US rats at any dose of isoprenaline infusion. However, in DS rats the largest dose (450 ng/kg/min) produced a significant rise. Isoprenaline infusion increased the heart rate in both groups, but the increases in the DS group were significantly lower than in the US group for the 200-ng/kg/min dose (p less than 0.01). The drop in mean arterial pressure was found to be more pronounced in DS rats than in US rats at 50, 100 and 200-ng/kg/min isoprenaline doses. Recovery of the mean arterial pressure to basal levels was also found in US rats with the various doses of isoprenaline administered. However, in DS rats the different doses of isoprenaline produced a progressive drop in mean arterial pressure with no recovery at the end of 30 min of isoprenaline infusion. The present results provide no evidence of subsensitivity to isoprenaline in the resistance vessels of conscious DS rats and suggest that the greater hypotensive response observed in these rats may be due to the inability of the renin-angiotensin system to adequately compensate the vasodilation produced by isoprenaline.
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PMID:beta-adrenergic reactivity in conscious DOCA-salt hypertensive rats. 254

According to the report of the Health and Welfare Ministry's research committee on brain death (1985), "brain death is defined as an irreversible cessation of the total brain function including brain stem." However, in brain death patients, whether the hypothalamic function which belongs to the brain stem function has completely ceased or not is unknown. In order to evaluate the hypothalamic function in brain death patients, the blood levels of the pituitary hormones and hypothalamic hormones were measured, and anterior pituitary stimulation test with triple bolus injection (TRH 500 micrograms, LH-RH 100 micrograms, regular insulin 0.3-0.7 unit/kg) was performed. The subjects were 13 brain death patients whose clinical states fully satisfied the criteria proposed by the committee. 1) The average blood levels of anterior pituitary hormones in these brain death patients were within normal range, and that of growth hormone was more than the twice of the normal level. 2) The blood anterior pituitary hormones were detectable in almost all cases even several days after the diagnosis of the brain death. 3) LH reserve was maintained in three cases. FSH reserve was maintained in three cases. Prolactin reserve was maintained in two cases. TSH reserve was maintained in one case. 4) Blood ADH (antidiuretic hormones) were detectable in 7 cases out of 9 cases. The blood ADH level of one case, in particular, was rather high (above 10 pg/ml). 5) Histopathologically anterior pituitaries were examined in three autopsy cases. The central necrotic areas were observed in all cases, but normal pituitary tissues existed peripherally. And all anterior pituitary hormones could be recognized immunohistochemically. 6) The blood levels of the hypothalamic hormones (GRF, CRF, LH-RH) were measured in four cases. The hypothalamic hormones were detectable in all cases. In one case, the levels of GRF were within normal range even 9 or 15 days after the diagnosis of brain death.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hypothalamic pituitary function in brain death patients--from blood pituitary hormones and hypothalamic hormones]. 314 54


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