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Query: UNIPROT:P01185 (
vasopressin
)
23,126
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The renal function was evaluated by clearance (cl.) method during hypotonic polyuria and successive relative
antidiuresis
induced by lysine-8-
vasopressin
administration. Four 15 min and two 60 min cl. periods were performed in hypotonic polyuria and
antidiuresis
, respectively. Glomerular filtration rate was estimated by creatinine cl., the osmotic cl. (Cosm' CH2O), the absolute and fractional excretions of water, sodium, potassium and chloride were determined by usual methods. The urinary PGE2, 6-keto-PGF1 alpha and TxB2 excretions were determined by RIA method. The study protocol was applied on 14 healthy women in acute potassium depletion, treated with indomethacin (100 mg i.m. at the end of the oral water load). In Group D3 (n = 6) in the presence of a greater potassium cumulative deficit (198.4 +/- 22.2 meq), in hypotonic polyuria, indomethacin induces significant effects as an increase of fractional hydro-electrolytic reabsorptions and as a decrease of urinary prostanoid excretion. The indomethacin tubular action in potassium depletion differs significantly from that observed in normal potassium balance.
...
PMID:[Further research on the role of prostanoids in controlling renal function in humans in normal potassium balance and acute experimental potassium depletion. III: Effects of indomethacin in potassium depletion]. 275 84
The renal function has been evaluated by clearance (cl.) method during hypotonic polyuria and successive moderate
antidiuresis
induced by a low dose of lysine-8-
vasopressin
; four 15 min and two 60 min cl. periods were performed, respectively. Glomerular filtration rate was estimated by creatinine cl.; the osmotic cl. (Cosm, CH2O), the absolute and fractional excretions of water, sodium, potassium and chloride were determined by usual methods. The urinary concentrations of PGE2, 6-keto-PGF1 alpha (6KPGF) and TxB2 were measured by RIA. The study protocol was applied in normal potassium balance and experimental potassium balance (KD), both in absence and presence of indomethacin. In KD groups with a potassium cumulative deficit of 198.4 +/- 22.2 meq (D3; n = 6) during polyuria significant correlations are consistent with the hypothesis that the lower the plasma potassium concentration is the higher the urinary chloride excretion and the inhibition of distal fractional chloride reabsorption. Moreover, by utilizing the polyuria and
antidiuresis
data pool, the effects of urine flow rate changes on PGE2 and 6KPGF urinary excretions are blunted as compared to normal potassium balance (n = 14). After indomethacin treatment (D3.I) the following functional relationships are disclosed: a) the lower the kaliemia is the lower the urinary chloride and potassium excretions and the higher the fractional isosmotic reabsorption; b) the lower the urinary potassium excretion is the lower the urinary chloride excretion. In both D3 and D3.I experimental groups the positive correlation between urinary chloride excretion and urinary potassium excretion is significant.
...
PMID:[Role of prostanoids in the control of renal function in normal potassium balance and in acute experimental potassium depletion. 4. Relation of extrarenal parameters, renal function parameters and urinary excretion of prostanoids]. 277 40
In vivo and in vitro studies were performed to assess the mechanism of the diuretic effect of B-HT 933, a selective alpha 2-adrenoceptor agonist. In conscious Sprague-Dawley rats whose plasma
vasopressin
(AVP) levels were increased by infusion of hypertonic NaCl, B-HT 933 had no effect on AVP secretion. In Brattleboro homozygous (DI) rats, the antidiuretic dose response to AVP was shifted to the right by B-HT 933. In addition, a sustained
antidiuresis
induced in rats by infusion of 10 pg/min AVP was attenuated by B-HT 933 in a concentration-dependent manner. Pretreatment of DI rats with pertussis toxin (2 micrograms/kg iv) 4-5 days before testing abolished the inhibitory effect of B-HT 933 on AVP-induced
antidiuresis
. In outer medullary collecting ducts of DI rats, norepinephrine and B-HT 933 produced significant inhibition of AVP-stimulated adenosine 3',5'-cyclic monophosphate (cAMP) accumulation. In contrast, the selective alpha 1-adrenoceptor agonist cirazoline had no effect on AVP-induced cAMP formation. The inhibitory effect of norepinephrine was antagonized by the selective alpha 2-adrenoceptor antagonist rauwolscine but not by prazosin, a selective alpha 1-antagonist. In outer medullary collecting ducts dissected from the pertussis toxin-treated DI rats used in the in vivo studies, the inhibitory effect of norepinephrine and B-HT 933 on AVP-stimulated cAMP accumulation was abolished. The results indicate that the hydrosmotic action of AVP is inhibited by alpha 2-agonists via a pertussis toxin-sensitive mechanism.
...
PMID:Mechanism of alpha 2-adrenoceptor agonist-induced diuresis. 290 Jun 6
Recently, there has been an explosion of knowledge on
vasopressin
, including its neuro-anatomy, biochemistry and physiology. Recent work demonstrates extensive extra-hypothalamic vasopressinergic projections from the SON and PVN. Of particular importance are projections to the cardiovascular medullary centres. Conversely, the SON and PVN receive reciprocal catecholaminergic innervation from autonomic medullary centres. Vasopressin should now be regarded as a peptide hormone with important peripheral effects, as well as a neuropeptide acting as a neurotransmitter or neuromodulator with important CNS actions. The central and peripheral
vasopressin
systems are not only anatomically differentiated, but, although integrated, may also function independently. There is an important interaction between the central
vasopressin
system and the autonomic nervous system. Vasopressin has multiple and diverse actions on the cardiovascular system, including direct vasoconstriction,
antidiuresis
and hence volume control, central actions on cardiovascular neural centres, modulation of the baroreflex and direct cardiac effects. It also acts in concert with the sympathetic nervous system and the renin-angiotensin system as an integrated neurohormonal system in the control of blood pressure. Vasopressin appears to have an important role as a vasoconstrictor agent whenever volume is threatened, such as in dehydration, haemorrhage, adrenal insufficiency and orthostasis. It seems unlikely that
vasopressin
acts as a direct vasoconstrictor agent in the pathogenesis of any form of experimental or human hypertension. Although plasma
vasopressin
levels have been reported to be elevated in most forms of hypertension, this correlates best with the severity of hypertension. Furthermore, the levels are not elevated to the pressor range, so that increased vascular reactivity and sensitivity has to invoked. This does not appear to be specific for
vasopressin
. However,
vasopressin
may be indirectly involved through volume maintenance or interactions within the CNS. Indeed, its volume retaining properties have probably been underestimated. Whereas in acute situations the vasoconstrictor properties may be of some importance, it is difficult to sustain long-term hypertension without maintenance of an adequate plasma volume. Vasopressin's central actions on the cardiovascular medullary centres, the baroreflex, the autonomic nervous system and catecholamine metabolism may also be involved in some hypertensive processes.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:Vasopressin in circulatory control and hypertension. 293 70
Plasma renin activity (PRA), plasma renin concentration (PRC) and brain serotonin content were investigated 48 h after i.p. administration of central serotonin depletor p-chlorophenylalanine (pCPA) (300 mg kg-1) in male Wistar (Wi) and diabetes insipidus Brattleboro (DI) rats. Water-salt balance and systolic blood pressure were followed up to 7th day after treatment. In addition, PRA was studied 48 h after drug administration in adrenalectomized and renal denervated Wi rats. Similar decrease of brain serotonin concentration was observed in both Wi and DI rats 48 h after pCPA treatment. PRA in Wi rats was unchanged despite the observed negative water-salt balance, decreased in adrenalectomized and renal denervated Wi rats and increased in DI rats in comparison with respective vehicle-treated controls. In WI rats PRC was not affected by pCPA but increased in DI rats. Negative water-salt balance was observed in both Wi and DI rats on the first day following treatment due to polyuria and suppressed food intake. During next following days a mild elevation of systolic blood pressure was found in both groups associated with opposite urinary responses:
antidiuresis
in Wi and polyuria in DI rats. The results indirectly show that pCPA-induced suppression of renal renin secretion observed in Wi rats may be due to prevailing inhibitory action of
antidiuretic hormone
.
...
PMID:Renin release and water-salt balance after central serotonin depletion by p-chlorophenylalanine in Brattleboro and Wistar rats: possible role of ADH. 295 66
The interaction of exogenous synthetic human atrial natriuretic peptide (hANP), given in iv bolus doses of 100, 200, and 400 micrograms, and of various bolus-primed infusion of 1-deamino-D-Arg8-
vasopressin
(dDAVP), a nonpressor analog of
antidiuretic hormone
, were investigated in six normal men. A marked dose-dependent rise in plasma hANP concentrations occurred after the administration of hANP. The antidiuretic effect of dDAVP (P less than 0.01) was partially but not completely reversed by the concomitant administration of hANP (P less than 0.01). hANP-induced natriuresis was similar in the presence and absence of dDAVP-induced
antidiuresis
. While these results do not prove that hANP-dependent natriuresis and diuresis are independent phenomena, it is of clinical interest that natriuresis without diuresis can be induced by the simultaneous administration of hANP and dDAVP.
...
PMID:Effect of human atrial natriuretic peptide on 1-deamino-D-Arg8-vasopressin-induced antidiuresis in man. 296 82
The mechanisms responsible for the natriuresis encountered in the syndrome of inappropriate secretion of
antidiuretic hormone
(SIADH) are not fully understood. The present study explores the role of atrial natriuretic factor (ANF). Eight subjects unable to excrete ingested free water normally (three patients with SIADH and five healthy humans after intranasal administration of desmopressin) underwent a standard oral water loading test. Plasma ANF level and urinary sodium excretion increased during water retention, whereas plasma aldosterone value decreased later. The increment of urinary sodium excretion rate was significantly correlated with that of plasma ANF. In two patients with hyponatremia due to SIADH, plasma ANF levels were increased during the hyponatremic phase of their condition and decreased under water restriction. In one of them, marked natriuresis was observed when the plasma ANF level was high. It is concluded that secretion of ANF is acutely and chronically stimulated during water retention in SIADH and that ANF may be in part responsible for the natriuresis encountered in inappropriate
antidiuresis
.
...
PMID:Natriuresis and atrial natriuretic factor secretion during inappropriate antidiuresis. 296 80
Desmopressin (DDAVP) is used intramuscularly in the treatment of post operative diabetes insipidus as soon as the condition is diagnosed to ensure continuous replacement of
antidiuretic hormone
secretion during the first 5 days of therapy. Two successive studies, each involving 15 patients, were conducted. The first study was designed to test the effectiveness and detect the possible side effects of intramuscular DDAVP, while the purpose of the second study was to evaluate the clinical application of the drug. With seven 2 mcg doses of DDAVP, administered 12-hourly by intramuscular injection to patients weighing more than 30 kg, continuous
antidiuresis
during 96 hours was achieved. This method is simple and effective, but it should not be prolonged beyond that period of time. Moreover, to prevent plasma hypo-osmolality, fluid intake must be strictly controlled and kept at the same level as or below diuresis.
...
PMID:[Treatment of post-neurosurgical diabetes insipidus with desmopressin by intramuscular route]. 296 49
Differential interference contrast microscopy was used in combination with standard electrophysiological techniques in the in vitro perfused mouse medullary (mTALH) and cortical (cTALH) thick ascending limbs of Henle to evaluate the cell volume responses of these nephron segments to sudden increases in peritubular osmolality and to assess the role of
antidiuretic hormone
(
ADH
) and net NaCl absorption on hypertonic volume regulation. In the absence of CO2/HCO3- in external media, the cells of the mTALH behaved in a simple osmometric fashion, with an osmotic space equivalent to 70-80% of the total cell volume. However, in CO2/HCO3- -containing media, the cells of the mTALH, but not the cTALH, were able to increase their cell volume to the original volume after shrinkage in peritubular media made hypertonic with either NaCl or mannitol. This volume-regulatory increase response (VRI) in the mTALH was mediated by an increase in intracellular osmoles, and required peritubular
ADH
, at concentrations that stimulate maximally the rate of net NaCl absorption. This
ADH
effect on VRI could be mimicked by addition of dibutyryladenosine 3',5'-cyclic monophosphate to the bath in the absence of hormone. However, 10(-4) M luminal furosemide, a concentration that abolishes
ADH
-dependent NaCl absorption in the mTALH, had no effect on the VRI response. These results indicate that the cells of the mTALH, but not the cTALH, are capable of hypertonic volume regulation, that
ADH
(via adenosine 3',5'-cyclic monophosphate) is required for expression of the VRI response in the mTALH, and that the effects of
ADH
on net NaCl absorption and the VRI response in the mTALH are completely dissociable. Thus these results are consistent with a role for
ADH
in hypertonic VRI in the mammalian mTALH, which may operate to maintain constant cell volume in this nephron segment during
antidiuresis
.
...
PMID:Hypertonic cell volume regulation in mouse thick limbs. I. ADH dependency and nephron heterogeneity. 301 18
The effects of N-(cyclopropylmethyl)-19-isopentylnororvinol hydrochloride (M320) on urine excretion by rats were investigated. Further studies, using rabbit isolated vas deferens, investigated its interactions with kappa-opiate receptors. The output of urine for a 2 h period after M320, administered subcutaneously to normally hydrated Long Evans rats, showed a bell-shaped dose-response relationship, the maximum effect occurring after 10 micrograms kg-1. Urinary retention contributed to but did not fully account for the weaker diuresis after high doses. Attenuation of the ascending portion of the dose-response curve to M320 occurred after 1 and 10 mg kg-1 but not 0.1 mg kg-1 of naltrexone intraperitoneally. M320 in low doses (3-10 micrograms kg-1) caused a small but significant increase in sodium excretion. M320 (30 micrograms kg-1) reduced both sodium and potassium excretion. M320 (10 micrograms kg-1 s.c.) did not increase the volume of urine voided in 2 h by Brattleboro rats showing diabetes insipidus, even when urine excretion was reduced to normal by 1 week of
vasopressin
replacement. The volume of urine voided in 4 h by Brattleboro rats was progressively reduced to zero by M320 (10-100 micrograms kg-1 s.c.). Urinary retention contributed to but did not account for this reduction. Plasma levels of immunoreactive arginine vasopressin (ir-AVP) were reduced in both normal and dehydrated Long Evans rats after doses greater than 1 microgram kg-1 M320 s.c. In vitro, M320 caused persistent inhibition of twitches of the electrically stimulated rabbit vas deferens (IC50 1.7 nM). 8 These data suggest that M320 has potent opioid agonist activity at K-receptors and at higher concentrations stimulates mu- receptors. In the rat, its activity on K-receptors is associated with diuresis and suppression of plasma
vasopressin
levels. The
antidiuresis
seen after high doses may be due to its activity on mu-receptors, possibly at a central site.
...
PMID:The effects of N-(cyclopropylmethyl)-19-isopentylnororvinol (M320), a potent agonist at kappa- and mu-opiate receptors, on urine excretion of rats. 302 50
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