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)

Glomerular visceral epithelial cells (podocytes) undergo flattening and spreading of major processes detectable by scanning electron microscopy in early postischemic acute renal failure in both animals and man. The authors examined the kinetics of development of these epithelial cell changes in the renal pedicle-clamping model of ischemic renal failure in the rabbit. They found that these changes develop progressively, increasing with increasing length of ischemia, and occur while the pedicle clamp is still in place. To assess the possible role of angiotensin II and vasopressin in producing the epithelial changes, the authors compared glomerular morphology before and during pedicle clamping in hydrated rabbits and in dehydrated rabbits. Dehydration alone produced changes in glomerular epithelial cells comparable to those seen in the postischemic kidney. The angiotensin-converting enzyme inhibitor captopril did not prevent the podocyte changes in either group. In vitro incubation studies confirmed that both angiotensin II and vasopressin produce glomerular epithelial cell changes with a threshold between 10(-7) M and 10(-8) M, a concentration that may be physiologically significant for angiotensin II, which is synthesized at the glomerulus and may have local paracrine effects. Such local synthesis may not be inhibited by systemic administration of captopril. Angiotensin II may play a role in producing podocyte alterations during renal ischemia, as well as in the dehydrated state.
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PMID:Glomerular epithelial cell changes after ischemia or dehydration. Possible role of angiotensin II. 669 12

Thromboxane B2 (TxB) is excreted in human urine, but the mechanism of renal excretion and the quantitative relationship of urinary TxB to the active parent compound, thromboxane A2, of renal or extrarenal origin is not established. To determine the effects of vasoactive hormones, uricosuric agents and urinary flow rate on TxB excretion, urinary TxB was measured by radioimmunoassay and mass spectrometry, and renal metabolism of blood TxB was determined by radiochromatography of urine after i.v. [3H]-TxB infusions. Basal TxB was 6.7 +/- 1.1 ng/h during an oral water load, and TxB fell with s.g. antidiuretic hormone (to 3.4 +/- 0.4 ng/h, P less than 0.01) and with fluid restriction (to 2.6 +/- 0.5 ng/hr, P = 0.001) in parallel with urinary volume. Urinary excretion of unmetabolized [3H]-TxB also fell (by 56%) with fluid restriction, implicating altered metabolism rather than synthesis as the mechanism of the urinary flow effect. Angiotensin II infusions slightly reduced both TxB and urine volume, consistent with a flow effect. In contrast, probenecid did not alter urine volume, but increased urinary uric acid (by 244%), TxB (from 5.6 +/- 0.9 to 11.1 +/- 2.9 ng/h) and urinary excretion of blood [3H]-TxB (by 243%) by similar amounts (all P less than 0.05), suggesting that TxB is actively reabsorbed in the proximal tubule, similarly to uric acid. Thus, urinary excretion of TxB of renal and extrarenal origin is regulated by proximal and distal tubule factors.
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PMID:Regulation of urinary thromboxane B2 in man: influence of urinary flow rate and tubular transport. 671 53

The effect of leucine5 -enkephalin on angiotensin II (AII)-stimulated release of oxytocin and vasopressin (VP) was investigated in the conscious male rat. Changes in the plasma concentration ([]) of both oxytocin and VP were measured in animals: (1) 60 s after intracerebroventricular (i.v.t.) administration of either artificial cerebrospinal fluid (CSF) or CSF with AII (10, 50, 100 ng/5 microliter); (2) 30, 60, 90 and 300 s after single injection of AII (50 ng/5 microliter; i.v.t.) or CSF and (3) 60 s after AII (50 ng/5 microliter) or CSF in animals pretreated with leucine5 -enkephalin (100 ng/5 microliter; i.v.t.) or CSF (5 microliter). Oxytocin and VP were quantified by radioimmunoassay and values corrected for 100% recovery. The development of a sensitive radioimmunoassay for oxytocin is described. The antiserum for oxytocin enabled detection of greater than or equal to 0.8 pg/ml oxytocin with cross-reactivity of 0.01% with arginine vasopressin and 0.10% with arginine vasotocin. The inter- and intra-assay coefficients of variation were 3-9% and 3.2%, respectively. The hypotheses being tested were that i.v.t. injection of AII stimulates release of both neurohypophysial hormones non-selectively and that leucine5 -enkephalin inhibits both AII-stimulated oxytocin and VP release. Angiotensin II at doses ranging from 10 to 100 ng/5 microliter, i.v.t. increased the plasma concentration of both oxytocin and VP. Plasma levels of both neurohypophysial hormones were elevated 30 s after AII administration i.v.t. and remained elevated 300 sec later.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enkephalin inhibition of angiotensin-stimulated release of oxytocin and vasopressin. 672 45

Chronotropic responses to angiotensin I and angiotensin II, vasopressin and bradykinin were measured in guinea pig isolated right atria. Angiotensin II (100-30,000 pg/ml) was slightly more potent than angiotensin I and caused a maximum tachycardia of 30-40 b/min; only 20% of the maximum response to (--)-noradrenaline. Propranolol (1 micro M) or reserpine pretreatment (1 mg/kg i.p., 24 h) did not alter the response to angiotensin II or bradykinin. Converting enzyme inhibition by captopril (10 micrograms/ml) did not affect resting rate nor the response to angiotensin II but shifted the location of the angiotensin I curve by 40 fold to the right. Bradykinin (5-500 ng/ml) caused small increases in rate while vasopressin 1-100 ng/ml was completely without effect. These results suggest that angiotensin II has a small positive chronotropic effect that is not dependent on tissue noradrenaline release or beta-adrenoceptors and that tissue converting enzyme is active in right atria. Relatively high concentrations of angiotensin and bradykinin were required to directly stimulate the sino-atrial node compared with plasma levels measured during physiological stimuli. Therefore these effects on atria are probably of little physiological significance for peptide concentrations in plasma but may be important in relation to local tissue generation of angiotensin II.
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PMID:Chronotropic effects of angiotensin I, angiotensin II, bradykinin and vasopressin in guinea pig atria. 674 32

Rats with electrolytic lesions of the tissue surrounding the third ventricle (AV3V) of the hypothalamus exhibit hypernatremia and chronic drinking deficits in response to hypertonic NaCl. These findings are suggestive of impaired osmoreception. The organ-cultured rat hypothalamo-neurohypophyseal system (HNS) previously has been shown to release vasopressin (VP) in response to osmotic stimuli. The ventral portion of the region damaged by AV3V lesions is included in the HNS explant. Thus, these studies were initiated to evaluate the ability of HNS explants which were obtained from rats previously prepared with AV3V lesions to respond to an increase in osmolality, acetylcholine, or angiotensin II with an increase in VP release. Following electrolytic ablation of the AV3V region or sham lesions and a 2-week recovery period, HNS explants were removed from rats with sham or AV3V lesions. The explants were maintained in organ culture for 4 days. On the third day in culture, increasing the osmolality of the culture medium from 295 to 315 mosm/kg H2O by the addition of NaCl resulted in a 2.5-fold increase in VP release from the explants with sham lesions, but did not significantly alter VP release from the explants with AV3V lesions. On the subsequent day in culture, acetylcholine (10(-5) M) stimulated VP release from the explants with AV3V lesions as well as the explants with sham lesions. Angiotensin II (10-5 M) also stimulated VP release from explants obtained from rats with both AV3V and sham lesions. These data suggest that the osmoreceptors which are involved in controlling VP release from the organ cultured HNS may be located in the region of the AV3V.
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PMID:Effect of anteroventral third ventricle lesions on vasopressin release by organ-cultured hypothalamo-neurohypophyseal explants. 688 61

Using newly develop radioimmunoassay for 6-keto-prostaglandin F1 alpha and 6,15-diketo-13,14-dihydro-prostaglandin F1 alpha, the plasma concentrations of these two prostacyclin derivatives were measured in anaesthetized cats. After the administration of angiotensin II, which releases prostacyclin into the circulation, concentrations of both derivatives rose simultaneously, the major immunoreactivity being 6,15-diketo-13,14-dihydro-prostaglandin F1 alpha. Angiotensin II-induced prostacyclin release was not caused by vasoconstriction alone, since comparable vasopressor responses to noradrenaline and vasopressin were not accompanied by increases in prostacyclin plasma levels. Injection of exogenous prostacyclin resulted in a shortlasting peak of 6-keto-prostaglandin F 1 alpha, which rapidly declined (t 1/2: 1.29-1.52 min). 6,15-diketo-13,14-dihydro-prostaglandin F1 alpha appeared with an t 1/2 of 0.48-1.38 min and was eliminated with a t 1/2 of 8.0-9.0 min. Due to its longer half-life in the circulation 6,15-diketo-13,14-dihydro-prostaglandin F 1 alpha again was the predominant derivative after 3 min. These data suggest that in vivo prostacyclin is mainly inactivated by the 15-hydroxy-PG-dehydrogenase-, delta 13-reductase-pathway, rather than by hydrolysis. Therefore, 6,15-diketo-13,14-dihydro-prostaglandin F1 alpha seems to be a better indicator of prostacyclin plasma levels than 6-keto-prostaglandin F1 alpha, although under certain conditions the additional determinations of this product of hydrolysis can be valuable.
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PMID:Formation and elimination of prostacyclin metabolites in the cat in vivo as determined by radioimmunoassay of unextracted plasma. 703 51

The effect of the dopamine antagonist, haloperidol, on arginine-vasopressin (AVP) release induced by angiotensin II was studied in six dehydrated conscious dogs. Angiotensin II (10 ng/kg per min) alone caused a twofold increase (P less than 0.05) in plasma AVP concentration, a 25 mmHg increase (P less than 0.01) in mean arterial blood pressure (ABP) and a 70% decrease (P less than 0.01) in plasma renin activity (PRA). In the presence of haloperidol (3 micrograms/kg per min), angiotensin II caused similar changes in mean ABP (25 mmHg; P less than 0.01) and PRA (-65%, P less than 0.01), but a small insignificant decrease in plasma AVP (-22%). The AVP response to angiotensin II in the presence of haloperidol was significantly (P less than 0.05) different from its response to angiotensin II alone. Neither haloperidol alone nor the two vehicles had any effect on plasma AVP or mean ABP but PRA dropped slightly. The results suggest that a dopaminergic mechanism may be involved in angiotensin II-induced AVP release.
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PMID:Role of dopamine in the angiotensin II-induced vasopressin release in the conscious dehydrated dog. 705 Feb 80

Rat medial basal hypothalami were superfused in vitro. The effect of angiotensin II on vasopressin outflow was investigated. Angiotensin II (10 nM or 1 microM, added to the superfusion medium) increased the veratridine-evoked vasopressin release. The higher concentration also slightly elevated the basal outflow. The effect of angiotensin II was blocked by saralasin. We conclude that angiotensin II can act on the median eminence and/or on the stump of the pituitary stalk to promote the release of vasopressin, which then may influence anterior pituitary hormone secretion.
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PMID:Vasopressin release from rat medial basal hypothalamus induced in vitro by angiotensin. 710 81

The supraoptic-hypophyseal tract is a primary system for the synthesis and release of vasopressin. Angiotensin II (AII) has been shown to release vasopressin when injected into the cerebral ventricles (IVT). However, intravenous (IV) AII injections have not produced consistent results. The present studies were conducted to examine the effects of AII delivered by either route on the unit activity of supraoptic nucleus (SON) magnocellular neurons. Rats were prepared with intracranial cannulas to insure delivery of drugs to the left lateral ventricle and with polyethylene catheters in the left jugular vein, femoral vein, and femoral artery for systemic injections and arterial pressure recordings. A ventral approach permitted recording from the SON without violating the ventricular-SON partition. Magnocellular neurons were electrophysiologically identified. In the majority of identified cells, IVT AII increased activity. In others pressor doses of AII IV inhibited firing while blood pressure was elevated. After sino-aortic denervation, AII IV excited SON neurons. Based on latency, and the fact that lesioning the anteroventral third ventricle blocked the action of AII IVT, the results indicate that AII IVT acts on a periventricular site to influence SON magnocellular neurons. Furthermore, systemic AII may have two effects on SON neurons: a central excitatory action, and an inhibition due to a baroreceptor reflex.
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PMID:Two possible actions for circulating angiotensin II in the control of vasopressin release. 712 77

The further role of vasopressin in the pathogenesis of hypertension was studied in two different types of hypertensive rats in which the intravenous injection of a vasopressin antiserum reduced arterial blood pressure substantially. The increased secretion of vasopressin was demonstrated in deoxycorticosterone acetate (DOCA)-salt hypertensive and spontaneously hypertensive rats with high salt intake. Angiotensin II binding of the brain receptor which has been postulated to modify osmotically stimulated vasopressin release from neurohypophysis was not affected by sodium balance in these types of hypertensive rats, whereas the decrease in the brain receptor binding of angiotensin II was observed in the control rats. The lack of the adjusting control system in the brain angiotensin II receptors for sodium balance may be, at least in a part, responsible for the enhancement of vasopressin secretion in the hypertensive rats compared to that in the control rats with high salt intake. Since pressor responsiveness to vasopressin was increased in the rats with DOCA-salt hypertension, vasopressin may function as a direct pressor agent in the maintenance of high blood pressure in this type of hypertension.
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PMID:The importance of vasopressin in the mechanism maintaining hypertension in the rat. 730 21


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