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)

To test the hypothesis that angiotensin II releases antidiuretic hormone (ADH) after injection into ventricular cerebrospinal fluid, conscious adult male Sprague-Dawley rats with a lateral cerebroventricular cannula received an intraventricular injection of 0, 10, 50, or 100 ng angiotensin II. Trunk blood was collected 90 seconds later for radioimmunoassay of ADH. Plasma ADH, pg/ml (mean plus or minus S. E.), for the four dose levels were 2.8 plus or minus 0.7, 9.6 plus or minus 2.5, 22.6 plus or minus 5.6 and 25.0 plus or minus 5.0, respectively. The increases produced by angiotensin were statistically significant (p smaller than 0.05). Plasma ADH of the 10 ng group was intermediate between control and the two highest angiotensin doses (p smaller than 0.05), suggesting a dose-response relationship. These data provide direct evidence that angiotensin releases ADH by central mechanisms.
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PMID:Release of vasopressin by angiotensin II. 23 17

Studies were designed to determine whether angiotensin II has a direct stimulatory effect on arginine-vasopressin in man and to determine the role, if any, played by angiotensin II in the control of vasopressin release in physiological and pathological conditions. Acute infusion of angiotensin II in normal volunteers produced small but definite increases in plasma levels of arginine-vasopressin (5-4+/-0-3(S.E.M.) to 6-4+/-0-2 pg/ml) only when plasma angiotensin II levels were supraphysiological. Concurrent measurements of plasma arginine-vasopressin and angiotensin II were made during acute changes in fluid balance and posture in normal volunteers and in clinical conditions characterized by high plasma levels of angiotensin II (Addison's disease and Bartter's syndrome). The results of these studies allow us to conclude that there is little to suggest a direct effect of angiotensin II which is likely to be relevant to the normal physiological control of arginine-vasopressin in man.
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PMID:Effects of angiotensin II on arginine-vasopressin in physiological and pathological situations in man. 30 1

This review provides a summary and assessment of research involving renal prostaglandins. Arachidonic acid released from phospholipids is converted by prostaglandin cyclo-oxygenase in the kidney to PGF2, PGF2alpha, PGD2, and, possibly, to PGI2 and thromboxane A2. Production of PGE2 and PGF2alpha is predominately but not exclusively in the medulla, whereas degradative enzymes are present in both cortex and medulla. Prostaglandins enter the tubular lumen by facilitated transport and are partially reabsorbed from the urine in the distal nephron. Urine prostaglandins probably reflect renal synthesis. PGE2 and endoperoxides stimulate and PGF2alpha and indomethacin inhibit renal renin synthesis. In response to ischemia, vasoconstriction, or angiotensin II the kidney increases prostaglandin synthesis to modulate renal vascular resistance. In conscious animals or man no role has been established for prostaglandins in the maintenance of basal renal blood flow or renal sodium excretion. PGE influences renal water excretion by inhibiting the action vasopressin. Despite conflicting data there is evidence that renal prostaglandins are involved either primarily or secondarily in many types of hypertension. Inhibitors of prostaglandin cyclooxygenase have been used with success in Bartter's syndrome. Conflicting results in many areas of investigation may be resolved by the use of more accurate and reliable assays, careful handling of samples, and the use of urine to further investigate renal prostaglandin synthesis.
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PMID:Prostaglandins and the kidney. 33 46

Production, transport, storage and release of antidiuretic hormone (ADH) in the hypothalamo-neurohypophysial system were investigated. ADH produced by nerve cells in the paraventricular and supraoptic nuclei of the hypothalamus is present in a form bound to the specific protein neurophysin, in the neurosecretary granula. Electric and chemical stimulation of these nuclei results in evoked release of ADH in ionic association with neurophysin from the neural lobes. Acetylcholine, norepinephrine, histamine, angiotensin II, gamma-aminobutyric acid and L-glutamic acid have been regarded as candidates of chemical transmitters for the release of ADH in the hypothalamus. Prostaglandin (PG) E2 may be another important compound for central regulation of water metabolism. The possibility that PGE2 may be the transmitter or a modulator in the nuclei has to be considred. Serotonin, dopamine and taurine, however, may not be involded in the ADH releasing mechanisms in the hypothalamus. It appears that norepinephrine, histamine, angiotensin II, PGE2 and bradykinin stimulate directly the neural lobe to release ADH. The ADH release is regulated by intracellular Ca++. The existence of a "readily-releasable pool" of ADH can be ruled out and any limitation in the amount of ADH released under experimental conditions may be due to insufficient activation of the neural lobe. A physiological significance other than a carrier was proposed for neurophysin.
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PMID:[The hypothalamo-neurohypophysial system and antidiuretic hormone (author's transl)]. 33 45

Angiotensin II is dipsogenic, and vasopressin (ADH) regulates renal water excretion. Together, these hormones govern overall mammalian water balance. The Brattleboro rat with inherited diabetes insipidus (DI) lacks ADH and is therefore a convenient model with which to elucidate mechanisms regulating water metabolism. In the present studies, angiotensin II has also been removed from DI rats by the administration of an inhibitor (captopril, SQ 14225; D-2-methyl-3-mercaptopropanoyl-L-proline) of the enzyme which converts angiotensin I, the relatively inert component of the renin-angiotensin system, to angiotensin II, the biologically active substance. SQ 14225 reduced the drinking rates, and after 6 days lowered peripheral plasma aldosterone concentrations were associated with hyperkalaemia. We conclude that the polydipsia of diabetes insipidus partly results from elevated plasma renin activities and angiotensin II concentrations seen in this syndrome. Further, the apparent hypoaldosteronism of DI Brattleboro rats reflects differences in both tissue usage of the steroid and adrenocortical sensitivities associated with polyuria, hyperosmolarity and possibly potassium wasting.
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PMID:Captopril (SQ 14225) depresses drinking and aldosterone in rats lacking vasopressin. 38 37

The action of prostacyclin (PGI2) on arterial pressure, heart rate, plasma concentration of angiotensin II and vasopressin was studied in groups of normal, renal hypertensive and DOC hypertensive rats. PGI2 was given by continuous iv. infusion at successive doses of 0.25, 0.5 and 1.0 microgram/kg x min, each rate for one hour. Arterial pressure was reduced to normal or below normal in the hypertensive rats, though the fall of blood pressure was greatest in the DOC hypertensive animals. Mean arterial pressure at the end of infusion was 89 mm Hg for normal rats, 87 mm Hg for renal hypertensive rats and 69 mm Hg for DOC hypertensive rats. Diastolic pressure fell more than systolic pressure suggesting a vasodilator mechanism. Heart rate was reduced significantly at the end of the infusion in the three groups of rats. Prostacyclin was also infused for 3 hours at a constant rate of 0.5 microgram/kg x min. The arterial pressure lowering effect was maintained throughout the infusion period.
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PMID:The vasodepressor action of prostacyclin (PGI2) and its effect on plasma angiotensin II and vasopressin in unanaesthetized normotensive and hypertensive rats. 39 17

The dose-response relationship of the mesenteric resistance vessels to vasopressin was studied in anesthetized laparotomized cats before and after hypophysectomy and again during the plateau phase of the response to a prolonged infusion of [Sar1-Ala8] angiotensin II (saralasin), a competitive antagonist of angiotensin II. Hypophysectomy and saralasin each caused an increase in superior mesenteric arterial conductance. Before hypophysectomy infusion of 0.5 mU/(min.kg) of vasopressin caused mesenteric conductance to decrease from 0.168 to 0.156 ml/(min.kg.mmHg), a change of only 0.012 units. After hypophysectomy, the same dose reduced conductance from 0.227 to 0.179 mU/(min.kg.mmHg), a change of 0.048 units. During the plateau phase of the response to saralasin, 0.5 mU/(min.kg) of vasopressin reduced conductance from 0.281 to 0.201 ml/(min.kg.mmHg), a change of 0.079 units. Hypophysectomy and saralasin had little effect on the mesenteric vasoconstrictor response to high doses of vasopressin (2.0-10 mU/(min.kg). The ineffectiveness of low doses of vasopressin on the mesenteric resistance vessels of the intact anesthetized, surgically stressed animal may be due in part to the already constricted state of the bed caused by endogenous vasopressin and angiotensin and in part due to an opposing vasodilator influence, the reflex withdrawal of the vasoconstrictor effect of endogenous vasopressin.
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PMID:Hypophysectomy and saralasin on mesenteric vasoconstrictor response to vasopressin. 42 Mar 2

The effect of furosemide on plasma renin, vasopressin (AVP), and aldosterone concentrations was studied in 10 control and 6 nephrectomized lambs during the 1st 2 wk of life. In a separate study in 10 newborn lambs, 1-sarcosine-8-alanine-angiotensin II (saralasin acetate, 5 mug/kg per min) was infused alone for 40 min, after which furosemide 2 mg/kg i.v. was injected in association with continuing saralasin acetate infusion. Plasma renin activity increased from a mean (+/-SEM) of 21.3+/-3.4 ng/ml per h in the 10 control lambs to 39.4+/-8.2 ng/ml per h at 8 min (P < 0.001) and remained high through 120 min after furosemide. Plasma AVP and aldosterone concentrations increased from respective mean values of 2.1+/-0.4 muU/ml and 12.8+/-2.5 ng/dl to 9.8+/-2.0 muU/ml (P < 0.01) and 23.0+/-7.7 ng/dl (P < 0.05) at 35 min and 13.8+/-2.1 muU/ml and 23.0+/-4.4 ng/dl at 65 min after furosemide (each P < 0.01). There was an insignificant AVP response in the 10 lambs treated with angiotensin inhibitor: from a mean base line of 4.7+/-0.9 to 8.3+/-2.0 muU/ml at 35 min, and 7.4+/-2.0 muU/ml at 65 min after furosemide. There was no increase in AVP in the anephric lambs. The mean increment AVP response from base line in the newborn lambs without saralasin, Delta 10.8+/-2.0 muU/ml, was greater than in the lambs with saralasin, Delta4.0+/-1.9 (P < 0.05), and greater than in the anephric lambs, Delta3.3+/-2.1 muU/ml (P < 0.05). The mean blood pressure fell 6 mm Hg in the 10 control lambs (P < 0.05), 7 mm Hg in the anephric lambs (P < 0.05), and 16 mm Hg in the lambs treated with angiotensin inhibitor (P < 0.05) by 35 min after furosemide. However, the changes in plasma AVP were not related to the fall in blood pressure. These data support the view that the observed AVP response to furosemide in the newborn lamb was mediated through the renin-angiotensin system.
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PMID:Endogenous angiotensin stimulation of vasopressin in the newborn lamb. 42 54

In unanesthetized water-loaded rats, intracerebroventricular (IVT) angiotensin II (AII) injections produce centrally mediated pressor effects and antidiuresis. Experiments were performed to evaluate the role of antidiuretic hormone (ADH) release versus neurogenic mechanisms in the antidiuretic responses to central AII median eminence lesions used to block ADH release abolish antidiuretic effects but only attenuated pressor responses to IVT AII infusions. Pretreatment with an intravenous infusion of ADH antibody had a similar effect. Central administration of AII in water and saline-loaded rats produced no change in effective renal plasma flow or glomerular filtration rate, Natriuretic and kaliuretic responses to IVT AII injections were similar to those observed to intravenous ADH infusions. These data are consistent with the suggestion that antidiuresis and osmotic excretion observed after IVT AII injections in the rats are the result of ADH release, and that neurogenic mechanisms play a major role in the blood pressure but not in the antidiuretic responses.
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PMID:Central effects of angiotensin II in water and saline loaded rats. 44 May 32

Ablation of anteroventral third ventricle (AV3V) periventricular tissue renders animals temporarily adipsic with no compensatory change in urine volume or concentration. The present experiment was designed to determine whether lesions of the AV3V region attenuate vasopressin (AVP) release in response to intraventricular (ivt) injections of angiotensin II (AII), hypertonic NaCl, and phenylephrine during the adipsic period. Blood pressure, urine conductance, and urine flow rate were monitored in awake, unrestrained animals during a continuous intravenous hydrating infusion. Changes in blood pressure and urine parameters were recorded following ivt injections of 100 ng AII, 500 ng AII, 1 microliter 3% NaCl, and 50 microgram phenylephrine. In addition, a radioimmunoassay (RIA) measured AVP following 500 ng AII ivt in lesioned and nonlesioned animals. Antidiuretic and pressor responses to ivt AII were attenuated after AV3V lesions. In addition, RIA analysis showed a significantly smaller concentration of AVP in lesioned animals following AII injections. These data suggest that the AV3V region is important for AVP release in response to central AII and osmotic stimuli.
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PMID:Anteroventral third ventricle lesions reduce antidiuretic responses to angiotensin II. 44 16


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