UNIPROT:P01185 - FACTA Search

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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The acute administration of ANG II into the brain of experimental animals produces transient pressor effects, a marked increase in drinking, release of the antidiuretic hormone, increase in total peripheral resistance, a diuretic and natriuretic effect and an increase in sympathetic outflow. The chronic administration of ANG II into a cerebrolateral ventricle produces sustained pressor effects only if 0.9% sodium chloride solution is used as the drinking fluid. The hypertension is due to an increase in total peripheral resistance which appears to be due to an increase in intrinsic tone of vascular smooth muscle. In addition there was enhanced responsiveness of the vasculature to norepinephrine and ANG II and a decrease in reflex vasodilatation of the hind limb of ANG II treated dogs. The chronic elevation of ANG II in the CSF plus an increase in NaCl intake produces a low renin, sodium dependent, expanded volume hypertension. Data are presented suggesting that this model of hypertension is induced by the central release of an inhibitor of the Na+,K+-Pump.
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PMID:The central effects of the renin-angiotensin system. 328 Jan 70

Circulatory variables and hormone concentrations in arterial plasma were measured in six normal subjects during angiotensin II (ANG II) step-up infusion of 0.25 and 1.00 ng kg-1 X min. During the 1.00 ng kg-1 X min infusion ANG II plasma concentrations increased from 11 +/- 2 to 48 +/- 6 pg ml-1; i.e., similar to those obtained during acute hypotensive hypovolaemia in man. Mean arterial pressure increased (P less than 0.05) from a resting value of 89 +/- 3 to 97 +/- 5 mmHg. Heart rate and catecholamine concentrations did not change. Plasma aldosterone increased (P less than 0.05) from 36 +/- 4 to 77 +/- 10 pg ml-1 during the infusion. Plasma concentrations of vasopressin, adrenalin and pancreatic polypeptide did not change during the investigation. During the 0.25 and 1.00 ng kg-1 X min infusion subcutaneous blood flow decreased (P = 0.06) to 67 +/- 20 and 66 +/- 26%, respectively, of control. It is concluded that: (1) ANG II in physiological doses in man may augment the sympathetic activity on the circulatory system since compensatory decreases in heart rate or in plasma catecholamines were not observed during the increased arterial pressure; (2) ANG II does not induce a general decrease in vagal tone as plasma pancreatic polypeptide concentrations were unchanged; (3) the obtained plasma concentrations of ANG II do not stimulate the release of vasopressin to plasma; and (4) the threshold for reducing the subcutaneous blood flow is reached within relatively small increments in plasma ANG II.
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PMID:Angiotensin II attenuates reflex decrease in heart rate and sympathetic activity in man. 334 55

The role of histamine (H) and prostaglandins (PGs) in the renal vasoconstriction prompted by a 10-min intrarenal infusion of norepinephrine (NE, 0.2 micrograms), antidiuretic hormone (ADH, 10 mU), or angiotensin II (ANG II, 0.05 micrograms) was evaluated in anesthetized dogs (amounts are per min per kg). Renal blood flow (RBF, flow probe) decreased four- to fivefold during the 1st min of infusion with each agonist but then gradually returned toward base line. This "escape" was greatest with ADH, less with NE, and small with ANG II. There was a postinfusion reactive hyperemia (RH) only after NE; NE-RH was 4.26 +/- 0.75 (SE) ml/g. Meclofenamate (MFA) reduced NE-RH to 60 +/- 11% of control and decreased NE escape. The H1-receptor antagonist, chlorpheniramine (CP), decreased NE-RH to 24 +/- 5% of control and reduced NE escape. MFA slowed, but did not block, ADH escape and had little effect on ANG II escape. CP did not affect ADH or ANG II escape. The histidine decarboxylase inhibitor, p-toluenesulfonohydrazine, did not affect NE escape but decreased NE-RH to 22 +/- 6% of control. Bolus injections of ADH during a constant infusion of the hormone were not vasoactive, indicating a tachyphylaxis-like phenomenon; this was not found with ANG II or NE. Finally, the excretion of histamine-like material increased from a control value of 0.69 +/- 0.08 to 1.28 +/- 0.28 micrograms/min during NE-RH. These results indicate that NE releases histamine and PGs from the kidney and that PGs account, primarily, for NE escape, whereas histamine accounts, primarily, for NE-RH.
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PMID:Vasoconstrictor-induced changes in renal blood flow: role of prostaglandins and histamine. 335 83

Experiments were done in urethan-anesthetized rats to investigate the effect of plasma angiotensin II (ANG II) and hypernatremia on the excitability of subfornical organ (SFO) neurons projecting directly to paraventricular nucleus of the hypothalamus (PVH), supraoptic nucleus (SON), and nucleus medianus (NM). Extracellular recordings were made from 106 antidromically identified neurons in the SFO. The firing frequency of 53 (50%) was increased by the intracarotid infusion of ANG II and/or 0.5 M hypertonic NaCl. The intracarotid infusion of isotonic saline or the intravenous infusion of phenylephrine did not alter the discharge rate of these SFO neurons. Of 38 PVH projecting neurons, 21 (55%) responded to ANG II and/or hypertonic NaCl: 9 to ANG II only, 8 to hypertonic NaCl only, and 4 to both. Similarly, of 42 SON projecting neurons, 30 (71%) responded to ANG II and/or hypertonic NaCl: 10 to ANG II only, 15 to hypertonic NaCl only, and 5 to both. Finally, of 26 NM projecting neurons, one increased its firing frequency to ANG II and one other to 0.5 M NaCl. An additional eight SFO neurons were found to send collateral axons to both the PVH and SON (n = 6) and PVH and NM (n = 2): four responded in various combinations to intracarotid infusion of ANG II and 0.5 M NaCl. These data suggest that blood-borne ANG II and plasma hypernatremia can influence arterial pressure and the release of vasopressin from the neurohypophysis by altering the discharge rate of SFO neurons projecting to forebrain structures that contain magnocellular neurosecretory vasopressin neurons and neurons that are components of sympathoexcitatory pathways.
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PMID:Effects of plasma angiotensin II and hypernatremia on subfornical organ neurons. 336 4

To evaluate the roles for catecholamines in angiotensin II (ANG II)-induced vasopressin (AVP) release, we examined in conscious rats the effects of intraventricular (ivt) administrations of catecholamine antagonists on plasma AVP responses to ivt applications of its agonists and ANG II. Plasma AVP was determined by RIA using trunk blood collected after decapitation. Dopamine (0.15 mumol), phenylephrine (an alpha-adrenergic agonist, 0.15 mumol) or ANG II (48.2 pmol) augmented plasma AVP 90 sec after the injection, whereas after isoproterenol (a beta-adrenergic agonist, 0.15 mumol) plasma AVP was unaffected. The plasma AVP responses to both dopamine and ANG II were significantly (P less than 0.01) inhibited by haloperidol (a dopamine blocker, 0.15 mumol) given 10 min before administration of these agents. Pre-administration of phenoxybenzamine (an alpha antagonist, 0.15 mumol) which was confirmed to abolish the effect of phenylephrine, or propranolol (a beta antagonist, 0.15 mumol) did not block the effect of ANG II. Administration of haloperidol, phenoxybenzamine or propranolol alone was without effect on plasma AVP level. On the basis of these results, we concluded that ANG II-induced AVP secretion may be mediated and/or modulated by dopamine.
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PMID:Central effects of catecholamine antagonists on angiotensin-induced vasopressin secretion in conscious rats. 338 51

Cultured rat glomerular mesangial cells (MC) were evaluated as a tool for reliable electrophysiological measurements as well as for fluorimetric determinations of intracellular Ca++. They had a resting potential similar to that observed in cultured vascular smooth muscle cells (VSMCs), in VSMCs of mouse kidney arterioles, or in glomerular--presumably mesangial--cells of kidney slices. The comparison with the other cell types was carried out in order to look for features distinguishing them from these cells, e.g., active and passive electrical membrane properties or electrical membrane responses to vasoactive pharmacological agents. In MCs, as well as in the other cell types, the average membrane potential was approx. -50 mV. The vasoconstrictor peptides angiotensin II (ANG II) and arginine-vasopressin (AVP) caused depolarizations that could be blocked by the respective specific inhibitors of these compounds. The agonist-induced depolarizations have to be attributed, at least in part, to a Ca++ inward current. Norepinephrine, if any, had only a weak action upon MCs, whereas isoproterenol either did not influence the membrane potential or hyperpolarized the cells. Other substances tested, which had no influences upon the membrane potential, were neuropeptide Y and atriopeptin 3. As to their resting electrical properties and their responses to pharmacological agents, cultured mesangial cells did not differ from glomerular, i.e., most probably mesangial, cells in the kidney slice. The difference between mesangial cells and VSMCs consists in their reaction to noradrenaline. Whereas VSMCs respond with a marked depolarization, the noradrenaline effect upon MCs in culture and in the kidney slice is either absent or very weak. Repeated passage of the cells (more than six passages) led to a gradual loss of their responsiveness to the agonists, indicating reduced receptor expression which may be interpreted as dedifferentiation. This held for both cultured MCs and VSMCs. Fluorimetric measurements using the Ca++-specific indicators quin-2 and fura-2 were performed with a purpose-developed, ultrasensitive photon-counting microspectrofluorimeter. Individual MCs as well as isolated glomeruli responded to the vasoconstrictors ANG II and AVP with an increase in Ca++-dependent fluorescence indicating that these agents indeed depolarize the cells partly via a Ca++ influx and increase cytosolic free Ca++.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The mesangial cell culture: a tool for the study of the electrophysiological and pharmacological properties of the glomerular mesangial cell. 344 61

The effect of intraventricular perfusion with hypertonic saline (HS) or angiotensin II (ANG II) on cerebrospinal fluid (CSF) vasopressin (AVP), blood pressure and heart rate was determined in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. There was a marked reduction in the central peptidergic response in the SHR. Pretreatment with the AVP (V1) antagonist abolished the pressor response to intraventricular HS in the WKY rats, but not in the SHR.
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PMID:A reduction of central peptidergic responses in the spontaneously hypertensive rat. 346 97

1. The role of the sympathetic nervous system and the effect of vasopressin (AVP) on the hypotensive action of nifedipine (Nf) were evaluated in conscious, unrestrained normotensive and DOCA-salt hypertensive rats. 2. The hypotensive response to Nf was much greater in DOCA rats than in the controls. 3. Solitary blockade of the sympathetic nervous system or AVP, did not alter the Nf effect in either DOCA or control rats. However, a combination clearly diminished the effect of Nf in the DOCA group, but enhanced it in the controls. The inhibition of angiotensin II (ANG II) augmented the hypotensive effect of Nf in control animals, but not in the DOCA rats. The percentage fall in blood pressure with Nf was much the same in both groups after the combined inhibition of the sympathetic nervous system and AVP. 4. The enhanced hypotensive action of Nf in DOCA rats may be dependent on the hyperactivity of the sympathetic nervous system and AVP, which facilitates calcium influx, and in the normotensive animals the depressor response to Nf may relate to blockade of the calcium influx, independent of the sympathetic nervous system, AVP and ANG II.
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PMID:Influence of the sympathetic nervous system and vasopressin on the blood pressure lowering effect of nifedipine in deoxycorticosterone acetate-salt hypertensive rats. 365 32

The role of pathways from the subfornical organ (SFO) to the hypothalamic paraventricular nucleus (PVN) through the median preoptic nucleus (MnPO) in regulating the activity of putative vasopressin (VP)-secreting neurons in the PVN was examined in urethane-anesthetized male rats. The activity of the majority (79%) of SFO neurons antidromically identified as projecting to the MnPO was excited by microiontophoretically (MIPh) applied angiotensin II (ANG II) and the effect was blocked by MIPh-applied saralasin (Sar), an ANG II antagonist. Identified SFO neurons that were excited by MIPh-applied ANG II were also excited by intravenously administered ANG II. Electrical stimulation of the SFO produced orthodromic excitation (48%) or inhibition (24%) of the activity of MnPO neurons antidromically identified as projecting to the PVN. Identified MnPO neurons that were excited by SFO stimulation were also excited by MIPh-applied ANG II, while the remaining neurons were not affected. The excitatory responses to SFO stimulation and to MIPh-applied ANG II were both blocked by MIPh-applied Sar, whereas the inhibitory responses to SFO stimulation were not affected. ANG II injected into the region of the SFO produced either an excitation (55%) or no effect (45%) on the activity of identified MnPO neurons. Electrical stimulation of the MnPO produced orthodromic excitation (27%) or inhibition (23%) of the activity of putative VP-secreting PVN neurons. ANG II injected into the region of the MnPO produced either an excitation (31%) or no effect (69%) on the activity of putative VP-secreting PVN neurons.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Subfornical organ and hypothalamic paraventricular nucleus connections with median preoptic nucleus neurons: an electrophysiological study in the rat. 369 28

In mammals, intracranial or peripheral administration of angiotensin II (ANG II) has a number of actions, including the release of antidiuretic hormone (ADH). Relatively little is known of the interactions between the renin-angiotensin and ADH systems in birds. In the present study [Asp1, Val5]ANG II (fowl ANG II) was infused intravenously into conscious White Leghorn cockerels to determine whether peripheral ANG II influences the release of arginine vasotocin (AVT), the avian ADH. Cannulas were inserted into a wing artery and vein under local anesthesia. ANG II was dissolved in 0.154 M NaCl and administered intravenously at 0, 2, 20, and 200 ng X kg-1 X min-1. In a second series of experiments, ANG II was infused in 0.1 and 1.0 M NaCl (200 ng X kg-1 X min-1) to examine the effect of the peptide on osmotic release of ADH. In the three groups administered ANG II in 0.154 M NaCl, plasma AVT before intravenous infusion averaged between 1.8 +/- 0.46 to 2.6 +/- 0.30 microU/ml. In these birds, infusion of ANG II at 2, 20, and 200 ng X kg-1 X min-1 caused plasma AVT to increase over preinfusion means by 39, 78, and 300%, respectively. The changes in AVT occurred in the absence of differences in plasma osmolality, electrolyte composition, or arterial blood pressure among the groups. In chickens that were administered ANG II in 0.1 and 1.0 M NaCl, significantly higher plasma AVT levels were observed compared with a control group receiving the saline infusions alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Peripheral angiotensin II stimulates release of vasotocin in conscious chickens. 374 Mar 16

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