Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The elimination from plasma of the peptide hormones vasopressin (VP) and atrial natriuretic peptide (ANP) as well as the time course of release and elimination of these hormones after a physiological stimulus were studied in anesthetized rabbits. As an inverse relationship was found to exist between carotid sinus pressure and plasma IR-ANP, a decrease in carotid sinus pressure to 60 mm Hg was used to stimulate ANP as well as VP release. The elimination of VP after iv injection involved a rapid initial phase and a slow late component, with corresponding half-life (t1/2) values of 0.9 and 5.4 min, respectively. After reduction of carotid sinus pressure to 60 mm Hg, plasma VP increased significantly within 1 min and reached a maximum at 10 min. When carotid sinus pressure was increased to 160 mm Hg to inhibit VP release, the t1/2 of VP was 1.3 min. The t1/2 of immunoreactive (IR) ANP after iv infusion was 1.2 min. Plasma IR-ANP was significantly increased 2 min after carotid sinus pressure was decreased, and a maximum was observed at 10 min. The t1/2 of IR-ANP after elevation of carotid sinus pressure to 160 mm Hg was 3.2 min. These studies indicate that both VP and IR-ANP are rapidly eliminated in the anesthetized rabbit.
 ...
PMID:Pharmacokinetics of vasopressin and atrial natriuretic peptide in anesthetized rabbits. 252 Dec 8

The influence of aortic baroreceptors and vagal afferent nerves on the release of immunoreactive vasopressin (iVP) and immunoreactive atrial natriuretic factor (iANF) was examined in anaesthetized rabbits. Changes in plasma concentrations of iVP and iANF, heart rate, mean arterial pressure, and right atrial pressure were measured in response to blood volume changes (+20, +10, -10, -20%). Carotid sinus pressure was maintained at 100 mmHg (1 mmHg = 133.3 Pa), and blood volume changes were performed before and after bilateral vagotomy (VNX) in all experiments. Two experimental groups were studied: rabbits with aortic depressor nerves intact (ADNI) and those with aortic depressor nerves sectioned (ADNX). Mean arterial and right atrial pressures decreased during haemorrhage and increased in response to volume expansion. Plasma iVP concentrations increased with haemorrhage and decreased with volume expansion in the ADNI group. Plasma iANF, however, decreased with haemorrhage and increased during volume expansion in both ADNI and ADNX groups. Vagotomy caused an increase in baseline plasma iANF in the ADNX group. The responses of iANF to blood volume changes were augmented after VNX and ADNX. The results show that neither the aortic baroreceptor nor the vagal afferent input are needed for the iANF response to changes in blood volume, over the range of +/- 20%. In contrast, intact aortic baroreceptors are essential for changes in circulating iVP in this preparation.
 ...
PMID:Plasma vasopressin and atrial natriuretic factor in response to blood volume changes in the anaesthetized rabbit. 252 82

1. The changes in plasma concentrations of immunoreactive vasopressin (iVP) and atrial natriuretic factor (iANF) in response to haemorrhage (10-30% blood volume) were measured in 10 anaesthetized rabbits before and after cardiac receptor denervation (vagal nerve section). Carotid sinus pressure was maintained constant (60 mmHg) to eliminate any changing input from carotid baroreceptors. 2. Haemorrhage increased iVP before and after vagal nerve section indicating that withdrawal of input from aortic baroreceptors may have contributed to the increase in iVP. 3. Section of the vagus nerves attenuated the iVP response to haemorrhage. 4. There was no correlation between release of iVP and iANF. 5. Haemorrhage decreased iAF before and after vagal nerve section. Section of the vagus nerves increased iANF. Plasma iANF was highly correlated with atrial pressure and mean arterial pressure suggesting iANF release was secondary to changes in cardiac haemodynamics.
 ...
PMID:Plasma vasopressin and atrial natriuretic factor during haemorrhage: influence of cardiac and aortic receptors. 255 49

The arterial baroreceptors are known to influence the release of vasopressin, but the quantitative relationship between baroreceptor stimulation and plasma vasopressin concentration has not been defined. These experiments examine the effect of stepwise changes in carotid sinus pressure (40-160 mmHg) on the plasma concentration of vasopressin in chloralose-urethan anesthetized rabbits. Plasma vasopressin concentration (9.2 +/- 1.2 pg/ml, n = 27) did not change in response to changes in carotid sinus pressure when the aortic depressor nerves were intact. These results were unaltered by bilateral cervical vagotomy. However, after aortic depressor nerve section, decreases in carotid sinus pressure were associated with increases in plasma vasopressin concentration. There appeared to be a greater redundancy in the baroreceptor control of plasma vasopressin than in the baroreceptor control of arterial pressure or heart rate. The results provided no evidence that receptors with vagal afferents have a tonic influence on the baroreceptor control of vasopressin release in the anesthetized rabbit.
 ...
PMID:Carotid sinus pressure and plasma vasopressin in anesthetized rabbits. 318 79

Our data indicate that vasopressin facilitates baroreflex inhibition of lumbar sympathetic nerve activity by two mechanisms: it sensitizes baroreceptors locally and shifts the stimulus-response curve so that a lower carotid sinus pressure results in a certain level of reflex sympathetic inhibition; it also produces a corresponding shift when given i.v. and excluded from baroreceptors implicating a second, central mechanism for facilitation of baroreflexes. In contrast, angiotensin II attenuates baroreflex inhibition of peripheral sympathetic function and this is accounted for totally by a central action. Why these differences occur present challenging new questions for future investigation.
 ...
PMID:Different effects of vasopressin and angiotensin II on baroreflexes. 398 16

The purpose of this study was to determine if there is an interaction between carotid baroreceptors (CBR) and cardiopulmonary receptors with vagal afferents (CPVA) in the control of plasma vasopressin (ADH). Changes in ADH (radioimmunoassay) in the superior vena cava were determined in 13 chloralose-anesthetized dogs with aortic nerves sectioned during concomitantly induced changes in CBR and CPVA input. CBR input was changed by altering pressure (CSP) in the isolated perfused sinuses. Carotid sinus pressure (CSP) was initially set at 50 mmHg. The CPVA input was reversibly interrupted by cooling the vagi to 0 degrees C while CSP was concomitantly increased to 135 or 200 mmHg or was held constant at 50 mmHg. Vagal cold block (VCB) with CSP held constant at 50 mmHg resulted in large increases in arterial pressure and plasma vasopressin. Increases in CSP to 200 mmHg resulted in significant decreases in arterial pressure and in plasma vasopressin despite concomitant VCB. VCB and concomitant increase in CSP to 135 mmHg resulted in a significant fall in arterial pressure, whereas plasma vasopressin tended to increase. Thus, the influence on arterial pressure of raising CSP to 135 mmHg exceeds that of VCB. In contrast, the influence of VCB on ADH equals or exceeds that of raising CSP to 135 mmHg. These differential responses of arterial pressure and plasma ADH suggest an interaction between CBR and CPVA in the control of ADH and arterial pressure.
 ...
PMID:Interaction between carotid and cardiopulmonary baroreflexes in control of plasma ADH. 728 51

The purpose of the experiments was to investigate the effect of changes in carotid sinus baroreceptor stimulation on plasma vasopressin (AVP) at different plasma osmolalities in the anesthetized artificially ventilated rabbit. Both carotid sinuses were isolated and perfused with blood at servo-controlled pressures. The vagus and aortic depressor nerves were sectioned bilaterally to eliminate input from atrial and aortic arch baroreceptors. Saline (0.3%, wt/vol) was infused to lower plasma osmolality, and 5% saline was infused to raise plasma osmolality. At three plasma osmolalities, the carotid sinus pressure (CSP) was changed from 100 mmHg to 40 and 140 mmHg and returned to 100 mmHg. There were no changes in plasma AVP in response to changes in CSP at low plasma osmolality (289 mosmol/kgH2O), but at medium (309 mosmol/kgH2O) and high (323 mosmol/kgH2O) osmolality, plasma AVP was higher at 40 than at 140 mmHg CSP. The relationship between plasma AVP and plasma osmolality was expressed as a linear regression at each CSP. Changes in CSP changed the sensitivity but not the threshold of the osmotic control of AVP release.
 ...
PMID:Regulation of plasma vasopressin by plasma osmolality and carotid sinus pressure in anesthetized rabbits. 816 Aug 73

To investigate the interaction between arginine vasopressin and the carotid sinus baroreflex, hemodynamic responses to bilateral carotid occlusion and to controlled reductions in carotid sinus pressure were examined. In the control state and during vasopressin infusion in conscious rabbits, mean arterial pressure, heart rate, mean aortic flow and total peripheral resistance were measured. Vasopressin infusion at 5 or 10 ng/kg/min did not raise arterial pressure, but increased resistance, and decreased heart rate and aortic flow in a dose-dependent manner. The pressure and resistance responses to carotid occlusion or changes in carotid pressure were not altered by vasopressin. The heart rate response was augmented significantly from 23 +/- 5 (mean +/- S.E.) to 40 +/- 8 and 43 +/- 8 beats/min with infusion of 5 and 10 ng/kg/min of vasopressin. Vasopressin did not augment the gain of carotid sinus reflex control of arterial pressure (3.7 +/- 0.5 in control and 3.5 +/- 0.5 during 5 ng/kg/min of vasopressin). With vasopressin infusion at 5 ng/kg/min, following vagal blockade with methylatropine both the arterial pressure and the heart rate responses to carotid pressure changes decreased to 73% and 32% of the response before blockade. The data indicate that vasopressin has little effect on control of arterial pressure by the carotid sinus baroreflex in conscious rabbits when vagal responses are activated.
 ...
PMID:Effects of vasopressin on the response to carotid occlusion in conscious rabbits. 822 61

The physicochemical properties of water enable it to act as a solvent for electrolytes, and to influence the molecular configuration and hence the function--enzymatic in particular--of polypeptide chains in biological systems. The association of water with electrolytes determines the osmotic regulation of cell volume and allows the establishment of the transmembrane ion concentration gradients that underlie nerve excitation and impulse conduction. Fluid in the central nervous system is distributed in the intracellular and extracellular spaces (ICS, ECS) of the brain parenchyma, the cerebrospinal fluid, and the vascular compartment--the brain capillaries and small arteries and veins. Regulated exchange of fluid between these various compartments occurs at the blood-brain barrier (BBB), and at the ventricular ependyma and choroid plexus, and, on the brain surface, at the pia mater. The normal BBB is relatively permeable to water, but considerably less so to ions, including the principal electrolytes Brain fluid regulation takes place within the context of systemic fluid volume control, which depends on the mutual interaction of osmo-, volume-, and pressure-receptors in the hypothalamus, heart and kidney, hormones such as vasopressin, renin-angiotensin, aldosterone, atriopeptins, and digitalis-like immunoreactive substance, and their respective sites of action. Evidence for specific transport capabilities of the cerebral capillary endothelium, for example high Na+K(+)-ATPase activity and the presence at the abluminal surface of a Na(+)--H+ antiporter, suggests that cerebral microvessels play a more active part in brain volume regulation and ion homoeostasis than do capillaries in other vascular beds. The normal brain ECS amounts to 12-19% of brain volume, and is markedly reduced in anoxia, ischaemia, metabolic poisoning, spreading depression, and conventional procedures for histological fixation. The asymmetrical distributions of Na+ K+ and Ca2+ between ICS and ECS underlie the roles of these cations in nerve excitation and conduction, and in signal transduction. The relatively large volume of the CSF, and extensive diffusional exchange of many substances between brain ECS and CSF, augment the ion-homeostasing capacity of the ECS. The choroid plexus, in addition to secreting CSF principally by biochemical mechanisms (there is an additional small component from the extracellular fluid), actively transports some substances from the blood (e.g. nucleotides and ascorbic acid), and actively removes others from the CSF. In contrast with CSF secretion, CSF reabsorption is principally a biomechanical process, passively dependent on the CSF-dural sinus pressure gradient. Pathological increases in intracranial water content imply development of an intracranial mass lesion. The additional water may be distributed diffusely within the brain parenchyma as brain oedema, as a cyst, or as increase in ventricular volume due to hydrocephalus. Brain oedema is classified on the basis of pathophysiology into four categories, vasogenic, cytotoxic, osmotic and hydrostatic. The clinical conditions in which brain oedema presents the greatest problems are tumour, ischaemia, and head injury. Peritumoural oedema is predominantly vasogenic and related to BBB dysfunction. Ischaemic oedema is initially cytotoxic, with a shift of Na+ and CI- ions from ECS to ICS, followed by osmotically obliged water, this shift can be detected by diffusion-weighted MRI. Later in the evolution of an ischaemic lesion the oedema becomes vasogenic, with disruption of the BBB. Recent imaging studies in patients with head injury suggest that the development of traumatic brain oedema may follow a biphasic time course similar to that of ischaemic oedema. Hydrocephalus is associated in the great majority of cases with an obstruction to the circulation or drainage of CSF, or, occasionally, with overproduction of CSF by a choroid plexus papilloma. In either case, the consequence is a ris
 ...
PMID:The normal and pathological physiology of brain water. 907 71

The hypothesis was tested that the carotid baroreceptor stimulation caused by a posture change from upright seated with legs horizontal (Seat) to supine (Sup) participates in the suppression of arginine vasopressin (AVP) release. Ten healthy males underwent this posture change for 30 min without or with simultaneous application of lower body negative pressure (LBNP) adjusted to maintain left atrial diameter (LAD) at the Seat level. Throughout Sup, mean arterial pressure and heart rate decreased from 98 +/- 2 to 91 +/- 2 mmHg and from 63 +/- 2 to 55 +/- 2 beats/min (P < 0.05), respectively, whereas the corresponding decreases during Sup + LBNP were attenuated and of shorter duration (98 +/- 2 to 93 +/- 2 mmHg and 62 +/- 2 to 58 +/- 3 beats/min, P < 0.05). During Sup, LAD increased from 30 +/- 1 to 33 +/- 1 mm, and arterial pulse pressure (PP) increased from 40 +/- 2 to 47 +/- 2 mmHg, whereas plasma AVP decreased from 0.9 +/- 0.2 to 0.5 +/- 0.1 pg/ml (P < 0.05), and plasma norepinephrine (NE) decreased from 176 +/- 20 to 125 +/- 16 pg/ml (P < 0.05). During Sup + LBNP, there were no changes in LAD, PP, plasma AVP, or NE. In conclusion, vasopressin secretion is suppressed during an antiorthostatic posture change, which increases carotid sinus pressure, PP, and LAD. The suppression is absent when PP and LAD are prevented from increasing and is thus critically dependent on at least one of these stimuli.
 ...
PMID:Mechanisms of inhibition of vasopressin release during moderate antiorthostatic posture change in humans. 1040 77


1