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)

Mesangial cells are smooth muscle-like cells of the renal glomerulus which contract and produce prostaglandins in response to vasopressin and angiotensin. These responses serve to regulate the glomerular capillary filtering surface area. We have used the membrane potential-sensitive fluorescent dye bis-oxonol and the intracellular fluorescent calcium-sensitive probe Indo-1 to study the changes in membrane potential (Em) and intracellular free calcium concentration ([Ca2+]i) in cultured rat mesangial cells in response to vasoconstrictor hormones. Basal [Ca2+]i was 227 +/- 4 nM, and stimulation by maximal concentrations of either vasopressin or angiotensin resulted in a transient 4-6-fold rise. Resting membrane potential was 45.8 +/- 0.9 mV and vasoconstrictor hormones caused a depolarization of 14-18 mV. The following extracellular ion substitutions indicated that chloride efflux was the predominant ion flux responsible for depolarization: 1) depolarization persisted when sodium in the medium was substituted with N-methylglucamine; 2) substitution of medium sodium chloride with sodium gluconate, which enhances the gradient for chloride efflux, augmented vasoconstrictor-stimulated depolarization; 3) suspension of cells in potassium chloride medium resulted in depolarization, following which, stimulation by either vasopressin or angiotensin resulted in hyperpolarization; and 4) this hyperpolarization did not occur when potassium gluconate medium was used to depolarize the cells. The calcium ionophore ionomycin also resulted in membrane depolarization. However, prevention of the rise in [Ca2+]i by prior exposure to ionomycin in calcium-free medium or by loading mesangial cells with the intracellular calcium buffer BAPTA did not abrogate the depolarization response to vasoconstrictor hormones. This indicates that a rise in intracellular calcium is not necessary for depolarization. In contrast, prior depolarization of the cells using varying concentrations of KCl in the external medium, which dissipated the electrochemical gradient for chloride efflux, resulted in a corresponding prolongation of the transient calcium response to vasopressin and angiotensin. These findings indicate that angiotensin and vasopressin depolarize mesangial cells by activating chloride channels and that this activation can occur by both calcium-dependent and -independent mechanisms. In addition, activation of chloride channels with resulting depolarization may serve to modulate the calcium signal.
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PMID:Vasoconstrictor hormones depolarize renal glomerular mesangial cells by activating chloride channels. 253 39

It has been suggested that abnormalities of thirst and vasopressin secretion commonly coexist with Kallmann's syndrome. Out-patient plasma osmolality, plasma sodium and 24-hour urine volume were similar in 10 patients with Kallmann's syndrome and 10 matched controls. Six patients underwent dynamic testing of osmoregulation with hypertonic sodium chloride infusion. There were similar rises in plasma AVP concentration in patients (0.4 +/- 0.1-6.2 +/- 1.2 pmol/l, P less than 0.001) and controls (0.4 +/- 0.1-5.7 +/- 1.0 pmol/l P less than 0.001). Thirst ratings rose in similar fashion in patients (0.7 +/- 0.3-6.2 +/- 1.0 cm, P less than 0.001) and controls (1.0 +/- 0.3-7.2 +/- 0.5 cm. P less than 0.001). Drinking rapidly abolished thirst and lowered AVP concentrations in both groups before major changes in plasma osmolality occurred. Linear regression analysis defined similar osmotic thresholds for thirst onset and vasopressin release in the two groups, and there was no difference in the calculated sensitivity of the osmoreceptor/vasopressin secretory unit as defined by the slopes of the regression lines. We conclude that osmoregulation is normal in Kallmann's syndrome.
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PMID:Osmoregulation of thirst and vasopressin secretion in Kallmann's syndrome. 260 90

Pulsatile administration of oxytocin was compared with continuous infusion of oxytocin for induction of labor in pregnant rats. The dosages consisted of intravenous injections of 0, 2.5, and 5 mU oxytocin every 10 minutes and intravenous infusion of 1 mU/minute of oxytocin in 0.9% sodium chloride. These doses are within the range of endogenously secreted pulses. All treatments began on day 22 at 2 p.m. and continued for 8 hours. Pulsatile administration resulted in a marked reduction in the dose of oxytocin required to induce labor. Using 5 mU pulses, birth was induced with 18.4%, and using 2.5 mU pulses, with 24% of the dose needed using continuous infusion. Parturition was advanced by 12 hours on the average by oxytocin treatment, but no significant differences were observed between the various oxytocin dosage regimens in this regard or in regard to gestation length, induction-delivery interval, duration of delivery, or the proportion of living or dead pups. Significantly more uterine activity was induced with each mU of oxytocin using pulsatile administration than using continuous infusion. There was no evidence for down-regulation of oxytocin receptors during a continuous infusion of oxytocin. We postulate that the greater efficacy of oxytocin pulses to induce uterine activity and delivery in comparison to continuous infusions is due to a more effective stimulation of prostaglandin F2 alpha release from the decidua. The amount of oxytocin needed for induction of labor with 2.5 mU pulses was similar to the decrease in neurohypophyseal oxytocin content during the first stage of spontaneous labor, and uterine activity elicited was also similar to that observed during spontaneous labor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulsatile administration enhances the effect and reduces the dose of oxytocin required for induction of labor. 271 12

A combination of autoradiographical techniques and computerized image analysis has been used to study the distribution and density of cholecystokinin receptors in the paraventricular and supraoptic nuclei of animals in which the magnocellular-posterior pituitary axis is activated, namely, in salt-loaded (2% sodium chloride) and homozygous Brattleboro rats. [125I]cholecystokinin octapeptide binding was greatly elevated in the paraventricular, supraoptic and accessory nuclei of salt-loaded and homozygous Brattleboro rats, compared to the respective control animals. Furthermore, under these conditions [125I]cholecystokinin octapeptide binding in the paraventricular nucleus was localized almost exclusively to magnocellular subdivisions, and especially to those containing predominantly oxytocin neurons. Autoradiographical competition studies revealed that the increase in [125I]cholecystokinin octapeptide binding in magnocellular nuclei reflected an increase in receptor number (Bmax) rather than affinity (Kd). These results suggest that cholecystokinin receptor density in the paraventricular, supraoptic and accessory magnocellular nuclei is closely linked to magnocellular neurosecretory activity and raises the possibility that cholecystokinin receptors may be involved in oxytocin and vasopressin release processes.
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PMID:Modulation of hypothalamic cholecystokinin receptor density with changes in magnocellular activity: a quantitative autoradiographic study. 272 63

Although the presence of mineralocorticoid binding sites have been demonstrated in brain, little is known about their physiological role. The purpose of this study was to evaluate possible interactions between a relatively short 2-day central infusion of aldosterone (5 ng/h) and a diverse group of centrally acting pressor agents. The intracerebroventricular infusion of aldosterone selectively attenuated the pressor response produced by the injection of arginine vasopressin (AVP, 10-400 ng) into the lateral ventricle without altering the responses to ventricular administration of 50-200 ng angiotensin II (ANG II), 150 ng carbachol, and 0.5 and 1 M hypertonic sodium chloride. No aldosterone-vasopressin interaction occurred in rats receiving a simultaneous central infusion of aldosterone and RU 28318 [7 beta-hydroxy-3-oxo-7 alpha-propyl(17 alpha)-pregn-4-ene-21-potassium carboxylate], a specific mineralocorticoid receptor antagonist. Baroreflex reactivity and the pressor response to intravenous AVP were not modified by the aldosterone treatment, indicating that overall cardiovascular reactivity was not depressed. Because the vascular reactivity of the mesenteric artery to AVP and norepinephrine remained unchanged after 2 days of central aldosterone infusion, and because plasma levels of aldosterone were not altered, the selective inhibition by this mineralocorticoid of the central AVP response appears to be purely central in origin. This specific central effect of aldosterone is mediated through interaction with mineralocorticoid receptors.
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PMID:Central interactions between aldosterone and vasopressin on cardiovascular system. 283 96

Pinealectomized (PX), sham-operated and non operated control rats were injected intraperitoneally (i.p.), once daily at 8.00 over five days, with: (a) 0.9% sodium chloride, (b) propranolol hydrochloride in a dose of 10 mg/kg (= 0.1 ml solution per 100 g b.w.). Three hours following the last injection the animals were decapitated and the content of vasopressin and oxytocin was bioassayed in the hypothalamus and neurointermediate lobe. PX was followed by known decrease of both vasopressin and oxytocin in the hypothalamus and neurohypophysis. In rats not-PX propranolol did not change the vasopressin and oxytocin content in the hypothalamus and neurointermediate lobe. In PX-rats, treatment with propranolol resulted in a distinct increase of the vasopressin in the neurohypophysis. It may be therefore supposed that the beta-adrenergic transmission is in some way involved in the regulatory mechanisms of pineal-neurohypophysial functional relationship.
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PMID:The effects of beta-adrenergic blockade on the hypothalamic and neurohypophysial vasopressin and oxytocin content in pinealectomized male rats. 288 9

Poorly controlled insulin-dependent diabetes mellitus is associated with considerable elevations of plasma vasopressin concentrations, although well-controlled diabetics have normal osmoregulated thirst and vasopressin release. We studied the effect of blood glucose concentration on osmoregulated thirst and vasopressin secretion in insulin-dependent diabetes mellitus. Blood glucose was maintained overnight, and for the duration of the study, in either the euglycemic (4-5 mmol/l) or hyperglycemic (10-12 mmol/l) range, and patients underwent infusion of hypertonic (855 mmol/l) sodium chloride solution. Plasma sodium was lower during the hyperglycemic study, but elevation in plasma sodium concentration by infusion of saline caused progressive linear increases in both thirst and plasma vasopressin concentrations in both studies. Linear regression analysis defined lowered plasma sodium thresholds for both thirst appreciation and vasopressin release during the hyperglycemic study, although the sensitivity of the osmoreceptors remained unchanged. Analysis of the data in terms of plasma osmolality, corrected for the increase in blood glucose in the hyperglycemic study, revealed no differences in the osmotic thresholds for thirst or vasopressin release; sensitivity of the osmoreceptors also remained the same. Drinking abolished thirst and lowered plasma vasopressin concentrations before major changes in plasma sodium were observed. These results show that insulin-dependent diabetic patients osmoregulate appropriately when moderately hyperglycemic but that the threshold plasma sodium for vasopressin secretion and thirst appreciation is lowered by an unknown mechanism.
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PMID:Effect of blood glucose concentration on osmoregulation in diabetes mellitus. 292 50

Plasma levels of immunoreactive alpha human atrial natriuretic peptide (IR-ANP) were measured in nine patients with chronic renal failure before and after removal of 1.3-3.7 litres of fluid by ultrafiltration and again during volume repletion with intravenous sodium chloride solution (150 mmol/l: saline). Baseline levels of IR-ANP were elevated but fell by 22% during ultrafiltration. Saline infusion induced a rapid and steep rise in IR-ANP levels which were 150% of baseline while body weight was still 2% below baseline. Changes in plasma renin, angiotensin II, aldosterone and vasopressin during the study were slight compared with the change in IR-ANP, but noradrenaline levels rose threefold during ultrafiltration. There was a significant positive relationship between arterial pressure and IR-ANP levels before and after ultrafiltration. These results lend support to the suggestion that atrial peptides are of physiological importance, especially in states of chronic fluid overload such as chronic renal failure.
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PMID:Exaggerated responsiveness of immunoreactive atrial natriuretic peptide to saline infusion in chronic renal failure. 294 53

Intraventricular perfusion with a hypertonic sodium chloride solution elicits increases in cerebrospinal fluid vasopressin and blood pressure and a decrease in heart rate. The central peptide response was greatly reduced in the hypertensive rat. Central pretreatment with the vasopressin (V1) antagonist completely abolished the pressor response to hypertonic sodium chloride in the normotensive animal. Results suggest that a central vasopressin receptor may play a role in the control of blood pressure.
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PMID:Involvement of central vasopressin receptors in the control of blood pressure. 301 14

Rats dehydrated for 8 days and subsequently rehydrated were given intracerebroventricularly (i.c.v.) methoxamine hydrochloride (MX) or dihydroergotamine methanosulphonate (DHE), each in a daily dose of 10 micrograms dissolved in 10 microliter of 0.9% sodium chloride. A single dose of MX injected to normally hydrated animals increased the release of hypothalamic and neurohypophysial vasopressin but did not affect significantly the oxytocic activity in the hypothalamus as well as in the neurohypophysis. Under conditions of dehydration MX did not influence the hypothalamic vasopressin content but it stimulated the neurohypophysial vasopressin depletion. On the contrary, MX distinctly inhibited the decrease of hypothalamic and neurohypophysial oxytocin content in dehydrated animals. In rehydrated animals MX restrained some what the renewal of hypothalamic vasopressin and oxytocin storage but intensified this process in the neurohypophysis. A single dose of DHE decreased the vasopressin content in the hypothalamus as well as the oxytocin content both in the hypothalamus and neurohypophysis. Under conditions of dehydration DHE stimulated the depletion of hypothalamic vasopressin and oxytocin. On the contrary, DHE strongly inhibited the depletion of oxytocin in the neurohypophysis of dehydrated rats. DHE restrained the renewal of hypothalamic vasopressin and oxytocin stores as well as intensified this process in the neurohypophysis of subsequently rehydrated rats.
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PMID:The hypothalamic and neurohypophysial vasopressin and oxytocin content under various states of adrenergic transmission in dehydrated and subsequently rehydrated rats. 301 81


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