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)

An organ culture system of a male guinea pig hypothalamo-neurohypophyseal complex (HNC) was established. On day 5 in culture, (Na+ -K+) ATPase activity was 0.83 +/- 0.11 mM Pi/mg prot/hr (mean +/- SEM): that is 67% of that on day 1 in culture. 3H-thymidine incorporated into DNA in the explants of HNC was 1,205 +/- 185 cpm/microgram DNA. The explants responded to the elevated KCl medium and the hypertonic solution of sodium chloride with a 470 +/- 38% and 298 +/- 31% increase in arginine vasopression (AVP) release, respectively. This response was inhibited by the addition of tetrodotoxin to the culture medium. AVP release from the explants in res-onse to angiotensin II increased significantly in a dose dependent manner. [Sar1, Ile8] angiotensin II, however, attenuated the response of the explants to angiotensin II when administered simultaneously with angiotensin II. These results suggest that angiotensin II and its analogue cause the AVP release from the explants in a competitive manner. The concentrations of AVP in the culture media made hypertonic with sodium chloride, sucrose and mannitol were 298 +/- 31% (p less than 0.01), 251 +/- 36% (p less than 0.01) and 255 +/- 59% (p less than 0.05) of their control values, respectively. The hypertonic solutions of sodium chloride, sucrose and mannitol caused AVP release from the explants in vitro, while the hypertonic solutions of glucose and urea were revealed to be poor osmotic stimuli on AVP release. These results support the concept of osmoreceptors to release AVP from the hypothalamo-neurohypophyseal axis.
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PMID:[Osmotic pressure and angiotensin II stimulation of arginine vasopressin release from a guinea pig hypothalamo-neurohypophyseal complex in organ culture (author's transl)]. 644 94

Hypertonic solutions of different substances were injected into the vertebral artery of dogs anesthetized with chloralose, preventing their access to the hypothalamic osmoreceptors by ligating the basilar artery and both the external carotid arteries. The hypertonic solution of sodium chloride produced graded inhibition of water diuresis and a concomitant rise in plasma antidiuretic hormone (ADH) level; hypertonic solution of glucose produced lesser effect. Hypertonic urea solution, on the other hand, did not alter the course of water diuresis. It was concluded that osmoreceptors are also present in the medulla which sense the changes in blood osmolarity and accordingly modify the ADH release.
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PMID:Evidence for the presence of osmoreceptors in medulla of the dog. 649 Jan 24

Diuretics have a central role in the treatment of edema and hypertension. This function is primarily an induction of a net negative balance of solute and water. Reviewed herein are the transport properties of each nephron segment that governs salt and water reabsorption with specific reference to the mechanisms by which the various diuretic agents affect those transport processes. Under normal circumstances, the proximal tubule reabsorbs about 50 to 66 percent of the filtered fluid by both active and passive mechanisms. However, diuretics that inhibit proximal reabsorption are "weak" diuretics since distal compensatory mechanisms can overcome their effect. The thin descending limb of Henle is highly permeable to water and relatively impermeable to solutes. Thus, its main physiologic function is to allow osmotic water abstraction. Although diuretics have no direct epithelial effect on this segment, many of the diuretics decrease fluid reabsorption from it by abolishing the papillary osmotic gradient. The decreased water absorption from the descending limb of Henle has a major role in over-all increased diuresis since nephron segments distal to the descending limb are impermeable to water in the absence of vasopressin. The thin ascending limb of Henle is impermeable to water while being highly permeable to sodium and chloride. Diuretics have no direct effect on the thin ascending limb of Henle. The medullary and cortical segments of the thick ascending limb of Henle absorb sodium chloride by active mechanisms as a result of a secondary active chloride transport mechanism that depends on the presence of sodium (co-transport mechanism). This transport mechanism is located on the luminal membrane. Most of the "loop" diuretics effect this process from the luminal side by having a direct inhibitory effect on this co-transport process. The diuretics that have a primary effect on the medullary segment (furosemide, bumetanide, ethacrynic acid) inhibit the concentrating mechanisms, whereas the diuretics that are effective primarily in the cortical segment (thiazides plus the diuretics affecting the medullary segment) inhibit the urinary diluting mechanism. The loop diuretics are physiologically the most potent family of diuretics. The cortical collecting duct segment reabsorbs sodium by active mechanisms. These processes are stimulated by aldosterone. The diuretics that affect these processes are considered weak diuretics, but they do have the metabolic effect of potassium sparing.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Site and mechanism of action of diuretics. 649 55

The effects of hemorrhage and parenteral hypertonic saline on the behavioural responses to centrally-administered arginine vasopressin (AVP) were examined in rats. Both hemorrhage and hypertonic saline act as potent stimuli for neurohypophysial vasopressin release, and may serve as potential stimuli for cerebral AVP release. When administered into a lateral cerebral ventricle of the rat brain, AVP has a potent convulsant action; this effect increases in severity upon subsequent administration. Removal of 15% of the estimated blood volume from the conscious rat or infusion of 1.0 ml of 1.5 M sodium chloride solution into the peritoneal cavity can mimic the effect of a central injection of AVP in 'sensitizing' the brain to the behavioural effects of subsequent injections of AVP. This suggests that these stimuli which are known to activate posterior pituitary secretion of AVP also induce the release of AVP (or a closely related molecule), from neuronal fibres within the brain.
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PMID:Increased motor disturbances in response to arginine vasopressin following hemorrhage or hypertonic saline: evidence for central AVP release in rats. 661 33

Participation of vasopressin and the renin-angiotensin system in the maintenance of systemic arterial pressure was evaluated in unanesthetized adrenalectomized rats. Adrenalectomized and sham-operated rats with implanted arterial and venous catheters were given 1% sodium chloride and 2.5% glucose as drinking fluid for 72 hours following adrenalectomy. Serum and urine samples were obtained for measurement of electrolyte and solute concentration. The pattern of serum electrolytes, serum osmolality, and renal excretion of electrolytes, solute, and water observed in the adrenalectomized rats was entirely consistent with previous observations in this model. Mean arterial pressure of unanesthetized unrestrained adrenalectomized rats was significantly lower than controls. In adrenalectomized rats, dPMeTyrAVP reduced mean arterial pressure 9 +/- 1 mm Hg, p less than 0.001; captopril then caused an additional reduction of 17 +/- 2 mm Hg, p less than 0.01. Neither antagonist altered arterial pressure in the control group. Our results indicate that vasopressin and the renin-angiotensin system play a compensatory pressor role in adrenal insufficiency, preventing a larger decrease of arterial pressure in this model of chronic hypotension.
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PMID:Maintenance of arterial pressure by vasopressin and angiotensin II after adrenalectomy. 665 64

The release of peptide hormones and uptake of radiolabelled calcium were measured in isolated rat neurohypophyses incubated in vitro. Neuropeptide release was provoked either by depolarising the tissue with raised extracellular potassium, or by application of biphasic electrical stimulus pulses. Potassium stimulation increased uptake of radiolabelled calcium, but electrical stimulation caused no measurable change, suggesting that non-neuronal elements unresponsive to electrical stimulation were responsible for the uptake. This possibility is supported by the results of 2 further series of experiments, in which the neurohypophyses were manipulated in vivo before incubation in vitro. First, the experimental animals were given a 2% solution of sodium chloride in place of drinking water for 3 days, to deplete the neuropeptide content of the incubated tissue. After such treatment, potassium-stimulated neuropeptide release was greatly reduced, but calcium uptake was increased relative to that of normal tissue. Secondly, the pituitary stalk was lesioned electrolytically 14 days before the incubation, thus completely eliminating the neural elements of the neurohypophysis. Potassium stimulation then released no neuropeptide, but calcium uptake increased as in normal tissue. It thus appears that calcium uptake does not always closely parallel neuropeptide release, in contrast with previous results, and that depolarisation of the non-neuronal elements is responsible for the measurable uptake of calcium. The results do not contradict existing concepts of the central role of calcium influx in stimulus-secretion coupling in neurohypophyseal terminals, but serve to emphasise the need for care in the interpretation of calcium uptake data in tissues which are not homogeneous. The neurohypophyseal glial cells (pituicytes) are a likely site for the calcium uptake caused by potassium depolarisation.
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PMID:The relationship between calcium uptake and hormone release in the isolated neurohypophysis. A reassessment. 673 14

Animal and human studies demonstrate the dependence of renal prostaglandin (PG) production on dietary sodium chloride intake. The effect of 5 days' low salt diet (10 mmol Na/day plus 0.5 mg/kg Furanthril daily), and 5 days' high salt diet (250 mmol Na/day) on PGE2 and PGF2 alpha plasma levels and their excretion, on plasma renin activity (PRA) aldosterone (A) and vasopressin (VP) was evaluated on 30 normal subjects. Sodium restriction significantly increased plasma PGE2 and PGF2 alpha and their excretion in the urine. High salt intake reduced renal PG production to normal levels. Under low salt conditions PRA and A increased significantly and fell to normal values on high salt regimen. A negative correlation between renal PG production and VP plasma levels and excretion was demonstrated during the changes of dietary sodium intake.
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PMID:Humoral factors involved in the regulation of sodium-fluid balance in normal man. I. Effect of dietary sodium chloride intake on renal prostaglandins, vasopressin and renin-angiotensin-aldosterone system. 674 63

The hypotheses of passive salt accumulation predict an enhancement of renal concentrating ability by urea. We tested this prediction in rabbits, a species whose nephons when studied in vitro show tansport properties that support these hypotheses. We used calm, unanesthetized, hydropenic, vasopressin-treated rabbits with intact kidneys fed a 16% protein diet, and we observed the effect of urea administration at two rates of solute excretion (60 and 190 microOsm/min . kg body wt; N = 10 and 5, respectively). After an i.v. mannitol infusion, when urea was infused, the i.v. solute excretion rate was unchanged, the changes in urine urea concentration were large (a change of 767 and 408 mumoles/ml), but only small and variable changes in urine osmolality occured (a change of 78 +/- 146, and 36 +/- 50 microOsm/g H20). In additional experiments, we removed the kidneys from antidiuretic, or urea- or mannitol-infused rabbits and measured the intrarenal distribution of sodium, potassium, urea, and chloride. When the urine urea level was greater than 400 mmoles, the urine-to-papilla ratios for urea were 1.6 to 3.6. This suggested that a low collecting duct permeability to urea could explain the absence of a marked enhancement of concentrating ability during urea administration. Further analysis, based on a model of inner medullary solute compartments, indicated that sodium chloride was the major (86%) osmotically active solute in the medullary central core of these rabbits and that it was not influenced by changes in urinary urea concentration. The results of tissue analysis were consonant with either active or passive sodium chloride reabsorption from the thin ascending limb of Henle's loop in these rabbits.
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PMID:Urea and renal concentrating ability in the rabbit. 677 Jan 67

Seven out of nine patients with chronic inappropriate secretion of antidiuretic hormone were successfully treated with 40 mg frusemide daily. One patient needed 80 mg, and the remaining patient achieved only a small increase in diuresis after 40 mg frusemide; this was probably related to his low creatinine clearance. In order to maintain a salt intake high enough to compensate for the loss of urine electrolytes 3 to 6 g sodium chloride was added as tablets to the sodium-free diet in six patients. Hypokalaemia occurred in five patients but was easily corrected with either supplements of potassium chloride or a potassium-sparing diuretic. These findings add further weight to evidence that Frusemide is a good alternative for the treatment of patients with inappropriate secretion of antidiuretic hormone who cannot tolerate water restriction.
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PMID:Inappropriate secretion of antidiuretic hormone treated with frusemide. 680 39

Sodium and the renin-angiotensin system (RAS) participate in the regulation of cardiovascular function, in part via activation of central nervous system (CNS) mechanisms. Because intraventricular (IVT) administration of either hypertonic sodium chloride (NaCl) or angiotensin II (ANG II) elicits similar effects (i.e., natriuresis, hypertension, increased drinking, and enhanced vasopressin release) a common and final pathway may be involved. With this in mind, we measured the effect of an IVT injection (third or lateral ventricle) of 0.6 M NaCl on postganglionic renal nerve activity (RNA) and blood pressure in morphine-pentobarbital-anesthetized dogs before and after blockade of the brain RAS with either captopril or [Sar1,Ile8]ANG II. Both vagus and carotid sinus nerves were cut to avoid impingement of the baroreceptor reflex on the measured variables. IVT injection of 0.6 M NaCl produced a prominent hypertensive response and tachycardia associated with a 59 +/- 9% increase in RNA. These changes were statistically significant (P less than 0.001), correlated with each other, and were abolished by administration of hexamethonium chloride (10 mg/kg iv). Blockade of central ANG II receptors with [Sar1,Ile8]ANG II was without effect. However, in dogs given IVT SQ 14,225, there was a slight increase in baseline RNA before injection of 0.6 M NaCl; in addition, both the pressor and heart rate responses to the stimulus of hypertonic NaCl were further augmented. These results demonstrate that central administration of hypertonic NaCl in baroreceptor-denervated dogs produces marked activation of sympathetic nerve activity via mechanisms other than activation of the brain RAS.
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PMID:Lack of interaction between a hypertonic NaCl stimulus and the brain renin-angiotensin system. 683 51


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