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L Share

Publications and source records attributed to L Share.

At least 91 records · Page 5Linked to original sources
PubMed1985

Subcellular localization of vasopressin-like material in platelets.

It has recently been reported that 90% of circulating vasopressin in humans appears to be in platelets. We have confirmed these results and studied the subcellular localization and secretion of vasopressin from human platelets. Sucrose density gradient analysis showed highest relative specific activity for vasopressin in the membrane fractions. Stirring of platelet-rich plasma with a number of different platelet-aggregating agents including epinephrine, norepinephrine, arachidonic acid, collagen, adenosine diphosphate, A23187, and platelet-activating factor failed to release significant amounts of immunoreactive vasopressin, despite the expected aggregation and secretion of platelet factor 4 by these agents. Thus vasopressin appears to be primarily a platelet membrane component and is not secreted in the usual way by agents modulating platelet function.

Adenosine Diphosphate↗
PubMed1985

Metabolism of vasopressin.

The clearance of vasopressin (VP) by the kidneys and splanchnic viscera was studied in the anesthetized dog. VP is bound to plasma protein, 10% at basal plasma VP levels and 40% at plasma VP concentrations greater than 20 microU/ml. The urinary clearance of VP is 70-100% of the glomerular filtration rate; the renal organ clearance of the hormone is 20-30% greater than its urinary clearance. There is evidence that the renal organ clearance of VP is affected by changes in both glomerular filtration rate and renal blood flow. The renal clearance of VP is a result of glomerular filtration, degradation, or reabsorption in the proximal nephron, and secretion into the distal nephron. In the short term, the renal clearance of VP is unaffected either by changes in the plasma VP concentration over a broad range or by moderate hemorrhage. The splanchnic clearance of VP is accomplished almost equally by the intestine and the liver. Because the sum of the splanchnic and renal clearances of VP is less than estimates of its metabolic clearance rate, there may be a physiologically significant clearance of VP by organs in addition to the kidneys and splanchnic viscera.

Animals↗
PubMed1985

Factors influencing the secretion of vasopressin into cerebrospinal fluid.

Vasopressin (VP) has been found in the cerebrospinal fluid (CSF) of several species of animals. Although it is known that hemorrhage, hypertonicity of body fluid, hypoxia, and hypercapnia all increase VP in plasma, little is known regarding the stimuli that cause the secretion of VP into the CSF. We therefore performed several studies to examine whether stimuli capable of increasing plasma levels of VP can also increase VP in the CSF of anesthetized dogs. We found that hemorrhage, intracerebroventricular infusion of hypertonic artificial CSF, hypoxia, and hypercapnia all produced increases in the concentration of VP in plasma and in CSF, but the time courses and the magnitude of the increases in the two compartments were different. In addition, an i.v. infusion of hypertonic saline or of hydrochloric acid produced an increase in plasma VP without significantly changing CSF VP. Thus, although the secretion of VP into plasma and CSF may be influenced by the same stimuli, changes in one compartment do not necessarily correlate with changes in the other. Taken together, our results are consistent with the hypothesis that the plasma and CSF VP may derive from different sources.

Acidosis↗
PubMed1984

Central indomethacin enhances volume-dependent vasopressin release.

The effect of centrally administered indomethacin on hemorrhage-induced vasopressin release was studied in the morphine-sedated, urethan/chloralose-anesthetized dog. Ventriculocisternal perfusion of indomethacin 1) significantly reduced the amount of prostaglandin E2 in the effluent from the cisterna magna, 2) significantly enhanced the vasopressin response to volume depletion, and led to a greater fall in mean arterial blood pressure during severe hemorrhage. The results suggest that central prostaglandins may have an inhibitory effect on vasopressin secretion during volume depletion.

Animals↗
PubMed1984

Cardiovascular response to vasopressin vasopressor antagonist administration during water deprivation in the rat.

The cardiovascular effects of intracerebroventricular (i.c.v.) and intravenous (i.v.) injection of a selective vasopressin vasopressor antagonist, [1-beta-mercapto-beta, beta-cyclopentamethylenepropionic acid-2-(0-methyl)tyrosine]arginine vasopressin (TMe-AVP) were examined in conscious rats under basal conditions and following 48 h of water deprivation. Pressor responses to i.v. vasopressin (50 ng/kg) were not blunted by i.c.v. treatment with either vehicle or 0.5 microgram/kg TMe-AVP. A dose of 5.0 microgram/kg TMe-AVP (i.c.v.) did reduce the pressor response to vasopressin, indicating peripheral leakage of the antagonist. Water deprivation for 48 h increased plasma vasopressin concentrations from 0.7 +/- 0.1 to 2.8 +/- 0.1 microU/ml and increased blood pressure from 112 +/- 2 to 123 +/- 1 mm Hg. No effect of the vasopressin antagonist on blood pressure could be detected following either i.c.v. (0.5 microgram/kg) or i.v. (5.0 micrograms/kg) treatment in water-deprived animals. However, a significant increase in heart rate was observed in water-deprived rats following i.v. injection of 5.0 micrograms/kg of TMe-AVP. Central vasopressin vasopressor receptor blockade appears to exert little effect on blood pressure either under basal conditions or during water deprivation. The data further delineate the relationship of plasma vasopressin concentrations to cardiovascular homeostasis.

Animals↗
PubMed1984

Effect of vertebral artery infusions of oxytocin on plasma vasopressin concentration, plasma renin activity, blood pressure and heart rate and their responses to hemorrhage.

Infusion of oxytocin into one vertebral artery of anesthetized dogs did not alter plasma vasopressin concentration, blood pressure or heart rate. However, there was a significant (p less than 0.01) increase in plasma renin activity (PRA; delta = 7.6 +/- 2.3 ng/ml X h). A 35% hemorrhage caused blood pressure to fall by 9.4 +/- 4.0 mm Hg (p less than 0.01) and PRA to rise by 8.8 +/- 2.7 ng/ml X h (p less than 0.05). In 8 dogs that were subjected to a similar hemorrhage and that also received an intravertebral infusion of oxytocin, blood pressure was maintained and PRA increased by 14 +/- 4.3 ng/ml X h (p less than 0.05). Heart rate and plasma vasopressin responses were similar in both hemorrhage groups. The results indicate that oxytocin prevented the fall in blood pressure associated with a hemorrhage, possibly by increasing renin release.

Animals↗
PubMed1984

Effect of vertebral, carotid and intravenous infusions of lysine vasopressin on plasma vasopressin and cardiovascular function.

The cardiovascular and vasopressin-releasing effects of vertebral artery, carotid artery and intravenous (i.v.) infusions of lysine vasopressin (150 microU/kg X min) were studied in anesthetized dogs. Vertebral and carotid artery infusions of lysine vasopressin led to similar decreases in cardiac output as i.v. infusions. Heart rate, however, decreased to a greater extent with vertebral and carotid artery infusions of lysine vasopressin than i.v. infusions. There were no changes in either mean arterial blood pressure or the plasma vasopressin concentration. The results indicate that peripheral vasopressin: has a central effect to reduce heart rate; has a peripheral effect on the heart to reduce cardiac output, and probably does not feed back to inhibit its own release.

Animals↗
PubMed1984

Role of vasopressin in regulation of renal kinin excretion in Long-Evans and diabetes insipidus rats.

To study the relationship between vasopressin and the renal kallikrein-kinin system we measured the rate of excretion of kinins into the urine of anesthetized rats during conditions of increased and decreased vasopressin level. The excretion of immunoreactive kinins in Brattleboro rats with hereditary diabetes insipidus (DI) (24 +/- 3 pg min-1 kg-1) was lower than in the control Long Evans (LE) rats (182 +/- 22 pg min-1 kg-1; P less than 0.05). The DI rats also exhibited negligible urinary excretion of immunoreactive vasopressin, reduced urine osmolality, and increased urine flow and kininogenase excretion. In LE rats, volume expansion by infusion of 0.45% NaCl-2.5% dextrose to lower vasopressin secretion reduced (P less than 0.05) kinin excretion, vasopressin excretion, and urine osmolality to 41, 26, and 15% of their respective control values, while increasing (P less than 0.05) urine flow and kininogenase excretion. On the other hand, the infusion of 5% NaCl, which promotes vasopressin secretion, increased (P less than 0.05) the urinary excretion of kinins and vasopressin to 165 and 396% of control, while increasing (P less than 0.05) urine flow and kininogenase excretion. Infusion of vasopressin (1.2 mU/h, intravenous) enhanced (P less than 0.05) kinin excretion by two to threefold in DI rats and in LE rats during volume expansion with 0.45% NaCl-2.5% dextrose, while decreasing urine flow and increasing urine osmolality. This study demonstrates that the urinary excretion of immunoreactive kinins varies in relation to the urinary level of vasopressin, irrespective of urine volume and osmolality and of the urinary excretions of sodium and kininogenase. The study suggests a role for vasopressin in promoting the activity of the renal kallikrein-kinin system in the rat.

Animals↗
PubMed1984

The response of vasopressin and blood pressure to hemorrhage in SHR and WKY rats.

The effects of hemorrhage on plasma vasopressin levels and blood pressure were examined in conscious, age-matched spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. Graded hemorrhage was produced by bleeding the rats at 10 min intervals over a total period of 65 min, to produce cumulative blood losses equivalent to 0.5, 1.0, 1.5, 2.0 and 3.0% of body weight in each animal. Hemorrhage progressively lowered blood pressure and increased plasma vasopressin levels in both SHR and WKY. At cumulative reductions in blood volume equivalent to 1.0 to 3.0% of body weight, there were greater reductions in arterial pressure and greater increases in plasma vasopressin concentrations in SHR than WKY. Basal blood volume in SHR was 10% lower than in WKY. In SHR, the greater vasopressin response to hemorrhage may have been due in part to the greater fall in arterial pressure. Although the lower blood volume may have contributed to the latter, derangements in baroreceptor function may also have been important.

Animals↗
PubMed1984

Effect of angiotensin II on vasopressin in plasma and platelets in SH and WKY rats.

A study was carried out of the effects of iv angiotensin II on vasopressin release and the distribution of vasopressin between platelets and plasma in 12 week old conscious unrestrained SH and WKY rats. Angiotensin II was infused at rates of 31.25 to 500 ng/kg X min for 20 min. There was an enhanced pressor responsiveness to angiotensin II in the SH rats. Angiotensin II caused a moderate increase in plasma vasopressin concentrations, but only at doses which produced maximal pressor responses (250 to 500 ng/kg X min). There were no significant differences in vasopressin responses to angiotensin II in SH compared to WKY rats. Approximately 30% of circulating immunoreactive vasopressin was found in platelets in both SH and WKY rats, and this distribution was not greatly affected by the iv infusion of angiotensin II.

Angiotensin II↗
PubMed1984

The role of vasopressin in hypertension.

There is evidence for an increased secretion of vasopressin in most models of hypertension, e.g., deoxycorticosterone (DOC)-salt hypertension, one- and two-kidney renal hypertension, partial nephrectomy-salt hypertension, the spontaneously hypertensive rat (SHR), the Dahl salt-sensitive rat on a high-salt diet, and human essential hypertension. In most forms of hypertension, there is also an increased pressor responsiveness to vasopressin as well as to other pressor agents. Blockade of vasopressin with either a competitive antagonist or a specific antiserum lowered blood pressure substantially in DOC-salt hypertension, two-kidney, one-clip hypertension, the stroke-prone SHR with well-established hypertension, and the Dahl S rat treated with captopril. In rats with diabetes insipidus, one- and two-kidney renal hypertension, but not DOC-salt hypertension, can be produced. There is evidence that vasopressin can contribute to some models of hypertension as either a pressor or an antidiuretic agent.

Animals↗
PubMed1983

Splanchnic clearance of plasma vasopressin in the dog: evidence for prehepatic extraction.

It is generally considered that the liver is primarily responsible for the extraction of vasopressin from the circulating blood by the splanchnic viscera. To investigate this matter further, measurements were made in the anesthetized dog of the concentrations of vasopressin in arterial, portal venous, and hepatic venous plasma, and of total splanchnic plasma flow and hepatic arterial plasma flow. The total splanchnic vasopressin extraction ratio was 12.9 +/- 1.0%. However, the concentration of vasopressin in portal venous plasma was consistently lower than in arterial plasma, and there was a substantial prehepatic extraction of vasopressin, averaging 10.5 +/- 0.8%. A quantitative evaluation of the contribution of the "prehepatic" viscera, i.e., viscera with venous drainage into the portal vein, is provided by the relevant clearances of vasopressin. The prehepatic and total splanchnic vasopressin clearances were 1.58 +/- 0.20 and 3.04 +/- 0.31 ml X min-1 X kg-1, respectively. Thus, the splanchnic viscera other than the liver were responsible for approximately half of the splanchnic clearance of vasopressin; the remainder could be attributed to the liver. Immunoreactive vasopressin was not found in the bile. In splenectomized dogs, in which venous blood was collected from the superior mesenteric vein, the vasopressin extraction ratio was 14.6 +/- 2.3%, suggesting that the prehepatic clearance of vasopressin occurs largely in the mesenteric bed. A more specific localization of the prehepatic clearance sites has not as yet been made.

Animals↗
PubMed1983

Intracerebroventricular captopril does not inhibit osmotically stimulated vasopressin release.

Experiments were carried out to determine the effect of intracerebroventricular (icv) administration of the angiotensin-converting enzyme inhibitor, captopril, on osmotically stimulated vasopressin secretion. During icv infusion of captopril (3.1 micrograms/kg . min), dogs were infused intravenously (iv) with either 2.5 or 0.15 M NaCl. Control groups received an osmotically equivalent mannitol solution icv with the 2.5 or 0.15 M NaCl iv infusion. As a result of the iv hypertonic saline infusion, plasma vasopressin concentrations increased progressively and in concert with the plasma osmolality; this response was not altered by icv captopril. Plasma vasopressin levels were unchanged during iv isotonic saline infusion, and, again, icv captopril was without effect. At the completion of the icv infusions, injection of angiotensin I icv (310 ng/kg) produced a markedly greater increase in plasma vasopressin levels in animals which had received mannitol icv, compared to those which had received captopril icv. On the basis of these findings, a role for an intrinsic brain renin-angiotensin system, if such a system exists, in the osmotic control of vasopressin secretion is seriously questioned, but not ruled out.

Animals↗
PubMed1983

Hypothalamic knife cuts alter fluid regulation, vasopressin secretion, and natriuresis during water deprivation.

To investigate central neural pathways involved in release of vasopressin and in fluid electrolyte regulation, a retractable wire knife was used to make coronal knife cuts posterior to the organum vasculosum lamina terminalis (OVLT). 4 days following cuts or control surgery, animals were housed in metabolism cages and: (1) deprived of food and water for 48 h; (2) deprived of water only for 48 h; or (3) allowed continuous access to food and water. Water ingestion, food ingestion, urine volume, sodium excretion and urine osmolality were recorded daily. Trunk blood was then collected following decapitation for determination of plasma vasopressin, sodium, and protein concentrations, and osmolality. Animals with knife cuts and ad libitum access to food and water had significantly higher plasma osmolality (310 +/- 2 mosm/kg), and plasma vasopressin concentration (2.02 +/- 0.5 microunits/ml) than controls (306 +/- 1 mosm/kg and 0.60 +/- 0.04 microunits/ml, respectively). When rats were deprived of both food and water, there were no significant differences between the two groups in plasma vasopressin concentration, although plasma osmolality wa higher in animals with cuts. However, rats with knife cuts deprived of water only had significantly higher plasma osmolality (358 +/- 8 mosm/kg), sodium (164 +/- 19 mEq/l) and vasopressin (17.7 +/- 4 microunits/ml), than similarly treated control animals (317 +/- 1 mosm/kg, 145.5 +/- 1.0 mEq/1, 5.5 +/- 3 microunits/ml, respectively). These data indicate that a neural pathway in this brain region is critical for normal fluid and electrolyte balance during ad libitum access to food and water, and during water deprivation.

Animals↗
PubMed1983

Effects of changes in steady state plasma vasopressin levels on renal and urinary vasopressin clearances in the dog.

A study was made of the effects of changes in the plasma vasopressin concentration on the extraction ratio and the renal organ and urinary clearances of vasopressin. Plasma vasopressin levels were increased in a stepwise fashion in anesthetized dogs by the iv infusion of vasopressin at rates of 100, 400, and 800 microU/min . kg. A steady state was achieved by infusing vasopressin for 60 min at each dose. Before the infusion of vasopressin, the extraction ratio and the renal and urinary clearances of vasopressin (one kidney) were 0.30 +/- 0.04, 1.8 +/- 0.2, and 1.4 +/- 0.1 ml/min . kg, respectively. The urinary clearance of vasopressin did not differ significantly from the inulin clearance (1.5 +/- 0.1 ml/min . kg). The infusion of vasopressin, which increased the plasma vasopressin concentration from an initial value of 4.3 +/- 1.3 to 54.6 +/- 2.4 microU/ml at the highest rate of infusion, was without effect on the vasopressin extraction ratio and the renal and urinary clearances of vasopressin. The MCR of vasopressin was estimated to be approximately 16 ml/min . kg. The renal clearance of vasopressin, calculated for both kidneys in all periods of all experiments, accounted for approximately 27% of the total clearance of vasopressin from the plasma. Thus, over a broad range of plasma vasopressin concentrations, a constant fraction of the vasopressin delivered to the kidney was removed from the blood perfusing the kidney, and the mechanisms for the renal extraction of vasopressin were not saturated.

Animals↗