Search PubMed⌕ Search

Biomedical subjects

L Share

Publications and source records attributed to L Share.

At least 109 records · Page 6Linked to original sources
PubMed1983

Effects of nonhypotensive hemorrhage on renal organ and urinary clearances of vasopressin in the dog.

A study was undertaken to investigate the effects of moderate nonhypotensive hemorrhage on the renal organ and urinary clearances of vasopressin in anesthetized dogs. A nonhypotensive hemorrhage was conducted in nine dogs by withdrawal of 12 ml/kg arterial blood over 10 min. This reduction in blood volume increased the plasma vasopressin concentration from a prehemorrhage value of 4.3 +/- 0.5 to 12.5 +/- 3.4 microU/ml (P less than 0.01) in the 15-min period immediately after hemorrhage and to 8.1 +/- 1.4 microU/ml (P less than 0.01) in the 45- to 60-min period after hemorrhage. The increased plasma vasopressin concentration was not associated with changes in either plasma osmolality or mean arterial blood pressure. The urinary excretion of vasopressin increased significantly after hemorrhage (P less than 0.01, 0-15 min after hemorrhage; P less than 0.05, 45-60 min after hemorrhage) and correlated significantly with the plasma vasopressin concentration (r = 0.92; P less than 0.001). However, this moderate nonhypotensive hemorrhage did not change the renal vasopressin extraction ratio or the renal organ and urinary clearances of vasopressin from their prehemorrhage values of 0.27 +/- 0.02, 2.00 +/- 0.20 ml/min X kg, and 1.43 +/- 0.13 ml/min X kg, respectively. At no time were these values different from those in nine time control dogs. Thus, changes in the renal handling of vasopressin do not contribute to the increase in the plasma vasopressin concentration after moderate nonhypotensive hemorrhage.

Animals↗
PubMed1983

Increased urinary vasopressin excretion in the DOCA-hypertensive pig.

A possible role for vasopressin in the development and/or maintenance of DOCA hypertension in pigs was studied. In control pigs mean arterial blood pressure (MABP), plasma lysine vasopressin (LVP) concentration, the 24-h urinary excretion of LVP (ULVPV) and plasma renin activity (PRA) did not change throughout the 30 days of the experiment. In DOCA-treated pigs MABP began to increase from the initial level of 95 +/- 2 mm Hg within 5 days and reached a level of 127 +/- 3 mm Hg between days 20-30 (P less than 0.01). At this time in the DOCA treated pigs, ULVPV increased threefold (P less than 0.05), although PLVP was unchanged and PRA was reduced to almost zero. After 30 days the pigs were fed a low sodium diet. This was without effect on MABP, PLVP and ULVPV in control pigs. However, in the DOCA-treated pigs, MABP fell from 133 +/- 2 to 112 +/- 6 mm Hg, accompanied by a 60% fall in ULVPV. PLVP was unchanged. Thus in DOCA-treated pigs, LVP appears not to be involved in the development of hypertension, but may be involved in its maintenance.

Animals↗
PubMed1983

Effect of intracarotid administration of morphine and naloxone on plasma vasopressin levels and blood pressure in the dog.

The effects of intracarotid injection of morphine and naloxone on plasma vasopressin levels and arterial blood pressure were examined in pentobarbital-anesthetized dogs. Morphine administration decreased blood pressure in a dose-dependent fashion with a threshold between 10 and 50 micrograms/kg. Plasma levels of vasopressin rose in parallel with the decrease in blood pressure and were significantly elevated after doses of 50 and 100 micrograms/kg of morphine. Intracarotid injection of the opioid antagonist naloxone (1 mg/kg) increased blood pressure slightly, but significantly, and increased plasma concentrations of vasopressin approximately 60%. Pretreatment with naloxone did not blunt the hypotensive effect of morphine at a dose of 50 micrograms/kg, but enhanced the secretion of vasopressin in response to the morphine stimulus; plasma vasopressin levels were 5-fold greater than those found in animals given morphine but not pretreated with naloxone. Pretreatment with the histamine receptor blockers chlorpheniramine and cimetidine blunted morphine-induced (50 micrograms/kg) hypotension by about 50% and prevented a significant increase in the plasma vasopressin concentration. The data are consistent with the hypothesis that stimulation of vasopressin secretion by systemically administered morphine is secondary to the blood pressure fall. However, it also appears that, in the pentobarbital-anesthetized dog, naloxone-sensitive systems exert a tonic inhibitory influence over both vasopressin secretion and blood pressure.

Animals↗
PubMed1982

Osmotic control of plasma vasopressin in anesthetized dogs.

The relation between plasma osmolality (pOsm) and the concentration of immunoreactive vasopressin in plasma from an external jugular vein (pAVP) was studied in dogs prepared with carotid loops and anesthetized with chloralose-pentobarbital. Control mean pAVP was 0.6-1.0 microM/ml, after 24 h of dehydration pAVP was tripled. Isosmotic volume expansion for 10 min elicited a decrease in pAVP in all cases not associated with low control values of pAVP. I.v. hyperosmotic infusions (delta pOsm: 9 or 18 mOsm/kg in 10 min) increased pAVP. No significant alterations in pAVP occurred in relation to infusions during which the head or the remainder of the body was selectively supplied by hyperosmotic blood. Statistically, the distribution of the pAVP values suggests the existence of two populations, in euhydrated animals high concentrations (greater than 8 microU/ml) were found in a small fraction of the samples. It is concluded that (i) in chloralose-anesthetized, non-traumatized dogs pAVP is very similar to values found in venous plasma from conscious dogs, (ii) the pAVP measurements support the concept of an episodic secretion of vasopressin, and (iii) under the present circumstances, an ubiquitous increase in pOsm is a more effective stimulus for vasopressin release than a similar but selective increase in the osmolality of the blood flowing towards the head.

Animals↗
PubMed1982

The relation between carotid solute concentration and renal water excretion in conscious dogs.

Verney's hypothesis of cerebral osmoreceptors controlling the renal excretion of water via vasopressin was reinvestigated in conscious trained dogs provided with bilateral skin loops containing the common carotid arteries. In multiple experiments in two dogs, bilateral intracarotid injections (0.25 ml. (kg b.wt.)-1 per artery in 10 s) of a hyperosmotic solution of sodium chloride (0.257 mol/l) during transient water diuresis failed to produce an antidiuretic response, although it is estimated that the injections elevated the osmolality of the carotid blood by 12-15%. In another 5 dogs, Bilateral intracarotid infusions of hyperosmotic saline (45 mumol.(kg b wt..min)-1 per artery for 10 min) during sustained water diuresis resulted in a 3% increase in jugular venous osmolality and an antidiuretic response without detectable changes in heart rate or mean arterial pressure. Equal intravenous hyperosmotic or intracarotid isosmotic infusions were not associated with antidiuretic response. Analysis of the concomitant concentrations of vasopressin in plasma fell short of supporting the hypothesis that the antidiuretic response to intracarotid hyperosmotic infusions was exclusively or mainly due to liberation of vasopressin, although the renal response could be mimicked by exogenous vasopressin. It is concluded that the present results-although discordant with several of Verney's results and assumptions-nevertheless support the concept of a cerebral solute receptor influencing the rate of renal water excretion.

Animals↗
PubMed1982

Central infusion of vasopressin decreased plasma vasopressin concentration in dogs.

The effects of increasing the cerebrospinal fluid (CSF) vasopressin concentration (CSFADH) by intracerebroventricular infusion of vasopressin on the plasma vasopressin concentration (PADH) were studied in four groups of anesthetized dogs. One group received an intracerebroventricular infusion of artificial CSF (ACSF) alone for 90 min; the other groups were infused intracerebroventricularly with vasopressin at rates of 10, 20, or 50 microunits/min for 90 min. Arterial blood and CSF samples were taken just before infusion and at 30-min intervals for 210 min. Vasopressin infused intracerebroventricularly at 10, 20, and 50 microunits/min resulted in peak CSFADH of 32.2 +/- 5.3, 82.6 +/- 4.5, and 131.4 +/- 12.5 microunits/ml and reductions in PADH of 32, 47, and 51%, respectively. Only the latter two responses were significant (P less than 0.5-0.01). Because the peak increases in CSFADH after intracerebroventricular infusion of vasopressin ranged from values that were similar to or five times higher than those seen after severe hemorrhage or intracerebroventricular hypertonic saline infusion, we suggest that centrally acting vasopressin may play a physiological role in control of vasopressin secretion.

Animals↗
PubMed1982

The effect of intracerebroventricular indomethacin on osmotically stimulated vasopressin release.

Experiments were carried out to investigate the effect of intracerebroventricular administration of a prostaglandin synthesis inhibitor on the osmotic control of vasopressin (ADH) secretion. During ventriculocisternal perfusion with indomethacin (7.6 microgram/min) or vehicle, dogs were infused intravenously with either 2.5 or 0.15 M NaCl. Hypertonic saline infusion elevated plasma osmolality approximately 60 mosm/kg H2O. In accordance, the plasma ADH concentration increased substantially in animals perfused ventriculocisternally with the vehicle (from 2.1 +/- 0.7 to 7.3 +/- 1.3 microU/ml); this response was markedly attenuated, however, in animals perfused with indomethacin (from 1.0 +/- 0.2 to 2.2 +/- 0.4 microU/ml). Isotonic saline infusion caused a decline in plasma ADH concentration which was similar in the indomethacin- and vehicle-perfused groups. Mean arterial blood pressure was unchanged during the experiments. In a companion study, ventriculocisternal perfusion with 152 ng PGE2/min was found to be as effective in stimulating ADH release in the presence of indomethacin as in its absence, indicating that the action of indomethacin in the first study was not nonspecific. The suppression of osmotically induced ADH release by intracerebroventricular indomethacin suggests that endogenous brain prostaglandins play a critical intermediary role in the osmotic control of ADH secretion.

Animals↗
PubMed1982

Effect of intravenous and intracerebroventricular infusion of hypertonic solutions on plasma and cerebrospinal fluid vasopressin concentrations.

In the anesthetized dog, intravenous infusion of 2.5 M saline (40 microliters/kg . min) increased plasma and cerebrospinal fluid (CSF) osmolality and the plasma vasopressin (ADH) concentration, but did not increase the CSF ADH concentration. The increase in the plasma ADH concentration coincided with the increase in plasma osmolality, but preceded the increase in CSF osmolality. Intracerebroventricular infusion of hypertonic artificial CSF (2,000 mosm/kg . H2O, 10 microliters/min) increased CSF osmolality and plasma CSF ADH concentrations; plasma osmolality did not increase. Thus, receptors which sense changes in plasma osmolality appear to be outside the blood-brain barrier; different receptors may sense changes in CSF osmolality.

Animals↗
PubMed1982

One-clip, one-kidney hypertension in rats with hereditary hypothalamic diabetes insipidus.

An attempt was made to produce one-clip, one-kidney hypertension in the rat with diabetes insipidus (DI). Renal artery constriction in unilaterally nephrectomized DI rats (DI-clip) resulted in an increased blood pressure in all 9 rats, but this response was only transient in 3 rats. The magnitude of the hypertension was less in the DI-clip rats than in Long-Evans rats subjected to the same protocol (LE-clip). Infusion of saralasin i.v. at doses of 10 and 30 micrograms/kg . min. 4 to 6 weeks after surgery was without effect on mean arterial pressure in LE-clip and control DI rats, but substantially lowered blood pressure in the DI-clip rats (p less that 0.05 - 0.01). It is concluded that vasopressin is not essential for the production of one-clip, one kidney hypertension in the rat, and that, in the DI rat, the renin-angiotensin system is an important factor in this form of hypertension.

Angiotensin II↗
PubMed1981

Changes in vasopressin concentration in plasma and cerebrospinal fluid in response to hemorrhage in anesthetized dogs.

In the anesthetized dog, the concentrations of vasopressin (ADH) in plasma and cerebrospinal fluid (CSF) were similar under basal conditions, and there was a highly significant positive correlation between them (r = 0.71, p less than 0.01). Although hemorrhage was capable of increasing the ADH concentration in both plasma and CSF, the threshold for the increase in plasma ADH was much lower than for the increase in the concentration of ADH in CSF. In addition, the magnitude of the increase in the concentration of ADH in plasma was considerably greater than that in CSF at a comparable degree of hemorrhage. Our results suggest that ADH released into CSF during hemorrhage may have a different origin from that released into blood.

Animals↗
PubMed1981

Central effects of dopamine and bromocriptine on vasopressin release and blood pressure.

In order to investigate the role of central dopaminergic receptors in the control of vasopressin release and in cardiovascular regulation, the effects of intracerebroventricular administration of dopamine (DA) and bromocriptine (BC), a specific DA agonist, were compared in the anesthetized dog. The drugs were infused over a 20-min period into a lateral ventricle. DA brought about a transient decrease in mean arterial blood pressure, a slight increase in heart rate toward the end of the experiment, and a suppression of vasopressin release. BC increased heart rate and decreased blood pressure to a greater extent than did DA, and doubled the plasma vasopressin concentration. The increase in vasopressin secretion preceded the fall in blood pressure, ans was, therefore, due to a direct central action of BC. Although in these circumstances it is difficult to determine the role of dopaminergic neurons in the control of vasopressin release, there is some reason to believe that this role may be expressed by the actions of BC under the present experimental conditions.

Animals↗
PubMed1981

The role of central adrenoreceptors in the control of vasopressin release and blood pressure.

In order to investigate the role of central noradrenergic neurons in the control of vasopressin (ADH) release and cardiovascular regulation, norepinephrine (1.4 microgram/kg), clonidine (0.1 microgram/kg), and isoproterenol (1.4 microgram/kg were infused into the lateral cerebral ventricle of the anesthetized dog. The drugs were given over a 20-min period, dissolved in 0.9% saline at a volume rate of 10 microliter/min. Both norepinephrine and clonidine markedly reduced ADH release and lowered arterial blood pressure and heart rate. Isoproterenol had no effect on ADH release and produced a slight reduction in arterial pressure and a large increase in heart rate. Pretreatment with phenoxybenzamine (100 microgram/kg, iv) completely blocked the effects of norepinephrine on blood pressure and heart rate but only partially (about 50%) inhibited the norepinephrine effect on ADH release. Intravenous isoproterenol lowered blood pressure and increased ADH release and heart rate. In none of the experiments could changes in ADH release be attributed to changes in plasma osmolality or plasma sodium and potassium concentrations. It is concluded that, in the anesthetized dog, intraventricular norepinephrine and clonidine decreased ADH release, blood pressure, and heart rate by stimulating alpha-adrenoreceptors. The increased release of ADH after peripheral administration of isoproterenol was presumably due to the reduction in blood pressure and decreased baroreceptor inhibition of ADH release.

Animals↗
PubMed1981

Characterization of the renal handling of vasopressin in the dog by stop-flow analysis.

The stop-flow technique has been used to characterize the renal handling of vasopressin in the anesthetized dog. To facilitate the measurement of vasopressin in small urine samples by a specific RIA, the plasma vasopressin concentration was elevated by the iv infusion of arginine vasopressin. Under control conditions, the urinary clearance of vasopressin did not differ significantly from the glomerular filtration rate. The data obtained with the stop-flow technique indicate that vasopressin was reabsorbed from or degraded in the proximal nephron and secreted into the distal nephron. Thus, vasopressin excreted in the final urine is the result of glomerular filtration (which is limited to the extent that vasopressin is bound to plasma proteins), proximal reabsorption or degradation of filtered vasopressin, and distal secretion of vasopressin. It is likely that the tubular secretion of vasopressin is an important component of the renal organ clearance of this hormone.

Animals↗
PubMed1981

Vasopressin in the rat with partial nephrectomy-salt hypertension.

The role of vasopressin in the pathogenesis of partial nephrectomy (PN)-salt hypertension was examined in the rat. Hypertension was produced by reducing renal mass 70% and substituting 1% saline for drinking water 2 to 4 days after surgery. PN alone resulted in an increase in systolic blood pressure. Subsequent salt loading led to a further large increase in arterial pressure. On the second to third day after substitution of saline for drinking water, urinary vasopressin excretion (UADHV) was increased six-fold and the plasma vasopressin concentration was increased two and one-half-fold. UADHV then fell to a level that was three-fold greater than control values 5 days later. Although there was a marked stimulation of vasopressin release during the period of salt loading, a vasopressin pressor antagonist had only a small effect on arterial pressure. This suggests vasopressin is not a major pressor agent in PN-salt hypertension.

Animals↗
PubMed1981

Vasopressin secretion in the New Zealand genetically hypertensive rat.

A study was undertaken to evaluate the role of vasopressin in the pathogenesis of hypertension in New Zealand genetically hypertensive (NZGH) rats. During the course of development of hypertension in NZGH rats from 4 to 11 weeks of age, the 24 h urinary excretion of vasopressin did not differ from that of the New Zealand normotensive control rats (NZNR). Furthermore, at the conclusion of the study (rats 13 to 14 weeks old), the plasma vasopressin concentrations in NZGH and NZNR rats were not significantly different. Although there was no evidence for a difference in secretion of vasopressin from the neurohypophysis in the NZGH rats, there was a substantially increased pressor responsiveness to vasopressin in these rats. This was not specific since NZGH rats also had an increased pressor responsiveness to angiotensin II. The importance of increased pressor responsiveness to vasopressin in the hypertensive process in the NZGH rat requires further study.

Angiotensin II↗
PubMed1980

Increased pressor responsiveness to enkephalin in spontaneously hypertensive rats: the role of vasopressin.

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection. 2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure. 3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats. 4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (D-Ala2)-methionine enkephalin. 5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.

Animals↗
PubMed1980

Effect of norepinephrine on plasma vasopressin concentration and renal water metabolism.

In the anesthetized, normally hydrated dog, the i. v. infusion of norepinephrine (NE; 0.5 microgram/kg/min) resulted in an increased blood pressure and a marked reduction in the plasma vasopressin (ADH) concentration (2.6 +/- 0.2 to 1.1 +/- 0.2 muU/ml). Urine flow and osmolar clearance, and urine osmolality fell. However, the negative free water clearance (TcH2O) increased, despite the reduction in plasma ADH levels. Thus, the NE-induced diuresis appeared to be due largely to the increased solute excretion, but the reduction in plasma ADH levels may also have been a factor. These data show that change in free water clearance is not a satisfactory index of change in the plasma ADH levels may also have been a factor. These data show that change in free water clearance is not a satisfactory index of change in the plasma ADH concentration when there are acute changes in renal hemodynamics and solute excretion. The norepinephrine-induced reduction in ADH secretion appeared to be due largely to increased activity of the arterial baroreceptors, but a central action cannot be ruled out.

Animals↗