PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Vasopressors”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1978

Neurohypophyseal vasopressor principle: vasopressor hormone as well as antidiuretic hormone?

Studies on the vasopressor role of the antidiuretic hormone arginine-vasopressin (AVP) in DOC hypertension, in two-kidney Goldblatt hypertension, and in spontaneous hypertension of rats, and during acute blood pressure elevation after intracerebroventricular injection of angiotensin II and in glycerol-induced acute renal failure of rats are reviewed. For the measurement of plasma AVP a radioimmunoassay has been developed. For this assay, a series of criteria has been met which allows the conclusion that, in plasma of rats, the antibody measures AVP only. For the blockade of vasopressor effects of AVP a specific antiserum has been used. On the basis of a series of control studies it has been concluded, but not proven that the antiserum lowers blood pressure exclusively by blockade of AVP. It could be shown that in the various animal models of hypertension and of acute blood pressure elevation AVP exerts systemic vasoconstriction when its plasma concentrations are elevated. In those models where the renin-angiotensin system played no role in blood pressure control, the height of blood pressure was closely related to the plasma AVP concentrations. When this relationship was compared with that obtained after the i.v. infusion or injection of AVP, a marked shift to the left became apparent. Hence, sensitization to the vasopressor effect of AVP had occurred, the factor of sensitization amounting to more than 1,000. It is concluded that AVP is not only an antidiuretic hormone but also a vasopressor hormone, and that any systemic vasopressor effect of AVP requires a mechanism of sensitization.

Acute Kidney Injury↗
PubMedDate not supplied

Identification of vasopressor constituents of amniotic fluid in pregnancy toxaemia.

The vasopressor activity of human amniotic fluid was assessed in 46 primigravidas during the third trimester of pregnancy. The subjects included 20 normal and 26 cases of pregnancy toxaemia. For identification of the vasopressor activity of the amniotic fluid, blood pressure measurements were made in the intact rat, and the smooth muscle contraction of the rat ascending colon preparation was determined in vitro. The samples of amniotic fluid showing vasopressor activity were lyophilized and subjected to gel filtration using Sephadex G-100. The various fractions thus obtained were monitored at 280 nm and the pressor activity was re-estimated. It was observed that most of the pressor activity of the amniotic fluid of the toxaemic patients was capable of causing contraction of the rat colon as well as a significant rise in the systolic blood pressure of the intact rat. Furthermore, this activity was found to be heat-labile and was completely blocked by cinnarizine. Fractionation of the amniotic fluid showing vasopressor activity by gel filtration further substantiated the findings reported above. On the basis of these results it was concluded that the pressor activity of the amniotic fluid was due to the presence of an angiotensin II-like substance. Its concentration was found to be higher in the toxaemic group than in normotensive subjects.

Amniotic Fluid↗
PubMed1975

Structure-activity relationships of the vasopressor activity of canine peptide-A from fibrinogen.

Canine peptide-A was demonstrated to be an active vasopressor substance. The effect of intravenous injection of canine peptide-A was a prolonged rhythmic vasoconstriction and is unlike any previously described vasopressor peptides. The intravenous administration of canine peptide-A resulted in a maximum increase in mean blood pressure of 19.0 mm of mercury at a dose level of 2.5-10-minus 2 mumol. This pressor effect exhibited a log proportionality to the injected dose of peptide. The duration of the vasopressor effect was 30 min or greater. A rhythmic variation in pressor response was also observed in all experiments. The canine AP and B peptides were inactive when tested under the same conditions. The relationship between structure and biological activity was investigated. Structural degradation of half of the peptide molecule was performed without loss of vasopressor activity. The canine peptide-A is postulated as assisting in local hemostasis by vasoconstriction.

Amino Acids↗
PubMed1978

[1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid),4-valine,-8-D-arginine]vasopressin, a potent and selective inhibitor of the vasopressor response to arginine-vasopressin.

As part of a program in which we are attempting the design and synthesis of an antagonist of the antidiuretic response to arginine-vasopressin (AVP) [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid),4-valine,8-D-arginine]vasopressin [d(CH2)5VDAVP] was synthesized and assayed for antidiuretic, vasopressor, and oxytocic activities. The required protected intermediate was synthesized by a combination of solid-phase synthesis and an [8 + 1] coupling in solution. d(CH2)5VDAVP has an antidiuretic potency of 0.10 +/- 0.02 unit/mg, less than 1/10000 that of its parent [deamino,4-valine,8-D-arginine]vasopressin (dVDAVP). d(CH2)5VDAVP is a specific antagonist of the vasopressor responses to AVP. It has an antivasopressor pA2 value of 7.68 +/- 0.05 when tested against AVP. It is also an antagonist of the in vitro oxytocic response to oxytocin (pA2 value = 6.62 +/- 0.07). With its negligible antidiuretic activity, absence of oxytocic activity, and its potent and specific ability to antagonize the vasopressor effects of AVP, d(CH2)5VDAVP is one of the most potent and selective vasopressor antagonists reported to date. It should thus be a useful tool with which to probe the possible role(s) that AVP may play in cardiovascular regulation under normal and pathological conditions.

Animals↗
PubMed1978

Design of potent antagonists of the vasopressor response to arginine-vasopressin.

As part of a program in which we are attempting to design and synthesize antagonists of the vasopressor response to arginine-vasopressin (AVP), [1-deaminopenicillamine]arginine-vasopressin (dPAVP), [2-O-methyl)tyrosine]-arginine-vasopressin [Tyr(Me)AVP], and [1-deaminopenicillamine,2-(O-methyl)tyrosine]arginine-vasopressin [dPTyr(Me)AVP] were synthesized by the solid-phase method and assayed for vasopressor, antidiuretic, and oxytocic activities. Tyr(Me)AVP has a vasopressor potency of 9.7 +/- 0.5 units/mg and an antidiuretic potency of 386 +/- 36 units/mg. These values are 2.5 and 120%, respectively, of the corresponding potencies of AVP. The analogue is an antagonist of the in vitro response to oxytocin (pA2 = 7.44 +/- 0.12). dPAVP has an antivasopressor pA2 of 7.45 +/- 0.11. Its antidiuretic potency is 42.2 +/- 2 units/mg, 2.5% that of its parent, 1-[deamino]arginine-vasopressin (dAVP). It is an antagonist of the in vitro response to oxytocin (pA2 value = 6.93 +/- 0.10). dPTyr(Me)AVP has an antivasopressor pA2 of 7.96 +/- 0.05 and an antidiuretic potency of 3.5 +/- 0.5 units/mg. It is also an antagonist of the in vitro oxytocic response to oxytocin (pA2 value = 7.61 +/- 0.14). It is thus one of the most potent vasopressor antagonists reported to date.

Animals↗
PubMed1977

[1-deaminopenicillamine,4-valine]-8-D-arginine-vasopressin, a highly potent inhibitor of the vasopressor response to arginine-vasopressin.

In attempting to design an antagonist of the antidiuretic response to arginine-vasopressin (AVP) [1-deaminopenicillamine,4-valine,8-D-arginine]vasopressin (dPVDAVP) was synthesized by the solid-phase method and assayed for antidiuretic, vasopressor, and oxytocic activities. dPVDAVP has an antidiuretic potency of 123 +/- 22 units/mg, one-tenth that of its parent [deamino,4-valine,8-D-arginine]vasopressin (dVDAVP). Like dVDAVP its antidiuretic effect in conscious diabetes insipidus rats is greatly prolonged when compared to AVP. dPVDAVP causes a prolonged inhibition of vasopressor responses to AVP but not to norepinephrine or angiotensin II. It has an antivasopressor pA2 value of 7.82 +/- 0.05 when tested against AVP. Thus the penicillamine substitution at position 1 in dVDAVP increased its antivasopressor activity sixfold (dVDAVP has a pA2 value of 7.03 +/- 0.11). dPVDAVP is thus the most potent vasopressor antagonist yet reported. dPVDAVP was also found to be a potent inhibitor of the in vitro oxytocic response to oxytocin (pA2 value = 7.23 +/- 0.04). dPVDAVP with its potent and specific ability to antagonize the vasopressor effects of AVP should be a useful pharmacological tool with which to explore the possible participation of AVP's potent vasoconstrictor properties in cardiovascular regulation in physiological and pathological states.

Animals↗
PubMed2026

Closed-loop vasopressor systems for hemodynamic control in perioperative and critical care settings: a systematic review and meta-analysis.

Maintaining mean arterial pressure (MAP) within a predefined target is central to haemodynamic management in surgical and critically ill adults receiving vasopressors. Closed-loop vasopressor (CLV) systems automate titration to optimise blood pressure control, but their clinical effectiveness remains uncertain. We performed a systematic review and meta-analysis comparing CLV with manual titration. This PRISMA 2020-compliant review was prospectively registered in PROSPERO (CRD420250655697). MEDLINE, Embase, Scopus, Web of Science, CENTRAL, and the Cochrane Library were searched (January 2000-June 2025). Randomised controlled trials enrolling adults receiving vasopressors in perioperative or intensive care settings were included. Primary outcomes were time within the MAP target range and time spent in hypotension or hypertension. Risk of bias was assessed using RoB 2.0 and certainty of evidence using GRADE. Random- or fixed-effects models were selected according to heterogeneity. Six randomized controlled trials (215 patients) were included in the systematic review, whereas five perioperative trials contributed to the meta-analysis of haemodynamic control outcomes, and one ICU-based study was summarized narratively because it did not report comparable MAP control endpoints. CLV increased time within the MAP target range (mean difference [MD] 33.94%, 95% CI 20.41-47.46; I2 = 77%) and reduced time in hypotension (MD - 18.24%, 95% CI - 28.95 to - 7.53; I2 = 73%). There was no significant difference in time in hypertension, cumulative norepinephrine dose, or major/minor adverse events. ICU length of stay was not pooled because of clinical and methodological heterogeneity. Certainty of evidence ranged from low to high (moderate for haemodynamic control outcomes). CLV systems improved haemodynamic control, primarily in perioperative settings, but heterogeneity and small samples limit confidence in effect size and generalisability. Evidence in critically ill populations remains limited, and larger trials are needed to determine whether improvements in these physiological surrogate endpoints translate into meaningful patient-centred outcomes.

Humans↗
PubMed1975

Intracranial pressure during hypotension and subsequent vasopressor therapy in anesthetized cats.

The effects of vasopressor therapy on intracranial pressure (ICP) during hypotension were evaluated in 45 adult cats anesthetized with pentobarbital and hyperventilated via an endotracheal tube with nitrous oxide, 70 per cent, and oxygen, 30 per cent, to maintain Paco2 25 plus or minus 5 torr. Hypotension was induced by intravenous administration of trimethaphan camsylate or sodium nitroferricyanide and by hemorrhage. Vasopressor (norepinephrine, ephedrine, or isoproterenol) administration in the absence of hypotension caused slight transient increases in ICP. Trimethaphan produced increases in ICP averaging 4.3 mm Hg, while sodium nitroferricyanide caused no change and hemorrhage decreased ICP by 3.9 mm Hg. After hypotension was established, vasopressors caused increases in ICP of 1-21 mm Hg. The greatest increase was seen with norepinephrine administration during sodium nitroferricyanide-induced hypotension. Increases in ICP were pronounced in absolute magnitude and rapidity of rise but were of short duration (2 to 5 minutes). The elevation of pressure might be of clinical significance in patients who have pre-existing intracranial hypertension or space-occupying lesions.

Anesthesia, Inhalation↗
PubMedDate not supplied

Effects of patient age, pH of cerebrospinal fluid, and vasopressors on onset and duration of spinal anesthesia.

Two hundred twenty-two spinal anesthesias were administered with 10 mg. of tetracaine and 1 ml. of 10 percent dextrose to investigate the effects of vasopressors, patients age, and pH of cerebrospinal fluid on the onset and duration of spinal anesthesia. Neither the differences in overall age, cerebrospinal fluid pH, nor the addition of vasopressors had any significant effect on onset. Duration, however, was significantly prolonged by the addition of vasopressors, 53 percent prolongation by 0.2 mg. of epinephrine and 72 percent prolongation by 2 mg. of phenylephrine.

Age Factors↗
PubMedDate not supplied

Distribution of oxytocic and vasopressor activity in the rat diencephalon.

The oxytocic and vasopressor activity was studied in five 1 mm thick, horizontal sections of the rat diencephalon. The diencephalon was cut frozen in dry ice. The sections obtained from identical parts of the diencephalon of 10 rats were homogenized together in 0.9% NaCl solution acidified with glacial acetic acid. The homogenate was heated to 100 degrees C for 5 min and centrifuged. The oxytocic activity of extracts was determined in vitro by, the method of Holton using the rat myometrium. The vasopressor activity was determined in vivo recording blood pressure in the carotid artery of rat by the method of Dekańaski. Oxytocic activity was found in all five sections of diencephalon and vasopressor activity in only two sections. The first section included the median eminence and ventral hypothalamus together with the supraoptic nucleus, the second section included the the dorsal hypothalamus with paraventricular nucleus, the third section--the ventral thalamus, the fourth section--the middle part of thalamus, the fifth section--the dorsal thalamus.

Animals↗
PubMed1977

Vasopressor role of ADH in the pathogenesis of malignant DOC hypertension.

During the onset of malignant hypertension (MH) in rats treated with deoxycorticosterone trimethylacetate (DOC), plasma arginine vasopressin (AVP) concentrations increase tenfold as a consequence of hypovolemia and hyperosmolality. In benign hypertensive (BH) rats, plasma AVP is increased threefold in comparison with control animals. Plasma renin is markedly suppressed in both BH and MH animals. In MH rats, biologically active AVP antiserum lowers blood pressure (BP) transiently to normal or subnormal levels; in BH rats, a small BP-lowering effect of the AVP antiserum is seen. (Biologically active angiotensin II antiserum does not lower BP in MH rats.) The relationship between the height of BP and plasma AVP concentration in DOC hypertensive rats indicates, when compared with that relationship in diabetes insipidus rats infused with AVP, a marked enhancement of the vasopressor effect of AVP. These findings and the earlier observation of vasopressin-induced vascular damage by Byrom (F. B. Byrom, The Hypertensive Vascular Crisis. London: Heinemann, 1969) strongly suggest that ADH is involved as a vasopressor hormone in the pathogenesis of malignant DOC hypertension.

Angiotensin II↗
PubMed1976

Contribution of vasopressor and plasma kininogen changes towards acute adrenaline pulmonary edema in the rat.

Acute pulmonary edema, evidenced by increased lung/body weight ratios, was evoked in rats within 5 min following the intravenous injection of 16-40 mug/kg of adrenaline. This change was accompanied by a decrease of 40% of circulatory kininogen not due to generalized plasma protein loss. Rats treated 10-20 min prior to adrenaline with 10 mg/kg of acetylsalicylate (Aspirin), 1000 KIU/kg of Kunitz anti-protease (Trasylol), or 10 mg/kg of soybean trysin inhibitor (SBTI), failed to exhibit pulmonary edema or decreased plasma kininogen levels, but were as sensitive as untreated animals to the arterial hypertensive effect of adrenaline. 4.8 mug/kg of carbamylcholine administered together with 40 mug/kg of adrenaline, prevented pulmonary edema. Carbamylcholine did not reduce plasma kininogen consumption by adrenaline, but effectively decreased the raised systolic arterial blood pressure, the increased systolic-diastolic pressure interval as well as the reflex slowing of the heart presented by adrenaline-treated rats. It seems that in the adrenaline-treated rat, pulmonary edema results from the joined action of vasopressor effects leading to hydrostatically forced outflow of vascular fluid, and of kinin release leading to increased peripheral vascular permeability.

Animals↗
PubMed1978

Identification of vasopressor phospholipid in crude soybean lecithin.

The vasopressor phospholipid in crude soybean lecithin was isolated by column chromatography on Sephadex LH-20. It represented 0.1% of crude soybean lecithin. The isolated phospholipid was identified to be lysophosphatidic acid by gas chromatography-mass spectrometry analysis of TMS-deacylated product and acetolysis product. Nuclear magnetic resonance analysis favored the 1-monoacyl isomer over the 2-isomer. By enzymic determination with L-3-glycerophosphate dehydrogenase, the isolated phospholipid was identified as 1-monoacyl-L-3-glycerophosphate. Gas chromatographic examination revealed that it was composed of a large percentage of unsaturated fatty acids, especially linoleic acid. The activity of isolated lysophosphatidic acid was slightly less than that of synthetic 1-linoleoyl-L-3-glycerophosphate.

Animals↗
PubMed1979

[The vasopressor role of ADH in the maintenance of blood pressure in experimentally hypertensive rats (author's transl)].

In order to investigate the vasopressor role of ADH in the regulation of blood pressure, passive immunization experiments with an antibody to AVP were carried out in experimentally hypertensive rats. In hypertensive rats treated with deoxycorticosterone acetate (DOCA), spontaneously hypertensive rats (SHR) and spontaneously hypertensive stroke-prone rats (SHR-sp), the intravenous injection of a specific vasopressin antibody resulted in a transient fall of blood pressure of 11 approximately 25mmHg, while in rats with two-kidney Goldblatt hypertension and normal rats, the blood pressure was not affected. This strongly suggests that ADH contributed to systemic vaso-constriction in DOCA hypertension and spontaneous hypertension in rats.

Animals↗
PubMed1976

[The effectiveness of vasopressors and vasodilators for pharmaco-dynamic renal angiography (author's transl)].

9,450 radiographs of 355 patients were analysed in order to determine the diagnostic values of pharmaco-dynamic renal angiography. In each case renal angiography was performed by a conventional techinique as the basis for a clinical experimental study of the effectiveness of a-renergic and cholinergic drugs. The comparison showed unequivocally that pharmacodynamic methods may increase the value of renal angiography. Vasopressors alter the pressure gradient during the arterial phase and improve filling of neovascular areas, which are themselves unreactive. The value of the vasodilators depends on the increased contrast values during the parenchymatous and venous phases of the angiogram. In this way structural changes in tne renal parenchyma and pathological changes in the veins can be emphasised. The value of adrenergic drugs consists in increasing the vascular supply to various tumours, focal inflammatory disease and renal contusion, whereas cholinergic drugs are suitable for improving the demonstration of parenchymal lesions, such as tumours, cysts, abscesses, tuberculomas and localised renal trauma. The results indicate clearly that pharmaco-dynamic methods represent an integral part of renal angiography.

Acetylcholine↗