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PubMed1995

Effects of variation in oxygen tension on responses of the human fetoplacental vasculature to vasoactive agents in vitro.

The human placenta perfused in vitro with Krebs' solution has been used to examine the effects of low oxygen tension on the vasoreactivity of the fetal placental vessels to several vasodilator and vasocontrictor autacoids. Increases in fetal arterial perfusion pressure (FAP) produced by endothelin-1 (ET-1, human), the thromboxane A2-mimetic U46619, 5-hydroxytryptamine (5-HT), angiotensin II (A II) and bradykinin (BK) were examined under conditions of high ( >or= 450 mmHg) and low <or= 50 mmHg) O2 tension. Similarly, decreases in pressure produced by adenosine triphosphate (ATP) and arachidonic acid (AA) were examined. The effects of these autacoids on the fetoplacental vasculature during low oxygen perfusion was compared to that obtained following nitric oxide synthase inhibition with N omega-nitro-L-arginine, (L-NOARG, 100 microns). Increases in FAP caused by ET-1, U46619, and 5-HT on fetoplacental blood vessels were not altered significantly at low oxygen tension, although that in response to BK was enhanced. Increases in FAP caused by A II were unchanged at low oxygen tension. ATP-induced decreases in FAP were reduced whereas AA-mediated changes were unchanged. Both low oxygen tension and L-NOARG produced an elevation in basal perfusion pressure. Perfusion of the human placenta with Krebs' solution of low oxygen tension may compromise placental vascular function. Impaired placental oxygenation may contribute to the development and severity of vasoconstriction in the placenta associated with pre-eclampsia/pregnancy induced hypertension.

Adolescent↗
PubMed1984

Place of vasoactive agents in the treatment of acute circulatory failure.

Increase in total cardiac output can improve oxygen delivery to the cells. Although inotropic drugs increase primarily myocardial contractility, they can adversely affect cardiac preload and afterload. Moreover, they can dangerously increase myocardial oxygen requirements. The combined use of vasodilating agents, with fluid challenge represents a challenging but more efficient treatment of acute circulatory failure.

Cardiac Output↗
PubMed1983

Species variation in the cerebrovascular response to neurotransmitters and related vasoactive agents.

Constrictory and dilatory responses of pial arteries to various receptor stimulants and modulators were evaluated in vitro and compared in rat, rabbit, cat and man. For the constrictory response, differences were noted especially in the rabbit, which responded strongly to histamine but poorly to noradrenaline and prostaglandin F2 alpha. Histamine was a prominent dilator, but only in rat and man. Isoprenaline induced effective vasodilation only in rat, and dopamine was efficient only in human pial arteries.

Animals↗
PubMed1994

Endothelium-denuded pulmonary resistance arteries from the fetal lamb: preparation and response to vasoactive agents.

A method was developed for preparing endothelium-denuded resistance arteries (mean internal diameter, 176 microns) from the term fetal lung to be used for tests in vitro. The endothelium was removed mechanically by passing a sandpaper-polished cat whisker through the lumen. Ultrastructurally, the preparation had a well-preserved internal elastic lamina which was facing the lumen without any endothelium superimposed. Its response to contractile agents (excess potassium, a thromboxane A2 analogue, endothelin-1) tended to be greater compared to the intact artery. Conversely, the relaxation to acetylcholine was abolished in the endothelium-denuded artery and, in its place, a modest contraction ensued. Sodium nitroprusside relaxation, unlike acetylcholine relaxation, was affected insignificantly by endothelium denudation. This preparation, in combination with the preparation of the intact resistance artery, is a useful, new tool for studying local factors responsible for pulmonary hemodynamic control in utero and through the transitional period at birth.

Acetylcholine↗
PubMed2005

Regulation of cerebral microvascular endothelial cell cyclooxygenase-2 message and activity by blood derived vasoactive agents.

We have investigated the effects of prolonged treatment of cerebral microvascular endothelial cells with vasoconstrictor products of blood clot hemolysis on prostanoid production and cyclooxygenase (COX)/prostacyclin synthase activity and message. Confluent primary cultures of endothelial cells derived from piglet cerebral microvessels were incubated with endothelin-1 (ET-1; 10 nM) or thromboxane A(2) analog U-46619 (1 microM), alone or combined, and COX/prostacyclin synthase activity determined following exposure of treated cells to arachidonic acid (10 microM) for 30 min. 6-KetoPGF(1)alpha and PGE(2) levels in the medium were determined using radioimmunoassay. Effect of treatments on COX-2 message was determined by RNAse Protection Assay. Combined treatment with ET-1 (10 nM) and U-46619 (1 microM) for 24h significantly reduced 6-ketoPGF(1)alpha and PGE(2) levels in the media by 57% and 33%. Treatment of cells with U-46619 alone increased both 6-ketoPGF(1)alpha and PGE(2) level in the media by 170% and 42%. Incubation of control cells with arachidonic acid (10 microM) for 30 min increased 6-ketoPGF(1)alpha and PGE(2) production by 163% and 567%. Pretreatment with ET-1 or U-46619 alone for 24h had no significant effect on 6-ketoPGF(1)alpha produced from exogenous arachidonic acid. However, PGE(2) production from exogenous arachidonic acid by cells pretreated with ET-1 but not with U-46619 was attenuated by 35%. Combined treatment with ET-1 and U-46619 reduced both PGE(2) and 6-ketoPGF(1)alpha production from arachidonic acid by 14% and 40%, respectively. Acute incubation of cells with ET-1 or U-46619 did not have any significant effects on COX-2 mRNA. In conclusion, combined ET-1 and U-46619 reduced prostanoid production. The reduction cannot be fully explained by changes in COX/prostacyclin synthase activity and/or message, but the changes could be due to reduced availability of free arachidonic acid potentially resulting from inhibition of endothelial phospholipase A(2).

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1993

Responses of placental arteries from normotensive and preeclamptic women to endogenous vasoactive agents.

OBJECTIVE: The hypothesis that preeclampsia may be associated with an increase in the response of the placental arteries to vasoconstrictors or a decrease in their response to vasodilators was tested. STUDY DESIGN: Concentration-response curves to various agents were determined on helical strips of fetal placental arteries from normotensive (n = 33) and preeclamptic (n = 8) women to calculate the potencies and maximal effects of the agents. RESULTS: Endothelin, prostaglandin F2 alpha, and serotonin caused concentration-dependent contractions; angiotensin II and norepinephrine produced little or no effects. The prostacyclin analog iloprost and atrial natriuretic factor, but not isoproterenol, relaxed placental arteries. Iloprost was more effective on preeclamptic than on normal arteries, but the effects of other agents on the two groups of arteries did not differ. Placental arteries exhibited spontaneous oscillations that were more marked in preeclamptic than in normal arteries and were inhibited by indomethacin. CONCLUSION: Preeclampsia is not associated with an increase in the responses of fetal placental arteries to vasoconstrictors or a decrease in their response to vasodilators. However, placental arteries from preeclamptic subjects exhibit increased oscillations.

Adult↗
PubMed1998

Effects of vasoactive agents in healthy and diseased human saphenous veins.

PURPOSE: Smooth muscle reactivity is one of the factors involved in the pathogenesis of varicose veins. We investigated the myotropic effects of the 3 main vasoconstrictor agents norepinephrine (NE), angiotensin II (Ang II), and endothelin-1 (ET-1) in isolated human saphenous veins. METHODS: Human saphenous veins were collected from 23 patients with primary chronic venous insufficiency who underwent elective varicose vein resections and who were stratified into the following 3 groups: group 1, 7 patients in clinical class 2; group 2, 9 patients in clinical classes 3 and 4; and group 3, 7 patients in clinical classes 5 and 6. Moreover, 6 patients who underwent arterial bypass grafting procedures represented the control group. The tissues were suspended in organ baths that contained Krebs solution, and their mechanical responses were measured isometrically. The cumulative concentration-response curves to Ang II, NE, and ET-1 were performed at 90-minute intervals in each tissue. RESULTS: In the control tissues, NE, Ang II, and ET-1 induced concentration-dependent contractions with apparent affinities (pEC50, the negative logarithm to base 10 of the molar concentration of the agonist, which produces the 50% of the maximal effect) and maximal effects (maximum effect, g of contraction) that were equal to 7.06 +/- 0.23, 8.53 +/- 0.34, 7.63 +/- 0.10, and 2.21 +/- 0.33, 1.65 +/- 0.31, 2.60 +/- 0.77, respectively. Two main findings were evident in comparison of varicose veins with control tissues. First, the maximum effect that was evoked by all of the stimulants was reduced progressively with the increasing severity of the disease, which raised the third group to statistical significance for both NE and Ang II (P <.05). Second, a marked reduction of Ang II apparent affinity was already evident in tissues that were taken from patients in an early stage of the disease (P <.05). CONCLUSION: The demonstration of a significant reduction in Ang II and NE contractile activities and the important reduction of that of ET-1 in the diseased veins as compared with the control tissues extends the previous observations regarding the impairment of smooth muscle contractility in primary chronic venous insufficiency. Moreover, the dramatic reduction of Ang II affinity, which appears in an early stage of the disease, supports the hypothesis that such abnormality within the venous wall could play a role in the pathogenesis of primary varicose vein disease.

Angiotensin II↗
PubMed2003

Influence of dietary salt intake on the response of isolated perfused mesenteric veins of the dog to vasoactive agents.

BACKGROUND: Previous work has established that a high dietary salt intake results in enhanced arterial vasoconstrictor responses to stimulation with agonists. This investigation was designed to investigate the effects of dietary salt on the responses of isolated capacitance vessels (third order mesenteric veins). METHODS: Dogs were fed diets containing low, intermediate, and high levels of dietary salt (0.4, 3.0, and 6.0 mmol kg/day). The animals were killed, and lengths of mesenteric vein were mounted in a perfusion myograph with changes in lumenal diameter measured using a video tracking device. Responses to cumulative doses of norepinephrine (NE) and acetylcholine (Ach) were then determined. RESULTS: The vasoconstrictor responses to NE were greater in the veins from dogs on a high salt diet. Acetylcholine also caused venoconstriction that also was greater in the high salt group of animals. Responses to Ach were unaffected by N(omega)-nitro-L-arginine methyl ester but were abolished by atropine. CONCLUSIONS: These results indicate that mesenteric veins from dogs fed a high salt diet constrict more powerfully in response to agonists, which could contribute to the hypertensive effects of high intakes of dietary salt.

Acetylcholine↗
PubMed1988

Potentiation of the anti-tumour effect of melphalan by the vasoactive agent, hydralazine.

The vaso-active drug hydralazine causes a considerable increase in the cytotoxic effect of melphalan towards the KHT tumour in mice. The enhancement in response, measured as the concentration of melphalan required to achieve a given tumour response, is 3.0 and 2.35 when determined using the regrowth delay assay and the technique for determining surviving fraction in vitro following treatment in vivo respectively. In contrast, measurement of systemic toxicity shows that the addition of hydralazine only causes a small increase (ER = 1.15) in melphalan damage. This suggests that the drug combination may have some therapeutic benefit. The tumour specificity for the action of hydralazine is supported by the finding that binding of 3H-misonidazole is increased in tumours but not in other tissues when mice are treated with hydralazine. Increased binding of labelled misonidazole is associated with an increase in the level and duration of hypoxia, which will occur as a consequence of changes in tumour blood flow brought about by hydralazine. However, hypoxia per se is not responsible for the enhanced effect of melphalan, since the agent BW12C, which also induces substantial tumour hypoxia as a result of changing the O2 affinity of haemoglobin, has no effect on melphalan tumour cytotoxicity.

Animals↗
PubMed2006

Alcoholic cirrhosis-associated hepatorenal syndrome treated with vasoactive agents.

BACKGROUND: A 35-year-old man with alcoholic cirrhosis, ascites and alcoholic hepatitis presented with new-onset renal insufficiency of unclear etiology after recovery from an episode of gastrointestinal bleeding. Renal function continued to worsen after cessation of diuretic therapy and initiation of volume resuscitation. INVESTIGATIONS: Physical examination, abdominal ultrasound, liver tests, basic metabolic panel, abdominal paracentesis, renal function tests, 24-h urine collections. DIAGNOSIS: Type 1 hepatorenal syndrome (HRS). MANAGEMENT: Intravascular volume resuscitation with normal saline and albumin followed by oral midodrine plus subcutaneous octreotide therapy. This regimen was continued until improvement and subsequent normalization of the serum creatinine.

Acute Kidney Injury↗
PubMed2000

The role of nitric oxide in the responses of the ovine digital artery to vasoactive agents and modification of these responses by endotoxin and cytokines.

1. Laminitis, an important cause of lameness in domestic ungulates, occurs as a result of altered digital perfusion. Endotoxin and cytokines may mediate the vascular derangements observed through alterations in nitric oxide production. In this study, the vascular responses of the isolated ovine digital artery were examined and the influence of endotoxin and cytokines investigated. 2. Neither removal of the endothelium nor incubation with N(G)-nitro-L-arginine methyl ester (L-NAME, 300 microM) altered the response to phenylephrine (PE, 1 nM to 300 microM). Indomethacin (10 microM) decreased PE log EC(50) from -6.22+/-0.08 to -6.55+/-0.07. Acetylcholine (1 nM to 1 mM) and bradykinin (BK, 100 pM to 3 microM) induced endothelium-dependent relaxation. Bradykinin-induced relaxation was reduced by L-NAME, E(max) falling from -61.7+/-7.4 to -34.0+/-2.1%. Addition of indomethacin further reduced BK E(max) to -9.6+/-2.8%. Sodium nitroprusside (1 nM to 300 microM) produced endothelium-independent relaxation that was unaffected by L-NAME or indomethacin. 3. Following a 6 h incubation with endotoxin (3 microml(-1)), arterial responses to PE and BK did not differ from polymyxin B-treated controls (10 microg ml(-1)). Arteries incubated for 6 h with interferon-gamma (IFN-gamma, 10 ng ml(-1)) and tumour necrosis factor-alpha (TNF-alpha, 5 ng ml(-1)) exhibited greater relaxation to BK (E(max)-50.0+/-5.1%) than polymyxin B-treated controls (E(max)-33.1+/-4.0%), but did not differ in their response to PE. 4. Prolonged incubation (16 h) with endotoxin (3 microg ml(-1)) did not alter the response to PE, however incubation with IFN-gamma (10 ng ml(-1)), TNF-alpha (5 ng ml(-1)) and interleukin-1beta (20 ng ml(-1)) for 16 h increased PE log EC(50) from -6.44+/-0.09 to -6. 10+/-0.11. 5. Nitric oxide is an important mediator of endothelium-dependent relaxation in ovine digital arteries but does not modulate PE-induced vasoconstriction. Incubation with cytokines decreased the sensitivity of digital arteries to PE.

Animals↗
PubMed2003

Effects of insulin on vascular responses to spinal cord stimulation and vasoactive agents in pithed rats.

1. Effects of insulin (2-600 pmol kg(-1) min(-1), i.v.) on vascular responses to spinal cord (lower thoracic vertebra, Th 9-12) stimulation (SCS) and to i.v. injection of noradrenaline (NA, 125-500 ng kg-1), angiotensin II (Ang II, 40-200 pmol kg(-1), acetylcholine (ACh, 1 nmol kg(-1), calcitonin gene-related peptide (CGRP, 0.1 nmol kg(-1) and sodium nitroprusside (SNP, 5 microg kg-1) were examined in pithed rats. 2.In euglycemic pithed rats, low and medium doses of insulin dose-dependently potentiated vasopressor responses to SCS (2-8 Hz), NA, while higher doses of insulin had little effect on SCS- and NA-induced pressor responses. All doses of insulin significantly augmented pressor responses to Ang II. 3. In pithed rats with artificially increased blood pressure, SCS (2 and 4 Hz) induced a frequency-dependent depressor response, which was blocked by infusion of CGRP(8-37) (CGRP receptor antagonist, 60 nmol kg(-1) min(-1). 4. In euglycemic pithed rats, low-doses of insulin significantly attenuated depressor responses to SCS and CGRP, but medium and high doses of insulin remained unaffected. 5. All doses of insulin significantly inhibited depressor response to ACh, while SNP-induced depressor response was not significantly affected by any doses of insulin. 6. These results suggest that insulin at low and medium concentrations increases adrenergic vasoconstriction, which is partly associated with inhibition of CGRPergic nerve function and endothelium function. It is also suggested that lack of insulin effect at higher concentrations may result from acute desensitization of insulin action, possibly via insulin receptors.

Acetylcholine↗