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PubMed1993

Effects of endothelin receptor antagonist on cyclosporine-induced vasoconstriction in isolated rat renal arterioles.

Recent evidence suggests that the potent constrictor peptide, endothelin (ET) has a mediating role in cyclosporine A (CsA)-related renal vasoconstriction. However, the nature of the CsA-ET interaction and effect on the renal vasculature is uncertain. The purpose of the present study was twofold: (a) to determine if CsA exposure caused direct local release of ET from the endothelium of the renal microvasculature and (b) to determine if locally generated ET has paracrine effects on the underlying vascular smooth muscle to induce vasoconstriction. Experiments were performed in isolated rat renal arterioles. First it was determined that both afferent arteriole (AA) and efferent arteriole (EA) exhibited concentration-dependent decreases in lumen diameter to increasing molar concentrations of CsA. The AA was more sensitive to the vasoconstrictive effects of CsA than the EA. Next, the blocking effect of a recently synthesized putative ETA receptor antagonist was verified in both the AA and EA, where it was found that the cyclic peptide cyclo D-Asp-L-Pro-D-Val-L-Leu-D-Trp totally inhibited the vasoconstriction observed with ET addition. Finally, the role of locally stimulated ET in CsA-induced vasoconstriction was tested by determining the effect of the ETA receptor antagonist on CsA-induced AA and EA constriction. In the AA the vasoconstrictor effect of 10(-11) M CsA was completely blocked by the ETA receptor antagonist. However, in contrast to AA, 10(-11) M CsA in EA in the presence of the ETA receptor antagonist decreased EA lumen diameter by a mean of 41% from baseline (4.80 +/- 0.75 microns vs 7.80 +/- 0.84 microns, P < 0.05). This change in lumen diameter was similar to that induced by CsA alone. These data suggest that CsA directly constricts renal microvessels. This effect is mediated by ET in the AA but not the EA.

Amino Acid Sequence↗
PubMed1997

ATP-sensitive potassium channels mediate contraction-induced attenuation of sympathetic vasoconstriction in rat skeletal muscle.

Sympathetic vasoconstriction is sensitive to inhibition by metabolic events in contracting rat and human skeletal muscle, but the underlying cellular mechanisms are unknown. In rats, this inhibition involves mainly alpha2-adrenergic vasoconstriction, which relies heavily on Ca2+ influx through voltage-dependent Ca2+ channels. We therefore hypothesized that contraction-induced inhibition of sympathetic vasoconstriction is mediated by ATP-sensitive potassium (KATP) channels, a hyperpolarizing vasodilator mechanism that could be activated by some metabolic product(s) of skeletal muscle contraction. We tested this hypothesis in anesthetized rats by measuring femoral artery blood flow responses to lumbar sympathetic nerve stimulation or intraarterial hindlimb infusion of the specific alpha2-adrenergic agonist UK 14,304 during KATP channel activation with diazoxide in resting hindlimb and during KATP channel block with glibenclamide in contracting hindlimb. The major new findings are twofold. First, like muscle contraction, pharmacologic activation of KATP channels with diazoxide in resting hindlimb dose dependently attenuated the vasoconstrictor responses to either sympathetic nerve stimulation or intraarterial UK 14,304. Second, the large contraction-induced attenuation in sympathetic vasoconstriction elicited by nerve stimulation or UK 14,304 was partially reversed when the physiologic activation of KATP channels produced by muscle contraction was prevented with glibenclamide. We conclude that contraction-induced activation of KATP channels is a major mechanism underlying metabolic inhibition of sympathetic vasoconstriction in exercising skeletal muscle.

Adrenergic alpha-Agonists↗
PubMed2006

Dissociation of local nitric oxide concentration and vasoconstriction in the presence of cell-free hemoglobin oxygen carriers.

Cell-free hemoglobin's (CFH) high affinity for nitric oxide (NO) could limit CFH's use as an oxygen-carrying blood replacement fluid because it scavenges NO, causing vasoconstriction and hypertension. However, the extent to which perivascular NO levels change following intravascular administration of hemoglobin (Hb) with different molecular dimensions correlates with vasoconstrictive responses in the microcirculation is unknown. The study objective was to determine vasoconstrictive effects following bolus infusions of (1) alphaalpha cross-linked Hb; (2) polymerized bovine Hb; or (3) polyethylene glycol-decorated Hb (PEG-Hb), by measurements of in vivo microvessel diameter, blood flow, perivascular NO concentration, and systemic hemodynamic parameters. All CFHs caused reductions in perivascular NO levels, not correlated to microvascular responses. PEG-Hb (largest molecular volume) maintained blood flow, while the others caused vasoconstriction and reduced perfusion. All solutions increased mean arterial pressure due to vasoconstriction and blood volume expansion, except for PEG-Hb, which increased blood pressure due to blood volume expansion and maintenance of cardiac output. In conclusion, perivascular NO reduction is similar for all Hb solutions because NO binding affinities are similar; however, effects on vascular resistance are related to the type of molecular modification, molecular volume, and oxygen affinity.

Animals↗
PubMed1995

Hematoma-induced enhanced cerebral vasoconstrictions to leukotriene C4 and endothelin-1 in piglets: role of prostanoids.

Cerebral hematoma enhances vasoconstriction induced by topical application of the vasoconstrictor agents endothelin-1 (ET-1) and leukotriene C4 (LTC4). We investigated the influence of dilator prostanoids on vasoconstrictions induced by ET-1 and LTC4 in piglets. Newborn pigs anesthetized with alpha-chloralose were fitted with closed cranial windows 4 d after cortical subarachnoid injections of artificial cerebrospinal fluid (aCSF) (control) or blood (hematoma). The responsiveness of pial arterioles to topical application of the vasoconstrictors ET-1 and LTC4 was examined in the control and hematoma groups before and after treatment with indomethacin (5 mg/kg, i.v.). Vasoconstriction to topical application of LTC4 and ET-1 was enhanced by hematoma compared with the control (28 +/- 2% versus 21 +/- 2% for 10(-8) M LTC4 and by 25 +/- 2% versus 15 +/- 1% for 10(-8) M ET-1, respectively). The lower dose of ET-1 (10(-12) M) dilated pial arterioles in the control group by 6 +/- 2%, hematoma blocked this dilation and it was converted to constriction (10 +/- 1%). Indomethacin treatment enhanced vasoconstriction to LTC4 in the control group to a similar constriction to that observed in the hematoma group. Indomethacin treatment also enhanced vasoconstriction to ET-1 in the control group (25 +/- 1% for 10(-8) M) to similar constrictions to those observed in the hematoma group (25 +/- 2% for 10(-8) M). Dilation to the lower dose of ET-1 was blocked and converted to constriction (17 +/- 2% for 10(-12) M) by indomethacin treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Bradykinin-induced pulmonary vasoconstriction is time and inducible nitric oxide synthase dependent in a peritonitis sepsis model.

In an isolated perfused lung model, bradykinin induced pulmonary vasoconstriction in rats made septic by the injection of lipopolysaccharide (LPS). To mimic the pathophysiology of sepsis in humans more closely, we investigated pulmonary endothelial injury in a peritonitis model (cecal ligation and perforation; CLP). Male Sprague-Dawley rats were randomly divided into nine groups (n = 6-8). LPS and CLP rats were compared after 6 h with and without treatment with a selective inhibitor of inducible nitric oxide synthase (iNOS), L-N(6)-(1-iminoethyl)-lysine. Time dependency was investigated in CLP-treated rats at 24 h. The pulmonary circulation was isolated and perfused with a constant flow after the rats' tracheas were intubated and ventilated. Bradykinin (1, 3, and 6 microg) was injected, and changes in perfusion pressure were measured. Lungs were harvested for Western blot analysis to determine the role of iNOS in pulmonary endothelial dysfunction. In contrast to CLP 24 h rats, dose-dependent bradykinin-induced pulmonary vasoconstriction was observed in LPS and CLP 6 h rats. Concomitant administration of L-N(6)-(1-iminoethyl)-lysine significantly attenuated this vasoconstriction in both groups. The iNOS protein was expressed in lung homogenates from LPS 6 h and CLP 6 h but not from CLP 24 h rats. Both sepsis models caused bradykinin-induced pulmonary vasoconstriction, with the CLP groups demonstrating a time dependency of this effect. In conjunction with the time-dependent decrease in iNOS protein, the attenuated bradykinin-induced vasoconstriction due to selective iNOS inhibition suggests an important role for iNOS in pulmonary endothelial injury for both sepsis models.

Animals↗
PubMed2005

Effect of adrenomedullin on adrenergic vasoconstriction in mesenteric resistance arteries of the rat.

Adrenomedullin (AM) is a hypotensive peptide that belongs to a family of peptides structurally related to calcitonin gene-related peptide (CGRP). The present study examined the effect of AM on adrenergic nerve-mediated vasoconstriction in rat perfused mesenteric vascular beds without endothelium. Perfusion of AM at 0.1 nM but not 10 nM increased vasoconstrictor responses to periarterial nerve stimulation (PNS) (1-4 Hz), while AM at 10 nM significantly attenuated vasoconstriction induced by bolus injection of norepinephrine (NE). In preparations treated with capsaicin (a CGRP depletor), pressor responses to both PNS and NE injection were markedly attenuated by AM. Perfusion of CGRP(8-37) (a CGRP-receptor antagonist) significantly potentiated the PNS- but not the NE-induced vasoconstriction. Combined perfusion of CGRP(8-37) and AM had no effect on the PNS-induced response and antagonized the inhibitory effect of AM on the NE-induced response. AM(2-52) (an AM-receptor antagonist) did not influence the effect of AM. These findings suggest that AM facilitates adrenergic vasoconstriction by inhibiting neurotransmission of CGRP-containing nerves, which counteract adrenergic nerve-mediated vasoconstriction.

Adrenomedullin↗
PubMed2005

Inorganic arsenite potentiates vasoconstriction through calcium sensitization in vascular smooth muscle.

Chronic exposure to arsenic is well known as the cause of cardiovascular diseases such as hypertension. To investigate the effect of arsenic on blood vessels, we examined whether arsenic affected the contraction of aortic rings in an isolated organ bath system. Treatment with arsenite, a trivalent inorganic species, increased vasoconstriction induced by phenylephrine or serotonin in a concentration-dependent manner. Among the arsenic species tested--arsenite, pentavalent inorganic species (arsenate), monomethylarsonic acid (MMAV), and dimethylarsinic acid (DMAV)--arsenite was the most potent. Similar effects were also observed in aortic rings without endothelium, suggesting that vascular smooth muscle plays a key role in enhancing vasoconstriction induced by arsenite. This hypercontraction by arsenite was well correlated with the extent of myosin light chain (MLC) phosphorylation stimulated by phenylephrine. Direct Ca2+ measurement using fura-2 dye in aortic strips revealed that arsenite enhanced vasoconstriction induced by high K+ without concomitant increase in intracellular Ca2+ elevation, suggesting that, rather than direct Ca2+ elevation, Ca2+ sensitization may be a major contributor to the enhanced vasoconstriction by arsenite. Consistent with these in vitro results, 2-hr pretreatment of 1.0 mg/kg intravenous arsenite augmented phenylephrine-induced blood pressure increase in conscious rats. All these results suggest that arsenite increases agonist-induced vasoconstriction mediated by MLC phosphorylation in smooth muscles and that calcium sensitization is one of the key mechanisms for the hypercontraction induced by arsenite in blood vessels.

Animals↗
PubMed1992

Cocaine produces coronary artery vasoconstriction independent of an intact endothelium.

Studies have demonstrated that cocaine causes coronary vasoconstriction, but this has been unassociated with myocardial ischemia. Therefore, cocaine seems unlikely to precipitate myocardial infarction in the absence of potentiating factors. We hypothesized that injury to coronary endothelium could potentiate cocaine-induced coronary vasoconstriction by decreasing EDRF. The effect of cocaine on LAD diameter was measured in dogs subjected to coronary endothelial denudation and compared with that in a non-denuded control group. Endothelial denudation was accomplished by abrasion with an inflated angioplasty balloon and confirmed in vivo by demonstrating a vasoconstrictive response to infused acetylcholine and by postmortem scanning electron microscopy. Cocaine produced a similar maximal reduction in LAD diameter in both groups. Thus, cocaine induces endothelium-independent coronary artery vasoconstriction. Failure of endothelial injury to potentiate the coronary vasoconstrictive effect by cocaine suggests that factors other than endothelial dysfunction may be important in pathogenesis of cocaine-associated myocardial infarction.

Acetylcholine↗
PubMed1985

Potential role of arachidonic acid metabolites in hypoxic pulmonary vasoconstriction.

Hypoxic vasoconstriction is important for lung ventilation/perfusion matching. The mechanism of hypoxic vasoconstriction remains elusive. Arachidonic acid is released from hypoxic tissues; possibly vasoconstricting arachidonate metabolites are involved in hypoxic pulmonary vasoconstriction. Data are presented that consider (a) lipoxygenase product(s) as "local," which could be involved in the hypoxia induced pulmonary vasoconstriction.

Animals↗
PubMed2005

Postpartum angiopathy and other cerebral vasoconstriction syndromes.

The phenomenon of reversible cerebral arterial segmental vasoconstriction has been associated with several conditions including pregnancy and puerperium ("postpartum angiopathy"), thunderclap headache, and use of vasoconstrictive medications. Patients with cerebral vasoconstriction typically present with sudden, severe, and recurrent ("thunderclap") headaches and can develop strokes. Cerebral vasoconstriction syndromes are under- recognized, are poorly characterized, and are frequently misdiagnosed as primary cerebral vasculitis. This article presents an illustrative case report and reviews the historical aspects, clinical and imaging characteristics, etiology, differential diagnosis, management, and prognosis of cerebral vasoconstriction syndromes.

Adult↗
PubMed1989

Almitrine bismesylate reduces hypoxic pulmonary vasoconstriction in isolated rat lungs.

The purpose of this study is to test how almitrine bismesylate (Alm) affects the function of pulmonary vasculature during normoxic ventilation, and whether low doses of Alm not causing detectable vasoconstriction during normoxic ventilation potentiate hypoxic pulmonary vasoconstriction (HPVC). Isolated Wistar male rat lungs were perfused with homologous blood at constant flow, and venous and ventilatory pressure. In the first experiment, after equilibration, dose-response curves to Alm (from 0 to 1000 ng/ml, n = 10) were measured under the ventilation with normoxic gas mixture (21% O2, 5% CO2, 74% N2). It was found that Alm causes a dose-dependent pulmonary vasoconstriction. In the second experiment, low doses of Alm (125 mg/ml) or diluent of Alm (malic acid) was injected to the blood reservoir. This doses of Alm did not cause significant vasoconstriction during normoxic gas ventilation compared with malic acid. After stabilization of pulmonary arterial pressure, the lungs were exposed to three cycles of normoxia (10 min) and hypoxia (10 min) through ventilation with gas containing 21% or 2% O2 and 5% CO2. It was observed that low doses of Alm significantly reduce HPVC (p less than 0.05) on the later periods of the first and the second hypoxic challenges. However, no significant difference was revealed among two groups in the third hypoxic challenge. Directly measured blood Alm concentration was significantly lower in the third challenge than in the first challenge. Responses to angiotensin II were not decreased by Alm. In conclusion, high doses of Alm constrict pulmonary vasculature dose-dependently, and low doses of the drug not causing vasoconstriction during normoxia reduce HPVC in rat.

Almitrine↗
PubMed1992

Recurrent coronary vasoconstriction caused by intranasal cocaine: possible role for metabolites.

OBJECTIVE: To define the temporal characteristics of cocaine-induced coronary vasoconstriction in humans and to assess the relation between cocaine-induced coronary vasoconstriction and the blood concentration of cocaine and its main metabolites. DESIGN: Randomized, double-blind, controlled clinical trial. SETTING: Cardiac catheterization laboratory of a large teaching hospital. PATIENTS: Eighteen patients (16 men and 2 women, 37 to 65 years of age) having catheterization for evaluation of chest pain. MEASUREMENTS: At catheterization, patients received intranasal saline (8 patients) or cocaine, 2 mg/kg body weight (10 patients). Cineangiographic examination of the left coronary artery and quantitation of the blood concentration of cocaine and its metabolites were done before (baseline) and 30, 60, and 90 minutes after administration of intranasal saline or cocaine. RESULTS: In response to cocaine, proximal coronary arterial diameter decreased from 2.4 +/- 1.6 mm (mean +/- SD) at baseline to 2.0 +/- 1.4 mm at 30 minutes (P less than 0.05). This change corresponded temporally to the peak blood concentration of cocaine. At 60 minutes, the cocaine concentration decreased and coronary artery diameter returned to baseline (2.3 +/- 1.6 mm) (P greater than 0.05 compared with baseline). At 90 minutes, all patients had recurrent vasoconstriction (1.9 +/- 1.4 mm, P less than 0.05) despite a further decrease in the blood cocaine concentration. This vasoconstriction corresponded temporally with an increasing blood concentration of cocaine's main metabolites, benzoylecgonine and ethyl methyl ecgonine. No changes were observed in the control group. CONCLUSION: Intranasal cocaine causes recurrent coronary vasoconstriction, which may be due to its metabolites.

Administration, Intranasal↗
PubMed1999

Renal vasoconstriction induced by oxidized LDL is inhibited by scavengers of reactive oxygen species and L-arginine.

BACKGROUND: Low density lipoprotein (LDL) may be involved in the pathogenesis of glomerulosclerosis and progressive renal dysfunction associated with atherosclerotic renal artery stenosis (RAS). This study was undertaken to investigate the effects of native (n-LDL) and oxidized LDL (ox-LDL) on renal vascular response and function in an isolated perfused rat kidney (IPRK) model. MATERIAL AND METHOD: IPRK model was used for the study at a constant pressure of 100 mm of Hg in the renal artery with continuous monitoring of pressure and renal perfusate flow. Urine and perfusate samples were collected to determine [14C] Inulin clearance and fractional reabsorption of sodium. To elucidate the role of nitric oxide (NO) urinary c-GMP, nitrate and nitrite excretion were measured and the responses to the NO synthase inhibitor N-monomethyl-L-arginine (LNMMA) and the NO donor Nitroso-glutathione (GSNO) were assessed. The effect of L-arginine supplementation and the role of reactive oxygen species were also studied by adding superoxide dismutase (SOD) and catalase. RESULTS: Ox-LDL but not n-LDL caused vasoconstriction in IPRK, as evidenced by a significant dose dependent reduction in renal perfusate flow. [14C] Inulin clearance and fractional reabsorption of sodium were reduced during ox-LDL infusion whereas no significant change occured with n-LDL. There was a significant decrease in urinary excretion of c-GMP during ox-LDL infusion. 10 microM LNMMA significantly increased and GSNO (10 microM) significantly diminished the vasoconstrictory effect of ox-LDL. The presence of L-arginine (100 & 500 microM) significantly decreased ox-LDL induced vasoconstriction. SOD (150 U/ml) and catalase (1200 U/ml) both had a significant inhibitory effect and the combination of SOD and catalase almost completely abolished the vasoconstriction due to ox-LDL. CONCLUSION: These results suggest that ox-LDL induced vasoconstriction in IPRK is mediated by decreased activity of NO probably due to inactivation of NO by reactive oxygen species. The free radical scavengers SOD, catalase and L-arginine provided protection against ox-LDL induced vasoconstriction in this model.

Animals↗
PubMed2003

Association of vasoconstrictive exposures with risks of gastroschisis and small intestinal atresia.

BACKGROUND: Gastroschisis and small intestinal atresia are congenital anomalies that may arise from vascular disruption. It is hypothesized that maternal exposure to cocaine, amphetamines, decongestants and nicotine, all of which have vasoconstrictive actions, can contribute to these defects. The present study examined risks of gastroschisis and small intestinal atresia associated with combined exposure to vasoconstrictive drugs and cigarette smoking. METHODS: This was a retrospective study conducted from 1995 to 1999 in 15 cities across the United States and Canada. Mothers of 205 gastroschisis cases, 127 small intestinal atresia cases, 381 malformed controls and 416 nonmalformed controls were interviewed within 6 months of delivery. RESULTS: Reported vasoconstrictive drugs included pseudoephedrine, phenylpropanolamine, ephedrine and methylenedioxymethamphetamine. Combined exposure to vasoconstrictive drugs and cigarette smoking in the first 2.5 months of pregnancy was reported by 9% of gastroschisis cases, 9% of small intestinal atresia cases and 4% of controls. Multivariate-adjusted odds ratios, controlling for the effects of age, education, income, other drug use and alcohol intake, were 2.1 (95% confidence interval = 1.0-4.4) for gastroschisis and 2.8 (1.1-6.9) for small intestinal atresia. Risks of each defect increased with increasing level of cigarettes (P for trend = 0.019 and 0.012, respectively). Vasoconstrictive drug use among smokers of 20 or more cigarettes a day increased gastroschisis risk 3.6-fold (1.3-10.3) and small intestinal atresia risk 4.2-fold (1.1-16.2). CONCLUSIONS: These findings provide further evidence of vascular disruption as an etiology for gastroschisis and small intestinal atresia.

Adult↗
PubMed1992

[Effect of alpha-adrenergic receptor blockade on peripheral vasoconstriction induced by the cold pressor test. Evidence for functional integrity of alpha 1 and alpha 2 adrenergic receptors in patients with congestive heart failure].

Central sympathetic stimulation results in direct vascular vasoconstriction mediated by activation of alpha-adrenergic receptors. However, it is unknown whether this vasoconstriction is mediated by alpha 1 or alpha 2-adrenoceptor subtypes. In patients with congestive heart failure (CHF), both circulating and neuronally released catecholamines produces vasoconstriction via alpha-adrenergic stimulation. This vasoconstriction produces detrimental hemodynamic effect in CHF patients since it increases right and left ventricular filling pressures and pulmonary and systemic vascular resistances. While the myocardial alpha 1-adrenoceptors seems not to be down-regulated in heart failure, the functional integrity of vascular alpha 1 and alpha 2-adrenoceptors in CHF remains to be elucidated. Accordingly, the present study was designed to assess whether the limb vascular response to alpha 1 or alpha 2-adrenoceptor stimulation is impaired in patients with CHF. We studied 25 control subjects and 19 patients with CHF due to primary dilated cardiomyopathy. Forearm blood flow was measured by venous occlusion plethysmography. Sympathetic stimulation was produced by cold. The intraarterial pump-infusions of BHT 933 (a selective alpha 2-adrenoceptors agonist agent, 0.1, 1, 10 micrograms/kg/min for 5 min) produced the same peripheral vasoconstriction in CHF and in control subjects: 32 +/- 23.9%, 47.3 +/- 20% and 55 +/- 26.1% respectively at I, II, and III dose in CHF and 28.7 +/- 38.6%, 36 +/- 14.5%, and 57 +/- 13.8% respectively at I, II, and III dose in control subjects. The dose response to BHT 933 was not different in the 2 groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed2003

Cerebral vasoconstriction in neurally mediated syncope: relationship with type of head-up tilt test response.

BACKGROUND: The pathophysiology of neurally mediated syncope (NMS) is unclear. Cerebral vasoconstriction has been observed in NMS patients during tilt testing. To shed light on the pathophysiology of NMS, we attempted to establish whether the degree of cerebral vasoconstriction changes with the tilt test positivity type, scored in accordance with Sutton's classification. METHODS: Twenty-one patients (12 males and 9 females, mean age 41 +/- 15 years) consecutively admitted to tilt test evaluation were studied through simultaneous recordings of their electrocardiogram, blood pressure, electroencephalogram and transcranial Doppler sonography (TCD) of the middle cerebral artery. TCD allowed computation of the Gosling's pulsatility index [PI = (systolic velocity--diastolic velocity)/mean velocity], as an index of cerebrovascular resistance. RESULTS: In the 13 tilt-positive patients (62%), TCD revealed a significant PI increase at the onset of prodromic symptoms in comparison with baseline (2.01 +/- 0.94 vs 0.77 +/- 0.20, p < 0.001, paired-sample Student's t-test). No significant TCD alterations were seen in tilt-negative patients. Furthermore, the percentage change in the PI from baseline was significantly higher in cardioinhibitory types (254 +/- 51%, 5 patients) than in mixed and vasodepressor types (101 +/- 22%, 8 patients, p < 0.001, independent-sample Student's t-test). CONCLUSIONS: Our data show that the degree of cerebral vasoconstriction at the onset of prodromic symptoms changes with the tilt test positivity type. We suggest that in NMS patients the degree of cerebral vasoconstriction may depend on the amount of sympathetic activation. The sympathetic modulation of cerebral vasoconstriction may therefore be a turning point in the explanation of the pathophysiology of NMS.

Adult↗
PubMed1992

[Endothelin-induced vasoconstriction in man: variable modification caused by endothelium-derived relaxing factor, Sodium nitroprusside and calcium antagonists].

The vascular effects of endothelin-1 (ET) were investigated in 25 healthy volunteers by measuring changes of forearm blood flow in response to brachial artery ET infusions. ET in a low dose (0.5 ng/min/100 ml tissue) resulted in a small but significant increase of forearm blood flow (FBF) from 2.3 +/- 1.5 to 2.5 +/- 1.5 ml/min/100 ml (n = 25, p less than 0.05) while higher dosages (25 and 50 ng/min/100 ml) resulted in significant decreases of FBF to 1.78 +/- 1.3 and 1.1 +/- 0.9 ml/min/100 ml (p less than 0.01). Neither sodium nitroprussid (n = 6) nor acetylcholine (n = 7) prevented ET-induced vasoconstriction. In contrast, both verapamil (n = 6) and nifedipine (n = 6) not only prevented ET-induced vasoconstriction but resulted in additional vasodilatation to values above those seen with the calcium antagonists alone. Thus, in human resistance vessels ET has a dual action with vasodilation occurring at low dosages and vasoconstriction at high dosages. Blockade of voltage-operated calcium channels prevents ET-induced vasoconstriction and unmasks the vasodilatory effects of high ET-dosages. Blockade of voltage-operated calcium channels but not cyclic GMP dependent vasodilation appears to be an effective tool in preventing ET-induced vasoconstriction.

Acetylcholine↗
PubMed2005

ERK1/2 signaling pathway is involved in 15-hydroxyeicosatetraenoic acid-induced hypoxic pulmonary vasoconstriction.

Hypoxia-induced 15-hydroxyeicosatetraenoic acid (15-HETE) is an essential mediator to constrict pulmonary arteries (PA). The signaling pathway involved in 15-HETE-induced PA vasoconstriction remains obscure. The aim of the present study was to test the hypothesis that hypoxic PA constriction induced by 15-HETE was possibly regulated by the extracellular signal-regulated kinase-1/2 (ERK1/2) pathway. PA ring tension measurement, Western blot and immunocytochemistry were used in the study to determine the possible role of ERK1/2 in 15-HETE-induced PA vasoconstriction. The organ bath for PA rings tension study was employed. Adult male Wistar rats were raised in hypoxic environment with fractional inspired oxygen (FIO2, 0.12) for 9 d. PA 1~1.5 mm in diameter were dissected and cut into 3 mm long rings for tension study. ERK1/2 up-stream kinase (MEK) inhibitor PD98059, which blocks the activation of ERK1/2, was used. The results showed that pretreatment of PD98059 significantly blunted 15-HETE-induced PA vasoconstrictions in the rings from hypoxic rat. Moreover, in endothelium-denuded rings, PD98059 also significantly attenuated 15-HETE-induced vasoconstriction. Phosphorylation of ERK1/2 in pulmonary arterial smooth muscle cells (PASMCs) of rat was enhanced evidently when stimulated by 15-HETE. Thus, the data suggest that ERK1/2 signaling pathway is involved in 15-HETE-induced hypoxic pulmonary vasoconstriction.

Animals↗