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PubMed1990

Endothelin-1-induced constriction in the coronary resistance vessels and abdominal aorta of the guinea pig.

The purpose of this study was to examine contractile properties of endothelin-1, a newly discovered vasoactive peptide, in guinea pig coronary resistance vessels and abdominal aorta. Changes in perfusion pressure after injections of endothelin-1 were measured using a constant-flow modified Langendorff preparation. The ED10 values of coronary perfusion pressure were about 100-fold less for endothelin-1 than for prostaglandin F2 alpha. After the endothelium was damaged by exposure to free radicals, maximal coronary constriction in response to endothelin-1 (10(-9) moles) was not altered, whereas dilator responses to low doses of endothelin-1 were converted to constrictor responses. Removal of the endothelium from aortic rings significantly increased responsiveness to endothelin-1 and the maximal response to the peptide. In calcium-free medium, endothelin-1 induced small increases both in perfusion pressure in coronary vessels and in tension in the aorta. Reintroduction of calcium in the coronary and aortic preparations produced a rapid increase in perfusion pressure and tension, respectively. Further, endothelin-1-induced coronary constriction was inhibited 59% +/- 7% by nifedipine (10(-7) moles). We conclude that endothelin-1 is a more potent constrictor than prostaglandin F2 alpha in the coronary vasculature. Endothelin-1-induced constriction in the coronary vasculature of the guinea pig is not mediated through an endogenous constricting factor released from the endothelium or a constrictor prostaglandin. Further, endothelin-1-induced dilation in the coronary vasculature and attenuation of endothelin-1-induced contraction in the abdominal aorta of the guinea pig are mediated through the release of a factor from the endothelium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Acute Cerebral Artery Constriction in the Spontaneously Hypertensive Rat following Blood and Plasma Administration into the Subarachnoid Space.

The purpose of the present study was to demonstrate, using a vascular casting technique, acute vasoconstrictive changes in the cerebral vasculature 1 h following whole-blood or plasma infusion into the subarachnoid space of conscious spontaneously hypertensive rats. Vascular casts from animals infused (over 20 min) with 0.45 ml of heparinized autologous arterial blood or plasma exhibited incomplete filling, while casts from saline-infused controls exhibited virtually no filling defects. Significant elevations in intracranial pressure were noted in blood, but not in plasma- or saline-infused rats. Two characteristic forms of constriction occurred, depending upon the vessel lumen diameter. Vessels with lumen diameters >100 &mgr;m were flattened longitudinally with deep endothelial nuclear imprints, while smaller vessels had focal circular constrictions resembling beads. Arterial cast filling terminated in vessels with lumen diameters from 70 to 120 &mgr;m with focal signs of constriction at or near the point of cast termination. The results indicate that the presence of both blood and plasma in the subarachnoid space produces acute small-artery constriction. This phenomenon is due to a noncellular blood component and does not correlate with increases in intracranial pressure. Copyright 1996 S. Karger AG, Basel

Journal Article↗
PubMedDate not supplied

Subtotal ear reconstruction for correction of type 3 constricted ears.

Constricted ears are characterized by four features: (a) lop deformity, (b) protrusion, (c) low ear position, and (d) decreased ear size. These deformities, resulting from inadequate length of the helix, have been described by Tanzer (1975) as a purse-string closure of the ear. Constricted ears are classified into types 1, 2, and 3 according to the severity of the deformity. Type 3 constricted ear, the most severe, with decreased size and loss of the upper half of the normal ear contour, is classified currently as a mild form of microtia. Therefore, autogenous rib cartilage was used to reconstruct the affected ear much as in correction of microtia. The expanded skin flap in the mastoid area was used to reconstruct auricles for 14 patients with type 3 constricted ear in the authors' center from 2001 to 2004. All the patients were satisfied with the final results. Therefore, the authors conclude that their operative technique is practical and reliable.

Adolescent↗
PubMed1984

Effect of conotruncal constriction on aortic-mitral valve continuity in the stage 18, 21 and 24 chick embryo.

The effect of conotruncal constriction on the development of aortic-mitral valve continuity in stage 18, 21 and 24 chick embryos was studied. A 10-0 nylon suture was tied around the conotruncus, constricting the outflow tract of the heart. The loop was removed after 4 or 24 hours or left permanently in place in 3 subgroups of the 236 experimental embryos. The embryo hearts were harvested at stages after completion of cardiac morphogenesis, fixed in end-diastole and microdissected. The distance between the mitral and aortic anuli was measured from the base of the heart with a calibrated filar micrometer eyepiece. This measurement was compared with the mitral-aortic separation in 72 normal and 132 control embryos. The mitral-aortic separation was similar among normal, control and 4- and 24-hour experimental embryo hearts. However, the mitral-aortic separation increased from 0.34 +/- 0.02 mm in normal hearts to 0.82 +/- 0.25 mm in stage 18, 1.11 +/- 0.36 mm in stage 21 and 0.75 +/- 0.33 mm in stage 24 permanent loop experimental hearts (p less than 0.01). In embryo hearts with an increased mitral-aortic separation, both great vessels arose from the right ventricle, the semilunar valves were at the same level and the ventricular septal defect was present beneath the aortic anulus. We conclude that conotruncal constriction modifies the relation of the aortic and the mitral valve. We speculate that conotruncal constriction alters the migration of mesenchymal tissue into the heart.

Animals↗
PubMed1988

Adrenoceptor subtypes involved in the baroreceptor reflex constriction of large coronary arteries in the anaesthetized dog.

The baroreceptor reflex was invoked by bilateral occlusion of the carotid arteries in anaesthetized dogs. The effect of bilateral carotid occlusion on the diameter of the left circumflex coronary artery and late diastolic coronary resistance was examined after bilateral vagotomy and antagonism of beta-adrenoceptors and then compared to responses after selective antagonism of alpha 1- and alpha 2-adrenoceptors. In the absence of any change in heart rate, bilateral carotid occlusion decreased coronary artery diameter (-8 +/- 1%) and increased coronary resistance (59 +/- 14%). Prazosin (0.01 mg/kg i.a.), a selective antagonist of alpha 1-adrenoceptors, significantly attenuated the bilateral carotid occlusion-induced changes in coronary artery diameter (-2 +/- 2%) and late diastolic coronary resistance (20 +/- 11%). Selective antagonism of alpha 2-adrenoceptors by the intra-coronary injection of idazoxan (0.05 mg/kg) significantly reduced the bilateral carotid occlusion-induced increase in coronary resistance (14 +/- 12%) but did not affect the large artery constriction (-8 +/- 4%). When injected into the coronary circulation the alpha 1-adrenoceptor agonist phenylephrine constricted both the large artery and the resistance vessels. In contrast B-HT 920, a selective alpha 2-adrenoceptor agonist, constricted the resistance vessels but did not affect large coronary artery tone. The responses to phenylephrine and B-HT 920 were selectively antagonised by prazosin and idazoxan respectively. Reflex activation of the sympathetic nervous system results in constriction of both large coronary arteries and coronary resistance vessels when there is no change in heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Cocaine constricts immature cerebral arterioles by a local anesthetic mechanism.

The effect of cocaine on cerebral arterioles was determined in newborn pigs and the mechanism of action was examined in terms of its local anesthetic and sympathomimetic properties. Forty-three newborn piglets were anesthetized, equipped with a closed cranial window, and the diameter of pial arterioles was measured by intravital microscopy. Increasing concentrations of cocaine (10(-7) M to 10(-3) M) applied onto the cortical surface resulted in a dose-dependent decrease in arteriolar diameter. Coadministration with phentolamine, an alpha-adrenoceptor antagonist, did not inhibit the contractile response to cocaine even though phentolamine blocked the constriction to topically applied norepinephrine. In contrast, coadministration of either tetrodotoxin (Na+ channel blocker), charybdotoxin (K+ channel blocker), or quinacrine (phospholipase A2 inhibitor), or pretreatment with indomethacin (cyclooxygenase inhibitor) attenuated vasoconstriction induced by cocaine. Topically applied lidocaine (10(-7) M to 10(-3) M), a local anesthetic without sympathomimetic properties, caused a dose-dependent constriction similar to cocaine, whereas topically applied nomifensine and desipramine (each 10(-7) M to 10(-3) M), inhibitors of dopamine and norepinephrine re-uptake, respectively, did not constrict cerebral arterioles. These results indicate that cocaine constricts cerebral arterioles by its local anesthetic properties rather than its sympathomimetic properties. The mechanism appears to involve an alteration in the flux of Na+ or K+ or prostanoid metabolism.

Anesthetics, Local↗
PubMed1994

Alpha 1B-receptors and intracellular calcium mediate sympathetic nerve induced constriction of rat irideal blood vessels.

The present study has investigated the receptors involved in the non-cholinergic nerve mediated constriction of the larger blood vessels (30-50 microns) within the rat iris. This response was blocked by the alpha-adrenoceptor antagonist, benextramine (10(5) M). Furthermore, the response was more sensitive to blockade by the alpha 1 antagonist, prazosin (IC50 9 x 10(-10) M), than to blockade by the alpha 2 antagonist, yohimbine (IC50 2 x 10(-7) M), or the adrenergic antagonist, WB4101 (IC50 2 x 10(-8) M), and was abolished by chloroethylclonidine (10(-5) M). These results suggest the involvement of alpha 1B-adrenoceptors. The nerve mediated constriction was not blocked by the voltage-dependent calcium channel blocking drugs, nifedipine (10(-6) M), verapamil (10(-6) M) or diltiazem (10(-6) M), but was completely abolished by the intracellular calcium mobilizer, caffeine (10(-3) M), supporting the hypothesis that alpha 1B-adrenoceptors are activated following nerve stimulation. Dantrolene (10(-4) M), which interferes with calcium release from the sarcoplasmic reticulum, reduced the nerve mediated constriction by 40% as did thapsigargin (2 x 10(-6) M), which inhibits the calcium ATPase responsible for uptake of calcium into intracellular stores. When influx of calcium was blocked by verapamil (10(-6) M), thapsigargin, but not dantrolene, completely abolished the response. Noradrenaline (10(-5) M) produced a vasoconstriction in the presence or absence of external calcium although the latter response was significantly smaller than the former. Vasoconstriction produced by a submaximal concentration of noradrenaline (10(-6) M), was completely prevented by pretreatment with chloroethylclonidine. The data indicate that noradrenaline released from sympathetic nerves causes a constriction of arterioles in the iris by activating alpha 1B-adrenoceptors and releasing calcium from dantrolene sensitive and insensitive intracellular stores, followed by inflow of calcium through verapamil sensitive calcium channels. Applied noradrenaline also activates chloroethylclonidine sensitive receptors on the arteriolar surface.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed2005

Alpha-1B adrenoceptors mediate neurogenic constriction in mesenteric arteries of normotensive and DOCA-salt hypertensive mice.

The contribution of alpha-1 adrenergic receptor (alpha1-AR) subtypes to neurogenic constrictions of mesenteric resistance arteries from SHAM and deoxycorticosterone acetate-salt (DOCA-salt) hypertensive mice was assessed. Frequency-response curves (0.5-30 Hz) for transmural stimulation-evoked contractions were examined in SHAM and DOCA-salt arteries in vitro in the absence (control) and presence of prazosin (0.1 microM), PPADS (10 microM), yohimbine (1 microM), 5-methylurapidil (5-MU; 0.1 microM), L-765,314 (1 microM) and BMY-7378 (0.3 microM); selective antagonists at alpha1-, P2X, alpha2-, alpha1A-, alpha1B-, and alpha1D-AR, respectively. In SHAM arteries, prazosin but not PPADS inhibited neurogenic responses. L-765,314 substantially inhibited neurogenic responses while 5-MU had a small inhibitory effect. BMY-7378 did not alter contractile responses at all. In DOCA-salt arteries, prazosin reduced neurogenic responses with no further significant inhibition seen with PPADS. L-765,314 antagonized neurogenic constrictions to a level similar to that seen in SHAM arteries. Furthermore, 5-MU and BMY-7378 did not affect these responses. The density of noradrenergic nerves (assessed using glyoxylic acid-induced fluorescence) or norepinephrine (NE) content was not altered by DOCA-salt hypertension. These results indicate that NE is the primary mediator of neurogenic constriction of murine mesenteric arteries. Nerve-released NE acts primarily at alpha1B-and to a lesser extent at alpha1A-ARs in SHAM arteries whereas NE mediates neurogenic constrictions in DOCA-salt arteries by acting at alpha1B-ARs.

Adrenergic alpha-Antagonists↗
PubMed2006

A pharmacogenetic exploration of vigabatrin-induced visual field constriction.

INTRODUCTION: Use of the antiepileptic drug (AED) vigabatrin is severely limited by irreversible visual field constriction, an adverse reaction to the drug reported in approximately 40% of patients. Given the evidence suggesting an idiosyncratic drug response, we set out to detect genetic variation of strong, clinically relevant effect that might guide clinicians in the safe, controlled prescribing of this otherwise usefuldrug. METHODS: Patients with a history of at least 1-year exposure to vigabatrin were enrolled at two independent referral centers. Using Goldmann perimetry, visual fields and the extent of constriction were calculated for each patient. We examined the correlation between the extent of vigabatrin induced visual field constriction and genetic variation across six candidate genes (SLC6A1, SLC6A13, SCL6A11, ABAT, GABRR1 and GABRR2). We availed of HapMap data and used a tagging SNP technique in an effort to efficiently capture all common variation within these genes. We attempted to replicate any positive associations before drawing conclusions from our results. RESULTS: The degree of visual field constriction correlated with three SNPs and one haplotype in a cohort of 73 patients. However we were unable to replicate these findings in a second independent cohort consisting of 58 patients, suggesting the initial results were possibly false positives, or variants of weak effect. CONCLUSION: Common variants of strong, clinically relevant effect do not appear to reside in the candidate genes studied here. This does not rule out the presence of genetic variants of weak effect in these genes, nor of variants of strong effect in other genes.

4-Aminobutyrate Transaminase↗
PubMed2006

Clinical features of mixed physiology of constriction and restriction: echocardiographic characteristics and clinical outcome.

AIMS: An entity of patients with mixed physiology of constriction and restriction has been reported, however, the characteristics of these patients have not been well documented. We evaluated the clinical features and the outcome of these patients. METHODS AND RESULTS: Study subjects consisted of 38 patients (57+/-14 years, 8 females, 30 males) who were diagnosed as having mixed physiology based on transthoracic and/or transesophageal echocardiography, MRI (or CT), cardiac catheterization, endomyocardial biopsy and/or surgical findings. Prior radiation therapy was the most frequent (50%) cause of mixed physiology followed by coronary artery bypass graft without prior radiation (24%) and heart transplantation (8%). The respiratory variation of peak early diastolic transmitral flow velocity by pulsed Doppler transesophageal echocardiography was 10.7% in patients with sinus rhythm and 18.1% in patients with atrial arrhythmia. Pericardial thickening was noted adjacent to the right-sided chambers in 19 patients, left-sided chambers in 10 patients, or both in 9 patients. All-cause 5-year mortality was 40% and unrelated to age, etiology, left ventricular systolic function and therapeutic course. There was a statistically significant difference (p<0.01) between the survival rates in patients with mixed physiology and in patients with pure constriction (n=125). CONCLUSIONS: Due to the high mortality in this disease, discrimination of the entity from the patients with pure constriction is mandatory. Transthoracic and transesophageal echocardiography are helpful noninvasive techniques in the diagnosis and the understanding of the physiology of patients with mixed constriction and restriction.

Adult↗
PubMed2000

Hypocapnic constriction in rabbit basilar artery in vitro: triggering by N(G)-monomethyl-L-arginine monoacetate and dependence on endothelin-1 and alkalosis.

This study tested whether hypocapnic constriction of the rabbit basilar artery in vitro can be triggered by a nitric oxide (NO) synthase inhibitor, and whether the resulting constriction is (1) due to the alkaline pH associated with hypocapnia, and (2) endothelin-1 mediated. Hypocapnic (25 mM NaHCO(3); pH 7.76; pCO(2) 14.2) or isocapnic alkaline solution (50 mM NaHCO(3); pH 7.73; pCO(2) 35.0) rarely altered basal tension. N(G)-monomethyl-L-arginine monoacetate (L-NMMA; 0.1 mM) challenge in hypocapnic or isocapnic alkaline solution resulted in near maximal tension that was maintained for 2-2.5 h even following L-NMMA washout. L-NMMA challenge in normal solution (25 mM NaHCO(3); pH 7. 42; pCO(2) 36.9) also induced near maximal tension, although the tension was maintained for only 25 min (mean). Ac-D-Bhg-L-Leu-Asp-L-Ile-L-Ile-L-Trp (PD145065), homopiperidinyl-CO-Leu-D-Trp(CHO)-D-Trp (BQ610), and N-cis-2, 6-dimethyl-piperidinocarbonyl L-gamma-MeLeu-D-Trp (COOCH(3))-Nle (BQ788; 1-3 microM), endothelin ET(A)/ET(B), endothelin ET(A), and endothelin ET(B) receptor antagonists, respectively, completely relaxed the tension that resulted from L-NMMA challenge in hypocapnic or isocapnic alkaline solution. These results demonstrate that constriction due to hypocapnia in vitro can be triggered by an NO synthase inhibitor and is endothelin-1 mediated. Additionally, alkaline pH in the absence of decreased pCO(2) is sufficient to elicit the constriction.

Acetylcholine↗
PubMed2000

Hypocapnic constriction in rabbit basilar artery in vitro: triggering by serotonin and dependence on endothelin-1 and alkalosis.

This study tested whether hypocapnic constriction of the rabbit basilar artery in vitro can be triggered by serotonin, and whether the resulting constriction is (1) due to the alkaline pH associated with hypocapnia, and (2) endothelin-1 mediated. Hypocapnic alkaline solution (25 mM NaHCO(3); pH 7.76; pCO(2) 14.2) or isocapnic alkaline solution (50 mM NaHCO(3); pH 7.73; pCO(2) 35.0) rarely altered basal tension. Serotonin (3 microM) challenge in hypocapnic or isocapnic alkaline solution resulted in near maximal tension. Washout of the serotonin did not decrease tension in 54% of the tissues, as plateau tension was maintained for 2-2.5 h. The plateau tension of washed tissues was relaxed by 1-3 microM PD145065 (Ac-D-Bhg-L-Leu-Asp-L-Ile-L-Ile-L-Trp), BQ610 (homopiperidinyl-CO-Leu-D-Trp(CHO)-D-Trp), and BQ788 (N-cis-2, 6-dimethyl-piperidinocarbonyl-L-gamma-MeLeu-D-Trp (COOCH(3))-Nle), endothelin ET(A)/ET(B), endothelin ET(A), and endothelin ET(B) receptor antagonists, respectively. In contrast, serotonin-induced tension in normal solution (25 mM NaHCO(3); pH 7.42; pCO(2) 36.9) was maintained for only 40 min (mean). These results demonstrate that (1) constriction due to hypocapnia in vitro can be triggered by serotonin and is endothelin-1 mediated and (2) alkaline pH in the absence of decreased pCO(2) is sufficient to elicit the constriction triggered by serotonin.

Acetylcholine↗
PubMed1995

Effect of preflaring on tactile detection of the apical constriction.

The efficacy of tactile detection of the apical constriction in flared and nonflared root canals was examined in 120 root canals of adult patients. In 68 nonflared (group 1) root canals, a #15 or #20 K-file was used to detect ("feel") the apical constriction. In 52 teeth (group 2), Hedstrom files, Gates Gliden drills #2 to #4, and ultrasonic files were used to enlarge the canal orifice and flare the coronal portion of the root canals before testing the apical constriction. After placing a #15 or #20 file in each root canal, a radiograph was taken, and the distance between the tip of the file and the radiographic apex was measured. The location of the file tip was classified into three categories: (a) within 1 mm short of the radiographic apex; (b) underextended, more than 1 mm short of the radiographic apex; and (c) overextended beyond the radiographic apex. In group 1 (nonflared), 32.3% of the root canals were classified in category a, as compared with 75.0% in group 2 (preflared). Over 26% of the root canals in group 1 and approximately 4% of the canals in group 2 were included in category b. Files inserted in preflared root canals had a significantly lower incidence of overextension than those placed in nonflared canals (21% versus 41%). The ability to determine the apical constriction by tactile sensation was significantly increased when the canals were preflared (p < 0.0001).

Adult↗
PubMed2003

Receptor mechanisms of prenodal lymphatic constriction by dopamine.

It has been proposed that alterations in lymphatic smooth muscle activity significantly impact lymphatic function. Numerous endogenous vasoactive agents are known to constrict prenodal lymph vessels. In this study, we assessed the ability of dopamine to alter lymphatic smooth muscle tone in perfused prenodal lymph vessels. Additionally, the receptor mechanisms of dopamine's actions were elucidated. Both intralymphatic (i.l.) and intra-arterial (i.a.) dopamine significantly increased lymphatic perfusion pressure. The increase in lymphatic pressure was completely blocked by i.a. phentolamine, suggesting involvement of alpha(1)- and/or alpha(2)-adrenoreceptors. Intra-arterial infusion of the specific alpha(1)-receptor antagonist prazosin completely abolished the constriction seen during i.l. phenylephrine but only attenuated that produced by dopamine. Intralymphatic infusion of the DA(1)-receptor agonist SKF 82526-J and the DA(2)-receptor agonist LY 171555 caused significant relaxation of lymph vessels that had been previously constricted by i.a. norepinephrine infusion. These data indicate that the constriction produced by dopamine, in the concentrations employed in this study, is mediated by both alpha(1)- and alpha(2)-adrenoreceptors. These lymph vessels do contain both DA(1)- and DA(2)-receptors but stimulation of these receptors results in lymphatic smooth muscle relaxation.

Animals↗
PubMedDate not supplied

Visualizing multiple constrictions in spheroidal Escherichia coli cells.

An Escherichia coli cell grows by elongation and divides in a perpendicular plane. Alternating planes of successive divisions in three dimensions can only be ascertained when multiple constrictions exist simultaneously in large, spheroidal cells (with extended constriction process), if the division signals are enhanced. Large, spheroidal cells are obtained by a brief mecillinam treatment, and more frequent divisions are achieved by manipulating the rate of chromosome replication without affecting cell mass growth rate. Such a procedure has recently been performed by thymine-limitation of E. coli K12 strain CR34 (Zaritsky et al., Microbiology 145 (1999), 1052-1022). Enhancing the replication rate in cells with multi-forked replicating chromosomes (by addition of deoxyguanosine) shortens the intervals between successive terminations and thus triggers divisions more frequently. Monoclonal antibodies against FtsZ were used to visualize the rings of secondary constrictions, but apparent shortage of FtsZ to complete rings over wide cells allowed assembly of arcs only. The arcs observed were not parallel nor perpendicular; the tilted constriction planes are consistent with our 3-D 'nucleoid segregation'model for division under conditions which relieve the cylindrical constraint for nucleoid segregation by the bacillari peptidoglycan sacculus (Woldringh et al. , J. Bacteriol. 176 (1994) 6030-6038). The shortage in FtsZ may explain the longer time required to complete the division process in wide cells with long circumferences, observed during thymine step-up. Overexpression of fusion protein FtsZ-GFP on a multi-copy plasmid should circumvent the shortage.

Bacterial Proteins↗
PubMed1997

Endothelin-1 causes luminal constrictions in rat cochlear veins.

Serum levels of the vasoconstrictor endothelin-1 (ET-1) increase in ischemia and systemic hypertension. We examined the effects of ET-1 on the cochlear microvasculature. Blood vessels were cast with methacrylate in adult male Wistar Kyoto rats, 10 min after intravenous injection of ET-1 (1.0 microg/kg); control animals received saline. Systemic blood pressure was recorded continuously. ET-1 increased the average systolic pressure by 18% and average diastolic pressure by 22% (P < 0.01). Scanning electron microscopy of cast vessels showed multiple circumscribed luminal constrictions on: (1) postcapillary venules; (2) collecting veins; (3) where collecting veins merged with the spiral modiolar vein; (4) on the spiral modiolar vein itself. Circumscribed constrictions in arteries were not observed. In ET-1 injected animals focal contractions of collecting veins reduced luminal width by 13.4% +/- 2.9 (P < 0.01). In control rats, constrictions on venous casts were minimal and constrictions on arteries were not observed. The present study shows that ET-1 is involved in local control of cochlear blood flow in that it focally contracts cochlear veins. It is suggested that this might be due to the high affinity of ET-1 receptors and/or the large number of ET-1 receptors on contractile cells in venous walls.

Animals↗
PubMedDate not supplied

Intracellular mechanisms of constriction of rat aorta by ethanol.

The intracellular mechanisms mediating vasoconstriction by ethanol are poorly understood. This investigation was designed to provide evidence on the role of protein kinase C (PKC) and calmodulin in vasoconstriction by ethanol. We studied helically cut strips of rat aorta that were exposed to ethanol before and in the presence of the PKC inhibitors calphostin C (79, 239, and 798 nM) or 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H7, 10 microM), and the calmodulin inhibitor, trifluoperazine (TFP, 10 microM). To test for the specificity of the PKC inhibitors, we measured the responses of aortas to potassium and phorbol 12-myristate 13-acetate (PMA) in the absence and presence of calphostin C and H7. To test for the specificity of TFP, we measured the responses of aortas to serotonin, potassium, PMA, and the thromboxane A2 mimic. 9,11-dideoxy-11 alpha, 9 alpha-epoxy-methanoprostaglandin F2a (U46619), in the absence and presence of TFP. We also studied the effect of the combination of calphostin C and TFP on constriction of the aorta by ethanol. We also measured the importance of intracellular and extracellular calcium in constriction of the aorta by ethanol. Force generation was measured before, and then during exposure of the strips to calcium-free buffer with EGTA, or calcium-free buffer with EGTA plus caffeine. We found that both PKC inhibitors antagonized vasoconstriction by ethanol and PMA. However, H7 antagonized contractions by potassium, but calphostin C did not. We found that TFP caused 99 +/- 1% inhibition of maximum contraction to serotonin, 90 +/- 4% inhibition of maximum contraction to potassium, 63 +/- 6% inhibition of maximum contraction to PMA, and 8 +/- 5% inhibition of maximum contraction to U46619. TFP caused a 22 +/- 8% inhibition of contraction to ethanol. The combination of TFP and calphostin C antagonized vasoconstriction by ethanol to a degree similar to that of calphostin C alone. We also found that contractions to ethanol were only 16 +/- 7% of control values in a calcium-free plus EGTA buffer. Contractions to ethanol were 0 +/- 1% of control values in calcium-free buffer with EGTA plus caffeine. We conclude that: 1-vasoconstriction by ethanol is, at least in part, mediated by PKC; 2-constriction by ethanol is mediated to a minimal extent by calmodulin, and 3-part of the constriction by ethanol of the aorta is mediated by a caffeine-sensitive pool of intracellular calcium.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1998

Fate mapping of the mouse midbrain-hindbrain constriction using a site-specific recombination system.

The mouse midbrain-hindbrain constriction is centrally involved in patterning of the midbrain and anterior hindbrain (cerebellum), as revealed by recent genetic studies using mice and embryological studies in chick (reviewed in [1,2]). This region can act as an organizer region to induce midbrain and cerebellar development. Genes such as Engrailed-1, Pax-2 and Pax-5, which are expressed in the embryonic cells that will form the midbrain and the cerebellum, are required for development of these regions. Fate-mapping experiments at early somite stages in chick have revealed that the cerebellar primordium is located both anterior and posterior to the midbrain-hindbrain constriction, whereas midbrain precursors lie more anteriorly. Fate mapping in mice has been complicated by the inaccessibility of the postimplantation embryo. Here, we report the use of a new in vivo approach involving the Cre-IoxP site-specific recombination system [3] to map the fate of cells in the mouse midbrain-hindbrain constriction. We show that cells originating in the mouse dorsal midbrain-hindbrain constriction during embryonic days 9-12 contribute significantly to the medial cerebellum and colliculi. Our data demonstrate the feasibility of using a recombinase-based lineage-tracing system for fate mapping in the mouse.

Animals↗