bluuebunny/crossref_metadata_2025_split huggingface dataset:
INFLUENCE OF SOMATOSTATIN ANALOGUE (SMS 201–995, OCTREOTIDE) ON BLOOD PRESSURE IN ADRENOCORTICOTROPHIN (ACTH) TREATED RATS: ROLE OF HYPERINSULINAEMIA IN ACTH HYPERTENSION
Authors: Li Ming , Wong Kok‐Seng , Whitworth Judith A. 
Published: June 2007

SUMMARY1. The hypothesis that adrenocorticotrophin (ACTH)‐induced hypertension is a consequence of steroid‐induced hyperinsulinaemia was tested using the somatostatin analogue (sandostatin, octreotide) to inhibit insulin release in Sprague‐Dawley (SD) rats (n= 41).2. Octreotide (20 μg, twice daily) did not modify blood pressure, plasma glucose, bodyweight, water and electrolyte balance, or organ weights but inhibited insulin secretion in the SD rat.3. Compared with sham injection, ACTH‐treated (0.5 mg/kg per day) SD rats showed an increase in blood pressure (sham 111 ± 4 mmHg; ACTH 140 ± 5 mmHg on treatment day 10 (P≤ 0.01), organ weights, water intake, urine volume, plasma glucose, insulin and sodium concentrations, and decrease of bodyweight and plasma potassium concentration.4. Systolic blood pressure in rats treated with combined octreotide and ACTH was similar to that in rats on ACTH alone. Plasma insulin concentration was lower in octreotide + ACTH treated rats than with ACTH treatment alone. There were no differences in body or organ weights, plasma glucose, water or electrolyte balance.5. Octreotide lowered plasma insulin concentration to the normal range but did not modify ACTH‐induced hypertension in SD rats. These data do not support the notion that insulin‐mediated alterations in blood pressure are a major mechanism for ACTH‐induced hypertension in the rat.
SUFENTANIL AND ALFENTANIL CAUSE VASORELAXATION BY MECHANISMS INDEPENDENT OF THE ENDOTHELIUM
Authors: Karasawa F. , Iwanov V. , Moulds R. F. W. 
Published: June 2007

SUMMARY1. The aim of these experiments was to determine if the vasorelaxation of the rat isolated aorta induced by sufentanil or alfentanil is mediated by the endothelium, and, if not, by α‐adrenoceptor blockade, or a direct effect on the smooth muscle.2. Both sufentanil (from 10−7 mol/L to 10−4 mol/ L) and alfentanil (from 10−7 mol/ L to 3 × 10−4 mol/L) relaxed rings, where endothelium was intact and precontracted with 40 mmol/L KC1, in a concentration‐related manner. Similarly, sufentanil and alfentanil relaxed rings, in the presence or absence of endothelium, which had been precontracted with phenylephrine.3. Naloxone (10−4 mol/L) had no significant effect on the relaxation induced by either sufentanil or alfentanil.4. In a similar manner as phentolamine, pretreatment with sufentanil protected α‐adrenoceptors from blockade by phenoxybenzamine (PBZ) in both endothelium intact and denuded rings, but the estimated potency of sufentanil was approximately 100‐fold less than that of phentolamine in α‐adrenoceptor protection. Treatment with alfentanil did not produce any receptor protection.5. We concluded that, in the rat aorta, vascular relaxation induced by sufentanil is mediated by both α‐adrenoceptor blockade and a direct effect on smooth muscle, whilst the relaxant effect of alfentanil is caused by direct effects alone. We also concluded that the endothelium has little role in relaxation produced by either drug.
NALOXONE STIMULATION OF ACTH SECRETION DURING PETROSAL SINUS SAMPLING IN CUSHING'S SYNDROME
Authors: Torpy David J. , Jackson Richard V. , Grice Jeffrey E. , Hockings Gregory I. , Strakosch Christopher R. , Topliss Duncan J. 
Published: June 2007

SUMMARY1. Petrosal sinus sampling has been used to establish the source of adrenocorticotropin (ACTH) in ACTH‐dependent Cushing's syndrome. Naloxone, an opioid antagonist, stimulates ACTH secretion, probably via release of endogenous hypothalamic corticotropin releasing hormone (CRH).2. Three patients with hypercortisolism were studied. Two showed suppressed (>50%) urinary‐free cortisol excretion with high‐dose dexamethasone treatment (2 mg every 6h for 2 days), one did not suppress. The patients were subjected to bilateral simultaneous inferior petrosal sinus sampling (BSIPSS) with simultaneous peripheral venous (forearm) samples. Basal (unstimulated) samples were taken and naloxone (125 pg/kg bodyweight) was given intravenously with subsequent simultaneous sampling. Plasma ACTH was measured by radio‐immunoassay (RIA).3. All cases exhibited a marked rise in immunoreactive (IR)‐ACTH levels (pmol/L) after naloxone injection, basal to peak: case 1, left 11.5–22.1, right 9.8 with no rise, peripheral 9.1–9.5; case 2, left 456–863, right 125–501, peripheral 59–82; case 3, left 12.7–13.0, right 277–431, peripheral 12.1–11.7. All results indicate pituitary Cushing's syndrome, with a central to peripheral ratio >2.3:1. Pituitary Cushing's syndrome was confirmed on the results of trans‐sphenoidal pituitary surgery in cases 1 and 3.4. It is suggested that naloxone injection during petrosal sinus sampling in Cushing's syndrome may assist in the diagnosis of ACTH source, by enhancing ACTH release from a pituitary micro‐adenoma.
A LOW AFFINITY, LOW MOLECULAR WEIGHT ENDOTHELIN‐A RECEPTOR PRESENT IN NEONATAL RAT HEART
Authors: Woodcock Elizabeth A. , Land Sarah L. , Andrews Robert K. 
Published: June 2007

SUMMARY1. Addition of endothelin‐1 (ET‐1) to [3H]‐inositol‐labelled neonatal rat hearts stimulated the accumulation of [3H]‐labelled inositol phosphates (InsP), but only at high concentrations; concentration at half maximum stimulation (EC50)>0.1 μmol/L). When similar experiments were performed using isolated myocytes, the potency of endothelin‐1 was higher and the EC50 value averaged 3.2 ± 0.5 nmol/L (mean±s.e.m., n = 4).2. The binding affinity of [125I]‐endothelin‐1 was higher for receptors on isolated cells than for receptors on membranes prepared from intact heart (72 ± 16 pmol/L compared with 3.9 ± 0.7 nmol/L, mean ± s.e.m., n= 4, P < 0.01; Students’t test).3. Receptors from both sources were cross‐linked to [125I]‐endothelin‐1 and their molecular weights measured using sodium dodecylsulfate gradient polyacrylamide gel electrophoresis (SDS‐PAGE). The receptors present on the isolated cells had a higher molecular weight (48 kD) than the receptor on the heart membranes (38 kD).
SPECTROPHOTOMETRIC STUDY OF α‐ADRENOCEPTORS AFFECTING MICROCIRCULATION OF RAT SKIN
Authors: Kakizoe Eiichi , Kobayashi Yuta , Shimoura Keiko , Hattori Keisuke , Jidoi Joji 
Published: June 2007

SUMMARY1. To determine the α‐adrenergic receptor subtypes that affect the microcirculation of skin, the relative absorption (RA) spectra of the skin on the backs of rats were measured using reflectance spectrophotometric methods. We injected α‐adrenergic agonists, noradrenaline (NA), phenylephrine (PE) and clonidine (CL), intravenously and determined changes in the RA value at 569 nm, one of the isosbestic points of the oxyhaemoglobin and deoxyhaemoglobin absorption.2. NA reduced the RA value and the reduction was inhibited significantly by pretreatment with phenoxybenzamine (PBZ; P<0.01). These findings suggested that the haemoglobin content in the skin tissue decreased as a result of vasoconstriction through α‐adrenoceptors.3. NA, PE and CL produced dose‐dependent reductions in RA. CL and NA produced virtually equipotent reductions except at the highest dose used. PE produced smaller effects. The potency of these drugs in terms of changes in RA did not correlate with their potency in terms of rises in systemic blood pressure (NA ≤ PE ≥ CL).4. Yohimbine (YO) inhibited the NA‐induced reduction in RA to a greater degree than bunazosin (BU). Midaglizole, a specific α2‐adrenergic antagonist, significantly and dose dependently inhibited the NA‐induced reduction in RA.5. Although BU inhibited NA‐induced reduction in RA only slightly, the effect was significant (P<0.05). BU significantly inhibited PE‐induced reduction (P<0.01), but did not inhibit CL‐induced reduction.6. These observations suggest that the microcirculation of the skin of the rat is affected mainly by α2‐adrenoceptor mediated vasoconstriction. However, α1‐adrenoceptor mediated vasoconstriction also has some effect.
MEDIATORS OF NICOTINE‐INDUCED RELAXATIONS OF THE RAT GASTRIC FUNDUS
Authors: McLaren A. , Li C. G. , Rand M. J. 
Published: June 2007

SUMMARY1. Relaxations of strips of rat gastric fundus were elicited with nicotine (100 μmol/L), nitric oxide (NO; 30 μmol/L), sodium nitroprusside (SNP; 100 nmol/L) and vasoactive intestinal polypeptide (VIP; 1 nmol/L).2. Methylene blue (30 μmol/L), an inhibitor of soluble guanylate cyclase, reduced relaxations elicited by NO and nicotine, but not those elicited by VIP.3. Chymotrypsin (1 U/mL) abolished VIP‐induced relaxations and reduced nicotine‐induced relaxations, but had no effect on SNP‐induced relaxations.4. NG‐nitro‐l‐arginine methyl ester (l‐NAME; 100 μmol/L), an inhibitor of NO synthase, reduced relaxations elicited by nicotine, but not those elicited by SNP or VIP.5. When nicotine‐induced relaxations had been reduced by either l‐NAME or chymotrypsin, the addition of the other agent produced a greater reduction. However, the relaxations were not abolished.6. Nicotine‐induced relaxations were abolished by tetrodotoxin (1 μmol/L) or hexamethonium (100 μmol/L), indicating that they were due to activation of neuronal nicotinic receptors. Their reduction by methylene blue and l‐NAME indicates that an NO‐like mediator was involved. Their reduction by chymotrypsin indicates that a VIP‐like peptide was involved. However, since they were not abolished by a combination of l‐NAME and chymotrypsin, it appears that at least one more as yet unidentified mediator may be involved.
EVIDENCE THAT IMIDAZOL(ID)INE‐ AND SULPHONYLUREA‐BASED ANTAGONISTS OF CROMAKALIM ACT AT DIFFERENT SITES IN THE RAT THORACIC AORTA
Authors: Challinor Joanne L. , McPherson Grant A. 
Published: June 2007

SUMMARY1. Ring segments of rat thoracic aorta were suspended in organ baths to record isometric tension. Tissues were precontracted with K+ (20 mmol/ L), and full concentration—relaxation curves constructed to cromakalim (0,01–30 μmol/L) in the absence and presence of increasing concentrations of glibenclamide, glipizide, tolbutamide (the sulphonylureas), alinidine (an imidazolidine), phentolamine (an imidazoline), and chlorpromazine (the phenothiazine derivative). Whereas the active sulphonylureas, glibenclamide and glipizide, displayed classical competitive antagonism, the remaining compounds (alinidine, phentolamine and chlorpromazine) caused shifts in the cromakalim concentration—effect curves associated with a reduction in the slope and maximum response.2. A single concentration of each antagonist was selected and the shift in the concentration—effect curve determined. The possibility that sulphonylurea and imidazol(id)ine antagonists act at different sites was tested using the concentration‐ratio method for combined antagonists described by Paton and Rang (1965). The combination of alinidine and phentolamine (collectively called imidazol(id)ines) at a number of different concentrations (10–30 μmol/L) resulted in a concentration‐ratio to cromakalim which was additive, suggesting a common site of action. Similar results were obtained when examining the interaction between two sulphonylurea compounds (glibenclamide and glipizide). However, the interaction between sulphonylurea (glibenclamide) and imidazol(id)ine (alinidine) produced concentration‐ratios which were multiplicative, suggesting a different or additional site of action for compounds from these two groups. Results indicated that chlorpromazine was able to block cromakalim via an action at the same site where alinidine and phentolamine act.3. The results from this study indicate that sulphonylurea—and imidazol(id)ine‐based K+ channel antagonists interact at different sites to produce their observed antagonism of the vasorelaxation induced by cromakalim. These results indicate the possibility of multiple sites of action underlying the effects of compounds which antagonize the actions of K+ channel opening drugs.
IDENTIFICATION OF ADENOSINE RECEPTORS IN HUMAN SPERMATOZOA
Authors: Shen Meng‐Ru , Linden Joel , Chen Shun‐Sheng , Wu Sheng‐Nan 
Published: June 2007

SUMMARY1. The effects of adenosine receptor agonists and antagonists on human sperm motility have been studied. Specific binding sites for adenosine and its analogues on human sperm were also investigated.2. Agonists stimulated human sperm motility in a dose‐dependent manner with a potency order of 5'‐N‐ethylcarboxamidoadenosine (NECA, EC50= 0.3 μmol/L)>2‐[p‐(carboxyethyl)phenylethylamino]‐5'‐N‐ethylcarboxamidoadenosine(CGS‐21680, EC50= 10 μmol/L)> adenosine (EC50= 100 μmol/L).3. NECA‐stimulated motility was competitively inhibited by various adenosine receptor antagonists. The potency order was 3,7‐dimethy‐l‐propargylxanthine>8‐(p‐sulfophenyl) theophylline > xanthine amino congener.4. The radioligand [3H]‐NECA bound to sperm membrane in a saturable manner with a Bmax of 21.3 pmol/mg protein and equilibrium Kd of 4 μmol/L. Adenosine agonists and antagonists competed for [3H]‐NECA binding with the same rank order of potency as for the stimulation of human sperm motility.5. GTPγs inhibited 63% of specific [3H]‐NECA binding with IC50 value of 11 nmol/L. This suggests that the [3H]‐NECA binding sites may be coupled to one or more G proteins.6. These results indicate the presence of adenosine A2 receptors on human sperm which are responsible for adenosine‐mediated enhancement of sperm motility.
THE INCREASE OF FEMORAL ARTERIAL FLOW BY STIMULATING THE DORSAL AND VENTRAL MEDULLA IN CATS
Authors: Wang M. R. , Chai C. Y. , J. S. Kuof  
Published: June 2007

SUMMARY1. In chloralose‐urethane anaesthetized cats, the dorsal cardiovascular reactive area (DCRA) in the parvocellular reticular nucleus dorsomedial to the facial nucleus, and the ventral cardiovascular reactive area (VCRA) ventromedial to the facial nucleus, were stimulated by microinjections of sodium glutamate (100–200 nmol) or electric current.2. Stimulation of DCRA, with a long latency of 15–20 s, elicited a marked increase of blood flow in the contralateral femoral artery with little change to moderate increase in systemic arterial blood pressure (ABP). In the relatively dorsal portion of DCRA, however, a smaller increase of blood flow in the ipsilateral femoral artery was elicited.3. On the other hand, stimulation of VCRA with a short latency (3–5 s) evoked an increase of blood flow in both femoral arteries which was more prominent on the contralateral side. The responses were accompanied with decreases in the blood flow of other vascular beds with only a slight increase or minimal change in ABP.4. The data suggest that DCRA and VCRA are both viscerotopically organized to alter the resistance of individual vascular beds for redistribution of blood flow.
ENHANCEMENT OF ENDOTHELIUM‐DEPENDENT RELAXATION IN THE AORTA FROM STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS AT DEVELOPMENTAL STAGES OF HYPERTENSION
Authors: Onda Takeshi , Mashiko Satoshi , Hamano Megumi , Tomita Isao , Tomita Takako 
Published: June 2007

SUMMARY1. Endothelium‐dependent relaxation (EDR) in aortic rings from young (8 weeks) and adult (16 weeks and 20 weeks) stroke‐prone spontaneously hypertensive rats (SHRSP) was investigated in comparison with age‐matched Wistar‐Kyoto rats (WKY).2. At 8 weeks, acetylcholine (3×10−‐9‐−10−‐5 mol/L) and ionomycin (4×10−8‐10−6 mol/L)‐induced EDR in SHRSP aortae was significantly enhanced compared to that in WKY aortae. Mechanical denudation of the endothelium completely abolished, and pretreatment of aortae with NG‐monomethyl L‐arginine (1 mmol/L), an inhibitor of nitric oxide formation, greatly reduced the relaxation in both strains. Indomethacin (10−5 mol/L), a cyclo‐oxygenase inhibitor that blocks the production of endothelium‐derived contracting factors, did not significantly alter the relaxation by acetylcholine at this age. There was no difference in endothelium‐independent relaxation of denuded aortae by sodium nitroprusside (10−9‐10−6 mol/L) and 8‐bromoguanosine 3‘, 5‘‐cyclic monophos‐phate (10−6‐10−3 mol/L).3. In adult SHRSP with established hypertension, however, the acetylcholine (10−8‐−10−5 mol/L)‐induced relaxation markedly diminished at any of the concentrations tested compared to that observed in 8 week old SHRSP and WKY at 8–20 weeks of age. This finding differed from other observations where the relaxation in SHRSP was impaired only at higher concentrations of acetylcholine. Indomethacin pretreatment of aortae from 20 week old SHRSP restored acetylcholine‐induced EDR to a level comparable with that in age‐matched WKY.4. These results suggest that the aorta from young SHRSP releases more endothelium‐derived relaxing factors in response to acetylcholine and ionomycin, but the relaxation greatly diminishes in adult SHRSP with established hypertension. This may be due to counteraction of endothelium‐derived contracting factors released from the endothelium with functional changes resulting from the long duration of the hypertension.
USE OF RECOMBINANT INBRED STRAINS FOR EVALUATION OF INTERMEDIATE PHENOTYPES IN SPONTANEOUS HYPERTENSION
Authors: Kuneš J. , Křen V. , Pravenec M. , Zicha J. 
Published: June 2007

SUMMARY1. The HXB/BXH recombinant inbred (RI) strains, derived from the spontaneously hypertensive rat (SHR) and the normotensive Brown Norway (BN.1x) rat, represent a very useful system for gene mapping and for genetic analysis of certain model diseases, such as spontaneous hypertension.2. These RI strains were genotyped in multiple genetic polymorphisms and characterized in blood pressure and some intermediate phenotypes.3. The analysis of RI strains has revealed that (i) a gene in the vicinity of the major histocompatibility complex (RT1) on chromosome 20, a kallikrein‐related gene on chromosome 4 and the renin gene on chromosome 13 were significantly associated with blood pressure, and (ii) Na+ leak in red blood cells correlated with blood pressure whereas relative heart and kidney weights as well as platelet aggregation did not.
RELATIONSHIP BETWEEN THE SUPPRESSIVE ACTIONS ON INTESTINAL ABSORPTION AND ON cGMP PRODUCTION FOR THE NATRIURETIC PEPTIDE FAMILY IN DOGS
Authors: Kagawa Koji , Suzuki Shunji , Matsushita Kohtaroh , Uemura Nobuhisa , Morita Hironobu , Hosomi Hiroshi 
Published: June 2007

SUMMARY1. The aim of this study was to investigate whether the suppressive effects of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C‐type natriuretic peptide (CNP) on net intestinal absorption were related to guanosine 3′,5′‐cyclic monophosphate (cGMP) production in the intestine.2. We measured the plasma cGMP concentration of the arterial, jejunal and ileal venous blood after intravenous infusions of natriuretic peptides (97 pmol/ kg per min for 30 min) in anaesthetized dogs.3. The infusion of ANP increased cGMP concentration of the aortic blood by 49.9 ± 9.0 (pmol/mL), BNP by 71.8 ± 12.3 and CNP by 5.5 ± 1.3. The increases in cGMP after ANP and BNP were larger than after CNP. The infusion of ANP increased jejunal arteriovenous differences in cGMP concentration by 69.9 ± 3.5 (pmol/mL) and ileal arteriovenous differences by 8.7 ± 3.2. In BNP infusion, the jejunal and ileal arteriovenous differences in cGMP concentration tended to increase by 15.6 ± 5.8 (pmol/mL) and by 14.8 ± 6.6 but neither were significant. CNP infusion did not change the jejunal and ileal arteriovenous differences in cGMP concentration.4. These results suggest that, while the actions of ANP on intestinal absorption may be mediated by cGMP, those of BNP and CNP are not.
EFFECTS OF GENTAMICIN, NEOMYCIN AND TOBRAMYCIN ON RENAL CALCIUM AND MAGNESIUM HANDLING IN TWO RAT STRAINS
Authors: Garland H. O. , Birdsey T. J. , Davidge C. G. , McLaughlin J. T. , Oakes L. M. , Smith A. J. , Harpur E. S. 
Published: June 2007

SUMMARY1. Standard renal clearance techniques were used to compare the acute effects of gentamicin, neomycin and tobramycin on renal calcium and magnesium handling in Sprague‐Dawley and Fischer 344 rats.2. Significant hypercalciuric and hypermagnesiuric responses to all three drugs (P<0.01) were apparent within 30 min of the onset of drug infusion.3. The magnitude of the acute hypercalciuric and hypermagnesiuric response to the three aminoglycosides was comparable. This contrasts with their nephrotoxic action where neomycin >> gentamicin > tobramycin. The magnitude of the acute physiological responses to these drugs do not therefore reflect their nephrotoxic potential.4. Sprague‐Dawley rats were at least as responsive as Fischer rats in their acute renal responses to gentamicin. If Fischer rats are more sensitive to aminoglycoside nephrotoxicity than Sprague‐Dawley rats, this is not reflected in their acute responses to gentamicin.
HUMAN INTERNAL MAMMARY ARTERY RESPONSES TO NON‐PEPTIDE VASOPRESSIN ANTAGONISTS
Authors: Liu James J. , Phillips Paddy A. , Burrell Louise M. , Buxton Brian B. , Johnston Colin I. 
Published: June 2007

SUMMARY1. OPC‐21268 and OPC‐31260 are newly developed orally active non‐peptide vasopressin (AVP) V1 and V2 receptor antagonists, respectively. The effects of the two compounds on human vessels have not been studied.2. The effects of the two compounds on AVP‐induced contraction of human internal mammary arteries (IMA) were investigated. Their effects were compared with the peptide V1 and V2 antagonists d(CH2)sSar7AVP (SAVP) and d(CH2)5D‐Ileu211eu4AVP (Ileu2 Ileu4AVP), respectively.3. The V1 antagonist OPC‐21268 failed to antagonize AVP‐induced contraction at low concentrations and potentiated the contraction at higher concentration (3 × 10−‐7 mol/L, P<0.05). It also caused a mild direct contractile effect on IMA. In contrast, the peptide V1 antagonist SAVP potently inhibited the AVP‐induced contraction, indicating that functionally constrictor V1 receptors exist in IMA. Both the nonpeptide and peptide V2 antagonists OPC‐31260 (3X10−‐6 mol/L) and Ileu2Ileu4AVP significantly antagonized the AVP‐induced contraction (P<0.01).4. The AVP‐induced contraction was reversed by high concentrations of OPC‐31260 (10−‐6 mol/L‐3×10−‐5 mol/L) but not by OPC‐21268 (up to 3X 10−‐5 mol/L).5. These studies indicate that, in human IMA, OPC‐21268 is a partial VI receptor agonist with no V1 receptor antagonist activity, while OPC‐31260 is a V1 receptor antagonist. The results also indicate that Ileu2 Ileu4AVP may be a Vl receptor antagonist in humans.
VASOCONSTRICTOR RESPONSES TO POLYMORPHONUCLEAR LEUCOCYTES FROM ATHEROSCLEROTIC RABBITS
Authors: Sobey Christopher G. , Hart Joanne L. , Woodman Owen L. 
Published: June 2007

SUMMARY1. The vascular contractile effects of polymorphonuclear leucocytes (PMN) isolated from control rabbits and from rabbits made atherosclerotic by 1% cholesterol feeding for 8 weeks were examined.2. Rings of control rabbit thoracic aorta with or without endothelium were mounted at 2g tension in 10 mL organ baths and were submaximally contracted by phenylephrine (0.1 μmol/L). After 30 min incubation at 37° C, the supernatant of PMN (5X107/mL, in Tyrode solution containing 0.25% bovine serum albumin) was obtained by centrifugation for addition to the vascular preparation.3. Control PMN supernatant (443 μL) caused contraction (0.58±0.15g, n= 11) of phenylephrine‐contracted aortic rings, which was prevented by removal of the endothelium (0.11 ± 0.07g, n= 5, P<0.05). However, the control PMN supernatant had no contractile effect on aortic rings at resting tension (0.00 ± 0.00g, n= 8).4. By comparison, atherosclerotic PMN supernatant (443 μL) caused a significantly greater contraction of the aortic rings (1.41± 0.13g, n= 9, P<0.05 vs control PMN supernatant) that was only partly inhibited by removal of the endothelium (0.45 ± 0.20g, n= 9, P<0.05). Moreover, PMN supernatants from four of seven atherosclerotic rabbits contracted aortic rings at resting tension (3.5 ±1.4g, n= 7).5. These results suggest that the release of a stable vasoconstrictor substance(s) by PMN is enhanced under conditions of atherosclerosis. The constrictor action of this substance(s) appears to be greater in the presence of a functional endothelium, and part of its action may involve inactivation of endothelium‐derived nitric oxide.