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At least 1,675 records · Page 93Linked to original sources
PubMed1998

Histamine receptor subtypes mediating hyperpolarization in the isolated, perfused rat mesenteric pre-arteriolar bed.

Histamine is a general dilator of rat blood vessels. We investigated the relative contribution of receptor subtypes to the rat mesenteric dilator responses initiated by histamine and related agonists. Histamine initiated dose, and endothelium-dependent, dilation of constricted mesenteric beds with an ED50 of 0.4 +/- 0.1 nmol. The ED50 was increased 10-fold by 0.1 microM chlorpheniramine (a histamine H1-receptor selective antagonist). Histamine H2 receptor blockade with tiotidine (0.1 microM) slightly decreased, while thioperamide (1 microM), a selective histamine H3 receptor antagonist, did not block histamine-induced dilation. Mesenteric bed dilation initiated by histamine H2 receptor selective agonists, amthamine and dimaprit, were antagonized markedly by tiotidine. However, the dilation initiated by the putative histamine H3 receptor selective agonists, R(-)- or S(+)-alpha-methylhistamine and imetit were not affected by thioperamide (1 microM). Histamine H2- and H3-receptor mediated dilator effects were endothelium-independent and were blocked by either excess (80 mM) extracellular K+, or 1 mM tetrabutylammonium (a non-selective K+ channel blocker), as well as by 1 microM dequalinium, a non-peptide blocker of the small conductance Ca2+-activated (SKCa) K+ channels. We conclude that (i) histamine H1 receptor subtype predominantly mediates endothelium-dependent dilator effect of histamine, and (ii) vascular hyperpolarization through opening of K+ channels (SKCa) mediate the dilator responses to histamine H2 receptor (amthamine and dimaprit) and the putative histamine H3 receptor (R(-)-alpha-methylhistamine and imetit) agonists.

Animals↗
PubMed1983

Localization of monoamine oxidase of type A and B in blood vessels with different innervation patterns.

Homogenates of dog mesenteric artery, dog saphenous vein, denervated saphenous vein, rabbit ear artery, denervated ear artery and human umbilical artery were prepared in phosphate buffer. Monoamine oxidase activity was determined with [3H]-5-hydroxytryptamine ([3H]-5-HT) as a preferential substrate for MAO type A and [14C]-beta-phenylethylamine as a preferential substrate for MAO type B. The endogenous noradrenaline content was compared with the MAO activities in these blood vessels. The results show that there is a good relationship of MAO type A content with the density of adrenergic innervation, but it is evident that this type of MAO is present even in vessels devoid of adrenergic innervation. Thus, MAO type A in these vascular structures has both intraneuronal and extraneuronal locations whereas MAO type B is predominantly or exclusively extraneuronal.

Animals↗
PubMed1992

Intestinal phase of superior mesenteric artery blood flow in man.

Duplex ultrasound was used to investigate superior mesenteric artery haemodynamics in humans in order to study the contribution of the small intestine to the postprandial splanchnic hyperaemia, and to determine the relative potencies of the major food components in the postprandial mesenteric flow response. Duplex parameters of vessel diameter, mean velocity, and volume flow were determined serially in the basal state and after stimulation. Flow parameters were significantly (p less than 0.05) increased after liquid and solid oral meals. Modified sham feeding did not alter mesenteric blood flow. Intestinal perfusion of an isocaloric liquid test meal induced flow increases comparable with oral intake. Superior mesenteric artery blood flow also significantly (p less than 0.05) increased after isocaloric and iso-osmolar loads of intraduodenal carbohydrate, fat, and protein meals. Responses were similar after the test meal, fat, and protein, but were significantly (p less than 0.05) less for carbohydrates. Different osmolar loads of saline did not affect flow responses. We conclude that the intestinal phase is the major regulator of the postprandial mesenteric blood flow response in healthy humans and that the chemical nature of food determines the mesenteric response pattern.

Adult↗
PubMed1985

Direct observations of responses of mesenteric microcirculation of the rat to circulating noradrenaline.

The responses of mesenteric microcirculation of the rat to circulating noradrenaline were studied by in vivo microscopy, using a photo-electric device placed on a television monitor to measure changes in diameter of individual vessels. Blood flow was measured in the anterior mesenteric artery with an electromagnetic flow transducer, mesenteric vascular conductance was computed on-line from mesenteric artery flow and arterial pressure. I.V. injection of noradrenaline induced a decrease in diameter of arterioles (less than 30 microns) which began simultaneously with the rise in arterial pressure and averaged 15% at 15-20 s. By contrast small and principal arteries (30-40 microns and 80-350 microns respectively) generally showed a diameter increase which averaged 10% and began at the peak of the pressor response. Venules and veins (12-560 microns) showed a diameter decrease which averaged 12-15% at 25-30 s. Meanwhile mesenteric vascular conductance fell by 65-75% in 10 s and rose to 30-50% above control in 25-30 s. The diameter increases of small and principal arteries were not reflex dilator responses initiated by the rise in systemic arterial pressure, nor due to beta-adrenoreceptor stimulation. However, local application of phentolamine abolished responses of all sections of the vascular tree indicating that they all depended on activation of alpha-adrenoreceptors. During I.V. infusion of noradrenaline small arteries showed a maintained increase in diameter which began at the peak of the pressor response, while arterioles initially decreased in diameter but then relaxed, often attaining resting diameter before infusion ceased. Meanwhile mesenteric flow and conductance decreased transiently, but then returned to near control levels, i.e. 'autoregulatory escape' occurred. It is argued that noradrenaline induced alpha-mediated contraction of all sections of the vascular tree; the tendency of arteries to constrict was counteracted by the rise in intravascular pressure caused by arteriolar constriction, active constriction of venous vessels may have been augmented by passive collapse secondary to arteriolar constriction. The secondary relaxation of arterial vessels reflects an inherent property of their smooth muscle to relax from the constrictor influence of noradrenaline and is more marked in proximal than distal vessels. It is proposed that the initial decrease in mesenteric vascular conductance in response to circulating noradrenaline may be attributed to active constriction of distal arterioles and the secondary increase in conductance ('escape') to secondary relaxation of more proximal arterial vessels.

Animals↗
PubMedDate not supplied

[Influence of angiotensin I on angiogenesis in vitro in the rat].

The regulation of angiogenesis involves complex interactions. The aim of our study was to assess the influence of angiotensin II (ANG II) on different vascular beds in rat. Aortic, renal and mesenteric rings from 10 male Sprague-Dawley rats were cultured using a three-dimensional culture system consisting of rat type I collagen lattice. We assessed the influence of different ANG II concentrations (10(-7) et 10(-9) mol/L) on these rings as well as the effect of AT1 blockade by losartan (10(-7 mol/L). ANG II inhibited angiogenesis at 10(-7) mol/L on renal artery. However, these was a angiogenic effect at 10(-9) mol/L on the mesenteric artery. Every time losartan prevented the effect of ANG II in any kind of vessel rings. No significant effect on ANG II was found on aortic rings but coadministration of losartan induced a dramatic decrease in the number of capillary sprouts. In conclusion, ANG II seems to be deeply involved in angiogenesis. However, its effect depends on the concentration of ANG II and the type of vessel. ANG II appears to be angiogenic on mesenteric arteries via an AT1 receptor effect and mostly anti-angiogenic on the renal arteries with possible involvement of AT2 receptors.

Angiotensin II↗
PubMed1985

Computed tomography in stage III neuroblastoma.

This multicenter study was designed to determine if CT can assess operability in stage III neuroblastoma. Nineteen children (11 boys, eight girls), aged 2-51 months, considered to have, by conventional clinical and radiographic examinations, localized neuroblastoma that crossed the midline were examined by CT. After intravenous and oral contrast media enhancements, CT was able to show the relation of the tumor to the adjacent vital vessels: aorta, celiac axis, and superior mesenteric artery. In all 15 patients, tumors that encased the aorta or its major branches were unresectable. However, three of four tumors crossing the midline but not coming into contact with the aorta or adherent only to one side of the vessel could be resected. Because surgery currently plays the major role in the treatment of neuroblastoma, the relation of the tumor to the aorta and great vessels is a more reliable and important factor in predicting the outcome of these children than the extension and location of the tumor with reference to the midline. CT after intravenous contrast enhancement can establish this relation and assess resectability.

Abdominal Neoplasms↗
PubMed1976

Relaxation of isolated rabbit arteries by fusaric (5-butylpicolinic) acid.

The influence of fusaric (5-butylpicolinic) acid on vascular contractile or relaxing response was examined in different isolated arterial preparations of the rabbit. Prior exposure (10 minutes) to 1 x 10(-4) to 1 x 10(-3) M fusaric acid decreased contractile responses elicited with norepinephrine, histamine, serotonin, acetylcholine, angiotensin II and KCl in helical strips of rabbit aorta and superior mesenteric, carotid, renal, and femoral arteries. Fusaric acid produced a shift to the right and down in the dose-response curves to all tested agonists, and antagonized acetylcholine and serotonin most effectively among these agonists. These results indicate that fusaric acid antagonized nonspecifically these contractile agonists. When blood vessels were contracted with prostaglandin F2alpha, fusaric acid caused relaxation of rabbit aorta and superior mesenteric, carotid, renal, and femoral arteries in a dose-dependent fashion. Among blood vessels tested superior mesenteric arteries were relaxed the most effectively by fusaric acid. The concentration of fusaric acid which induced 50% relaxation of aortic strips was about 10-fold higher than that of papaverine. Propranolol and atropine did not affect fusaric acid-induced relaxation, suggesting that fusaric acid did not work through beta adrenergic or cholinergic receptors. Ethylene glycol bis(beta-aminoethyl-ether)-N,N'-tetraacetic acid which chelates with Ca++ caused blood vessel relaxation in doses similar to those of fusaric acid. As fusaric acid is known to chelate Ca++, a possible mechanism of fusaric acid to relax blood vessel through Ca++ depletion is discussed briefly.

Aminophylline↗
PubMed2005

[Role of endothelium-derived hyperpolarizing factor in shear stress-induced endothelium-dependent relaxations of rats].

AIM: To investigate the role and mechanism of endothelium-derived hyperpolarizing factor (EDHF) in shear stress induced vasorelaxation of rat mesenteric artery. METHODS: The changes in vessel diameter in response to variable flow (0-300 microL.min(-1)) were continuously examined. The contribution of prostacyclin (PGI2), NO and EDHF to shear stress induced relaxation were analyzed by inhibitory effects of indomethacin, N(G)-nitro-L-arginine (L-NA) and KCl. The nature and hyperpolarizing mechanism of EDHF were examined by the inhibitory effects of inhibitors of cytochrome P450 pathway and of various K+ channels. RESULTS: The shear stress-induced relaxation were endothelium dependent and the contribution of NO was more prominent in large mesenteric arteries (400-500 microm) than that in resistance arteries (150-250 microm), whereas that of EDHF was noted in both-sized blood vessels. Tetrabutylammonium (a nonselective inhibitor of K channels) almost abolished, whereas the combination of charybdotoxin (an inhibitor of both large and intermediate-conductance Ca2+-activated K channels) and apamin (an inhibitor of small-conductance Ca2+-activated K channels) significantly inhibited the EDHF-mediated component of the shear stress-induced relaxations. CONCLUSION: EDHF plays an important role in shear stress-induced endothelium-dependent relaxations, and K channels especially calcium-activated K channels appear to be involved.

Animals↗
PubMed1989

Distribution of substance P in the enteric plexuses of the small intestine of the platypus, Ornithorhynchus anatinus.

A study was made of substance P-like-immunoreactive nerves within the small intestine of platypus, an Australian prototherian mammal. Both immunoreactive nerve cell bodies and fibers were present. No immunoreactive fibers were found in mesenteric nerves or on intramural blood vessels, suggesting that extrinsic sensory neurons containing substance P do not innervate platypus ileum. This was further supported by the result of in vitro experiments. Although applied substance P (10(-9) M-3 x 10(-8) M) caused contraction of the longitudinal muscle, neither mesenteric nerve stimulation nor application of capsaicin caused contractions.

Animals↗
PubMed1996

Calcium dependence of indolactam-mediated contractions in resistance vessels.

The protein kinase C activator, (-)-indolactam, has been shown to enhance reactivity of arterioles by a mechanism not requiring an increase in intracellular Ca++ (Ca++i). The aim of this study was to characterize the Ca++ requirement for indolactam-induced contraction of resistance vessels. Studies were performed in small mesenteric arteries (diameter, 260 +/- microm), using intact segments or after permeabilization with alpha-toxin (500 U/ml). Additional studies were preformed using isolated smooth muscle cells to allow electrophysiological assessment of the effect of indolactam on voltage-gated Ca++ entry. Intact and permeabilized vessel segments showed dose-dependent constriction to indolactam. Studies of Fura 2-loaded vessels and permeabilized segments maintained at low Ca++i, showed that the constriction occurred without an overt increase in Ca++i. That Ca++ was required was evident by near maximal relaxation after the removal of Ca++. Patch clamp studies indicated that indolactam potentiated voltage-gated Ca++ entry; however, nifedipine (0.5 microM) and La (0.2 or 1 mM) were relatively ineffective in reversing the contraction, indicating that voltage-gated Ca++ entry was not an absolute requirement. In intact vessel segments, the myosin light chain (MLC) kinase inhibitors, ML-7 and ML-9, reversed the indolactam contraction, suggesting the requirement of the MLC chain phosphorylation pathway. Furthermore, indolactam caused by a significant increase in MLC phosphorylation in permeabilized vessels, despite clamping of Ca++i at pCa 7.0. The data are consistent with the suggestion that the protein kinase C activator, indolactam, acts to modulate the Ca++ sensitivity of the smooth muscle contractile process such that higher than expected levels of MLC phosphorylation exist for a given level of Ca++i.

Animals↗
PubMed1982

The effect of surgical procedures on blood vessel innervation. A fluorescence histochemical study of degeneration and regrowth of perivascular adrenergic nerves.

Four commonly used surgical procedures have been shown to cause extensive damage to the sympathetic nerves which supply and accompany blood vessels. One of these procedures, which produced a localised crush lesion, was shown by fluorescence microscopy to cause extensive degeneration of adrenergic nerves in two densely innervated blood vessels of different character in the guinea pig: the elastic carotid artery and the muscular mesenteric artery. The extent of denervation was different in the two vessels: in the carotid artery the crush lesion destroyed all the nerves near the lesion, but left undamaged sparse nerves which reached the vessel wall along its length with the vasa vasorum; in the mesenteric artery all the nerves ran with the artery, consequently denervation could be extensive (at least 2 cm distal to the crush), although the largest nerve bundles were resistant to crush injury. The regrowth rate of nerves in the mesenteric artery was faster than that found in the carotid artery. A plexus of normal density and appearance was re-established between 3 and 8 weeks, and hyperinnervation was observed in some specimens. In the carotid artery this process was usually not complete by 8 weeks and involved both the regrowth of injured fibres and collateral sprouting distal to the lesion of the sympathetic nerve fibres that had not been injured. Axon sprouting was observed in both vessels near the lesion site. Explanations for these differences are discussed.

Adrenergic Fibers↗
PubMed2002

Endothelium-dependent blunting of myogenic responsiveness after chronic hypoxia.

Blunted agonist-induced vasoconstriction after chronic hypoxia is associated with endothelium-dependent vascular smooth muscle (VSM) cell hyperpolarization and decreased vessel-wall Ca(2+) concentration ([Ca(2+)]). We hypothesized that myogenic vasoconstriction and pressure-induced Ca(2+) influx would also be attenuated in vessels from chronically hypoxic (CH) rats. Mesenteric resistance arteries isolated from CH [barometric pressure (BP), 380 Torr for 48 h] or normoxic control (BP, 630 Torr) rats were cannulated and pressurized. VSM cell resting membrane potential was recorded at intraluminal pressures of 40-120 Torr under normoxic conditions. VSM cells in vessels from CH rats were hyperpolarized compared with control rats at all pressures. Inner diameter was maintained for vessels from control rats, whereas vessels from CH rats developed less tone as pressure was increased. Pressure-induced increases in vessel-wall [Ca(2+)] were also attenuated for arteries from CH rats. Endothelium removal restored myogenic constriction to vessels from CH rats and normalized VSM cell resting membrane potential and pressure-induced Ca(2+) responses to control levels. Myogenic constriction and pressure-induced vessel-wall [Ca(2+)] increases remained blunted in the presence of nitric oxide (NO) synthase inhibition for arteries from CH rats. We conclude that blunted myogenic reactivity after chronic hypoxia results from a non-NO, endothelium-dependent VSM cell hyperpolarizing influence.

Animals↗
PubMed2004

[Effect of low-intensity He-Ne laser irradiation on rat mesenteric microcirculation].

Changes in microcirculation during low-intensity He-Ne laser irradiation were studied by measurement of blood vessels and lymphangions' diameter in anesthetized rat mesentery using method of videomicroscopy in vivo. We demonstrated that the red coherent light induced a significant increase in contractility of vessels' smooth muscle cells. The flow decreased in the mesenteric microvessels during H2O2-mediated oxidant stress was restored after He-Ne laser irradiation.

Animals↗
PubMed1992

Characterization of a vasopressin-like peptide in rat and bovine blood vessels.

The present study examined the possibility that blood vessels of the rat and cow contain arginine vasopressin (AVP) and that the vascular stores of this potent vasoconstrictor are of local, rather than blood-borne, origin. Vessels from rat or cow were homogenized in acid, and the supernatants were assayed for AVP by radioimmunoassay. AVP immunoreactivity was detected in all vessels taken from the rat including aorta, mesenteric artery, renal artery, vena cava, and renal vein, as well as atria of the heart and also in cow aorta. Blood vessels from hypophysectomized and Brattleboro rats also contained AVP at levels similar to those of intact control rats. Further characterization of this immunoreactive material showed that, in both radioimmunoassay and radioreceptor assay, vascular extracts produced competition curves, which were parallel to those of synthetic AVP. Additionally, immunoreactive AVP in aortic extracts comigrated with synthetic AVP and pituitary extract on both high-pressure liquid chromatography and Sephadex G-25 chromatography. Furthermore, intravenous administration of the aortic extract produced pressor responses in conscious rats, and these responses were significantly attenuated by pretreatment with a specific AVP V1-receptor antagonist. These data demonstrate that blood vessels contain an AVP-like peptide that appears indistinguishable from authentic AVP and further suggest that this vascular peptide is of local origin.

Animals↗
PubMed2006

Pulmonary vasoconstrictor action of KCNQ potassium channel blockers.

BACKGROUND: KCNQ channels have been widely studied in the nervous system, heart and inner ear, where they have important physiological functions. Recent reports indicate that KCNQ channels may also be expressed in portal vein where they are suggested to influence spontaneous contractile activity. The biophysical properties of K+ currents mediated by KCNQ channels resemble a current underlying the resting K+ conductance and resting potential of pulmonary artery smooth muscle cells. We therefore investigated a possible role of KCNQ channels in regulating the function of pulmonary arteries by determining the ability of the selective KCNQ channel blockers, linopirdine and XE991, to promote pulmonary vasoconstriction. METHODS: The tension developed by rat and mouse intrapulmonary or mesenteric arteries was measured using small vessel myography. Contractile responses to linopirdine and XE991 were measured in intact and endothelium denuded vessels. Experiments were also carried out under conditions that prevent the contractile effects of nerve released noradrenaline or ATP, or block various Ca2+ influx pathways, in order to investigate the mechanisms underlying contraction. RESULTS: Linopirdine and XE991 both contracted rat and mouse pulmonary arteries but had little effect on mesenteric arteries. In each case the maximum contraction was almost as large as the response to 50 mM K+. Linopirdine had an EC50 of around 1 microM and XE991 was almost 10-fold more potent. Neither removal of the endothelium nor exposure to phentolamine or alpha,beta-methylene ATP, to block alpha1-adrenoceptors or P2X receptors, respectively, affected the contraction. Contraction was abolished in Ca2+-free solution and in the presence of 1 microM nifedipine or 10 microM levcromakalim. CONCLUSION: The KCNQ channel blockers are potent and powerful constrictors of pulmonary arteries. This action may be selective for the pulmonary circulation as mesenteric arteries showed little response. The results imply that the drugs act directly on smooth muscle cells and contraction requires voltage-dependent Ca2+ influx. It is concluded that the drugs probably act by blocking KCNQ channels in pulmonary artery myocytes, leading to membrane depolarization and Ca2+ influx through L-type Ca2+ channels. This implies a functional role for KCNQ channels in regulating the resting membrane potential of pulmonary artery myocytes.

Animals↗
PubMed1993

The effect of muscarinic receptor alkylation on endothelium-dependent vasodilation in SHR.

Possible hypertension-related alterations in the nature- and receptor reserve of the muscarinic (M) receptors mediating endothelium-dependent vasodilation remain to be elucidated. Therefore we used 4-diphenylacetoxy-N-(2-chloroethyl)-piperidine (4-DAMPmustard), an irreversible M3-receptor antagonist, to estimate the receptor reserve for the methacholine (MCh)-induced endothelium-dependent vasodilation in perfused mesenteric vascular bed preparations obtained from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) rats, respectively. The concentration-response curve parameters for the MCh-induced vasodilation were similar in both types of preparations. 4-DAMPmustard concentration-dependently decreased the maximal effect (Emax) of MCh without altering (N.S.) the pD2 in either type of preparation. The Emax was decreased to the same extent (N.S.) in both types of preparations. The dissociation constants of MCh for the response to muscarinic stimulation were comparable in preparations from SHR and WKY rats. The receptor reserve for this response, which is relatively low, does not appear to differ between vessels from SHR and WKY. It is concluded that an endothelial dysfunction does not seem to occur in perfused mesenteric resistance vessels from SHR. Also, the nature- and M-receptor reserves to not appear to differ. Therefore there are no important hypertension-related alterations in the M-receptor mediating endothelium-dependent vasodilation, at least in the experimental model used.

Alkylating Agents↗