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PubMed1994

Effects of Hoe 140 on systemic depressor responses to bradykinin and mesenteric vascular reactivity in vivo in pregnant Wistar-Kyoto rats.

1. To examine possible changes in vascular reactivity to exogenous bradykinin (BK) and the possible role of endogenous BK in reduced mesenteric vascular reactivity in pregnant rats. The authors studied the effects of Hoe 140 on systemic depressor responses to BK and on mesenteric vascular reactivity in in situ blood-perfused mesenteric resistance vessels of 18-20 day pregnant and age-matched non-pregnant Wistar-Kyoto rats (WKY). 2. Mean intra-arterial blood pressure (MBP) of pregnant rats was lower than non-pregnant controls. Basal mesenteric perfusion pressure (BPP) was slightly, but not significantly, reduced in the pregnant group. Neither MBP nor BPP was significantly influenced by Hoe 140 (1 mg/kg. s.c.) 3. Systemic depressor responses to BK (1-30 micrograms/kg, i.v.) were significantly increased in pregnant rats at 1 and 3 micrograms/kg. Hoe 140 completely abolished systemic depressor responses to BK in either pregnant or non-pregnant animals. 4. Mesenteric vascular responses to regional administration of noradrenaline, electrical stimulation of sympathetic nerve and angiotensin II were overall decreased in pregnant compared with non-pregnant groups, but those responses were not significantly affected by Hoe 140 in either groups. 5. The results suggested that although systemic depressor responses to exogenous BK were increased, endogenous BK does not contribute to decreased mesenteric vascular reactivity in vivo in pregnant WKY.

Animals↗

PubMed1991

Structural changes during the early onset of experimental hypertension: trophic influences of the renin-angiotensin system.

All forms of established hypertension are characterised by hypertrophy of the heart and blood vessels. Although these structural alterations are a normal adaptation to raised blood pressure, it has been suggested that hypertrophy may develop by a mechanism independent of pressure. Some investigators claim that in the young spontaneously hypertensive rat, hypertrophy of the blood vessels and heart is present at a time before the rise in pressure. Evidence also exists to support the role of angiotensin II in directly influencing growth within the vasculature. The present study confirms that hypertrophy of the mesenteric resistance vessels is present in the 3-week old spontaneously hypertensive rat. However, enhanced vascular structure was also associated with a higher mean arterial blood pressure. No increase in activity of the renin-angiotensin system could be detected. These observations raise doubts as to whether hypertrophy of the blood vessels can develop independently of raised pressure.

Animals↗

PubMed1990

Effect of pinacidil on ion permeability in resting and contracted resistance vessels.

Pinacidil is thought to cause vasodilatation by opening K+ channels and consequent hyperpolarization. This proposed mechanism of action is based mainly on membrane potential measurements and 42K or 86Rb efflux experiments under resting conditions. We have measured the simultaneous effect of pinacidil on force and membrane potential in resting and norepinephrine-contracted rat mesenteric resistance vessels. Also the effect of pinacidil on 42K and 36Cl efflux and 22Na uptake in the absence and presence of norepinephrine was examined. From the membrane potential and ion flux measurements the ion permeabilities were calculated. In both resting and norepinephrine-contracted vessels, pinacidil caused a large hyperpolarization, the latter situation being associated with an almost complete relaxation. In both resting and norepinephrine-stimulated vessels, pinacidil caused a large increase in K+ permeability and a decrease in Cl-permeability, whereas no significant change of Na+ permeability was found. Our results suggest that pinacidil causes vasodilation due to hyperpolarization. The major cause for the hyperpolarization is an increase in K+ permeability.

Animals↗

PubMed1978

Intestinal ischaemia associated with ileal carcinoid tumours.

A case of intestinal infarction due to multiple ileal carcinoid tumours is presented in which abdominal pain due to intestinal ischaemia was the first manifestation of the underlying tumour. It is postulated that intestinal ischaemia may be of more importance in the production of abdominal pain by carcinoid tumours than has been generally accepted, and that it is the result of functional and structural changes in the around the mesenteric blood vessels, caused by substances secreted by the carcinoid tumour.

Carcinoid Tumor↗

PubMed1994

Vasoconstrictor responses to components of the renin-angiotensin system in cyclosporin-induced hypertension in the rat.

1. Since plasma renin activity is increased in cyclosporin A (CsA)-induced hypertension in the rat, the role of the vascular renin-angiotensin system (RAS) in CsA-induced hypertension was investigated in rat mesenteric resistance vessels. 2. Female Wistar rats received CsA (10 mg/kg per day, s.c.) or vehicle for 30 days. CsA treatment increased tail-cuff systolic blood pressure (CsA treated 135 +/- 3 mmHg vs control 125 +/- 1 mmHg, P < 0.0001). 3. Mesenteric resistance arteries (200-300 microns) were isolated and mounted in a microvessel myograph. Concentration-response curves to tetradecapeptide renin substrate (10(-11)-10(-6) mol/L), angiotensin I (10(-11)-10(-6) mol/L) and angiotensin II (10(-12)-10(-6) mol/L) showed no differences between CsA-treated and control groups. 4. Mesenteric vascular angiotensin-converting enzyme (ACE) characteristics were determined by radioligand binding. There were no differences in the content or affinity of ACE between CsA-treated and control rats. 5. These results suggest that the mesenteric vascular RAS does not play a major role in CsA-induced hypertension in the rat.

Angiotensin I↗

PubMed2005

Vascular but not cardiac remodeling is associated with superoxide production in angiotensin II hypertension.

OBJECTIVE: Angiotensin (Ang) II increases reactive oxygen species (ROS), decreases nitric oxide (NO) bioavailability and promotes cardiovascular remodeling. ROS have been identified as critical second messengers of the trophic responses by Ang II. In rats with Ang II-induced hypertension, we investigated the role of ROS in cardiac hypertrophy as well as the remodeling of aortas and mesenteric (resistance) arteries. METHODS: Sprague-Dawley rats received Ang II (0.7 mg/kg per day by mini-pump, n = 7) or vehicle (n = 7) for 5 days. Endothelium-dependent relaxation to acetylcholine (EDR) in aortas was determined in organ baths and in mesenteric resistance vessels in a pressurized myograph. Superoxide (O2) production was measured by lucigenin chemiluminescence, laser-confocal fluorescence microscopy (LCM) and NADPH oxidase assay. RESULTS: Ang II-treated rats developed hypertension (183 +/- 3 versus 138 +/- 4 mmHg, P < 0.05), increased aortic O2 (50%), aortic hypertrophy (12%) and impaired EDR. Mesenteric arteries manifested impaired EDR, increased NADPH oxidase activity (356%) and eutrophic inward remodeling (decreased lumen diameter and increased wall/lumen ratio). However, although Ang II-treated rats developed cardiac hypertrophy (13%), this was not accompanied by an increase in cardiac O2, as measured by lucigenin, LCM or NADPH oxidase assay. On the other hand, cardiac calcineurin, a molecule that promotes cardiac hypertrophy linked to Ang II, was increased by 40% (52 +/- 8 versus 33 +/- 5 pmol/min per mg protein, P < 0.05). CONCLUSION: These studies demonstrate that the role of ROS in Ang II-induced vascular remodeling differ across vascular territories. Although in conduit and resistance vessels, vascular hypertrophy and endothelial dysfunction are linked to increased ROS production, cardiac hypertrophy is not. Instead, cardiac hypertrophy is associated, at least in part, with an increase in calcineurin. These studies unveil novel mechanisms that may play an important role in the pathogenesis of cardiac and vascular injury in hypertension.

Angiotensin II↗

PubMed1999

Kinetics of neovascularisation of splenic autotransplants in mice.

The aim of this study was to examine the kinetics of neovascularisation of splenic autoimplants into the abdominal cavity after splenectomy in mice. Sixty-eight female Swiss mice were submitted to splenectomy. The spleen from each animal was sliced and the slices were implanted into the abdominal cavity. Groups of animals were killed after 1, 2, 3, 5, 7, 15, 21, 28, 42, 56, 70 and 84 d. Fluorescent polystyrene microspheres were injected via the orbital venous plexus before killing and the splenules were removed 5 min later for light and electron microscopy. Mesenteric blood vessels were injected with coloured latex to study the origin of the nutrient vessels. Three days after the implant the microspheres were observed at the periphery and then migrating to the internal parts of the implant in the subsequent days. The blood supply to the implants originated from branches of the splenic, short gastric, mesenteric and gastroepiploic arteries. It is concluded that revascularisation of splenic autografts proceeds centripetally, starting as early as 3 d after implantation.

Animals↗

PubMed1991

Anatomical localization of the binding and functional characterization of responses to dopexamine hydrochloride in the rat mesenteric vasculature.

Dopamine receptors of the DA1 subtype have been identified in mesenteric blood vessels, stimulation of which leads to vasodilation. In this study, we have determined the anatomical localization of dopexamine-hydrochloride-binding sites and carried out functional characterization of responses to this DA1-receptor and beta 2-adrenoceptor agonist in rat mesenteric vasculature. Autoradiographic studies showed the presence of [3H]-dopexamine-binding sites in all the different layers of the mesenteric artery. The DA1 receptor antagonist, SCH 23390 (IC50 = 4.9 mumol/l), and the beta-adrenoceptor antagonist, propranolol (IC50 = 6.0 mumol/l), inhibited the binding of dopexamine. The inhibitory effect of these compounds on dopexamine binding was selective for different regions of the mesenteric artery. Also, dopexamine produced concentration-related increases in cAMP formation in membrane particles from superior mesenteric artery and its main branches. The presence of both SCH 23390 and propranolol was required to completely abolish dopexamine-induced increases in cAMP formation. In functional studies, dopexamine (1 and 3 micrograms/kg/min) produced dose-related increases in mesenteric blood flow (23 and 38%, respectively) which were accompanied by concomitant decreases in the calculated mesenteric vascular resistance. As seen with increases in cAMP, the vascular responses to dopexamine could be completely abolished only by prior treatment with both SCH 23390 and propranolol. These results suggest that in mesenteric vasculature of rat dopexamine binds primarily to DA1 receptors and beta 2-adrenoceptors. The activation of these receptors by dopexamine leads to vasodilation which is mediated by an increase in the intracellular levels of cAMP.

Adenylyl Cyclases↗

PubMed1989

Artificial induction of red gut in sheep.

Eight out of 10 lambs died within six to 11 hours after occlusion of the cranial mesenteric blood vessels by a snare placed around both the artery and vein. Death resulted from shock and was accompanied by post mortem findings identical to those seen in red gut. It is suggested that the cause of death in the naturally occurring disease is from arrested mesenteric blood flow following intestinal torsion.

Animals↗

PubMed1978

Time course of mesenteric vasodilatation following hypophysectomy and the stopping of a vasopressin infusion.

Hypophysectomy caused an increase in superior mesenteric arterial conductance that reached a new plateau approximately 20 min after removal of the gland in four pentobarbital-anesthetized cats. Intravenous infusion of arginine vasopressin (0.74 +/- 0.21 mU min-1kg-1) caused conductance to decrease to approximately prehypophysectomy control values. Stopping the infusion resulted in an increase in conductance and the time course of this vasodilatation was virtually identical to that which occurred following hypophysectomy. The results are consistent with the interpretation that the effects of acute hypophysectomy on the mesenteric resistance vessels are due primarily to removal of the vasopressin system and the concomitant elimination of circulating vasopressin.

Animals↗

PubMed1976

Reversible adrenergic alpha-receptor blocking action of 2,4'-dimethyl-3-piperidino-propiophenone (tolperisone).

The vascular action of 2,4'-dimethyl-3-piperidino-propiophenone hydrochloride (tolperisone hydrochloride), a centrally acting muscle relaxant, was investigated in pentobarbital anesthetized dogs. Tolperisone given intravenously produced a transient hypotension, tachycardia, and hyperventilation. The drug increased the femoral arterial flow, and decreased the superior mesenteric arterial flow following an initial transient increase. When injected directly into femoral and mesenteric arteries, tolperisone caused a rapid increase in both arterial flow (vasodilatation). However, femoral vessels were about 90 times as sensitive as mesenteric vessels to tolperisone. These results indicate that tolperisone shifts the blood volume from mesenteric (visceral) vessels to femoral (skeltal) ones. The femoral vasodilatation produced by i.a. tolperisone was not depressed by the pretreatment with i.a. propranolol, atropine or chlorphenylamine. Tolperisone decreased the contractile force in an isolated and cross-circulated papillary muscle. Tolperisone produced adrenaline reversal and antagonized the pressor response to noradrenaline. Moreover, femoral vasoconstriction caused by i.a. adrenaline was converted to vasodilatation and that caused by i.a. noradrenaline was depressed during an i.a. infusion of tolperisone. These results indicate that tolperisone blocks adrenergic alpha-receptors. The blocking action was rapid in onset, short-lived, and in addition, competitive.

Adrenergic alpha-Antagonists↗

PubMed2000

Effect of captopril on neurally induced contraction and relaxation of mesenteric arteries of renal hypertensive rats.

The effect of captopril treatment on neurally induced vasoconstrictor and vasodilator responses was examined in the isolated mesenteric arterial bed from normotensive and one-kidney, one clip hypertensive (1K1C) rats. In isolated mesenteric beds, electrical field stimulation (EFS) of perivascular nerves at basal tone induced a frequency-dependent increase in perfusion pressure that was greater in preparations from hypertensive rats compared with those from normotensive rats. Captopril treatment was associated with a decrease in vasoconstrictor responses in the hypertensive group compared with its non-treated control. Responses to norepinephrine (320 ng) were greater in hypertensive than normotensive groups; captopril reduced this response only in the hypertensive group. In preconstricted mesenteric arteries perfused with solutions containing guanethidine (5 microM) and atropine (1 microM), EFS elicited a frequency-dependent decrease in perfusion pressure that was abolished by tetrodotoxin (1 microM). Vasodilator responses to EFS were not affected by captopril treatment, although they were smaller in the hypertensive group. Acetylcholine (10 ng) induced similar decreases in perfusion pressure of normotensive and 1K1C groups; captopril did not influence these responses. These results indicate that captopril treatment does not affect the reduced neurogenic vasodilation but normalizes the augmented sympathetic-mediated vasoconstrictor responses of mesenteric resistance vessels of chronic 1K1C hypertensive rats.

Adrenergic Fibers↗

PubMed2001

Vascular changes in cyclosporine A-induced hypertension and nephrotoxicity in spontaneously hypertensive rats on high-sodium diet.

Functional and morphological changes of blood vessels in cyclosporine A (CsA)-induced hypertension and nephrotoxicity were studied in spontaneously hypertensive rats (SHR). The role of the L-arginine-nitric oxide (NO) pathway and the importance of oxidative stress in CsA toxicity were also assessed. SHR (7-8 week old) on a high-sodium diet were treated with CsA (5 mg kg(-1) d(-1) s.c.) for 6 weeks. A proportion of the rats were treated concomitantly with the NO precursor L-arginine (1.7 g kg(-1)d(-1) p.o.). CsA elevated blood pressure and caused renal dysfunction and morphological nephrotoxicity. CsA also impaired mesenteric and renal arterial function and caused structural damage to intrarenal and extrarenal small arteries and arterioles. Medial atrophy of the mesenteric resistance vessels and decreased viability of smooth muscle cells of the thoracic aorta were observed. Renal and arterial damage was associated with the presence of inflammatory cells. CsA did not affect markers of the L-arginine-NO pathway (urinary cyclic GMP excretion or endothelial or inducible NO synthase expression in kidney, aorta or heart) or oxidative stress (urinary excretion of 8-isoprostaglandin F2alpha, plasma urate concentration or total radical trapping capacity). Concomitant L-arginine treatment did not affect CsA-induced changes in blood pressure or histological findings but tended to alleviate the arterial dysfunction. The renal and cardiovascular toxicity of CsA was associated with arterial dysfunction and morphological changes in small arteries and arterioles in SHR on a high-sodium diet. The findings did not support the role of oxidative stress or a defect in the L-arginine-NO pathway.

Acetylcholine↗

PubMed1995

Endothelin receptor subtypes in mesenteric vascular smooth muscle cells of spontaneously hypertensive rats.

Calcium responses to the endothelin B receptor (ETB) selective agonist IRL-1620 (IRL) and to endothelin 1 (ET-1) in the absence and presence of the endothelin A receptor (ETA) antagonist BQ-123 were determined in primary cultured unpassaged vascular smooth muscle cells derived from mesenteric resistance vessels of 3-, 9-, and 17-week-old spontaneously hypertensive rats (SHR), Wistar rats, and Wistar-Kyoto (WKY) rats. Intracellular free calcium concentration ([Ca2+]i) was measured microphotometrically and by digital imaging using fura 2 methodology. ET receptor affinity and density were determined in membrane preparations from the mesenteric vascular bed from these rats. Binding studies were performed using [125I]ET-1 in the presence of increasing concentrations of ET-1, BQ-123, or IRL. Basal [Ca2+]i was significantly greater (p < 0.01) in adult SHR compared with age-matched normotensive groups. IRL (10(-7) mol/L) and ET-1 (10(-9) mol/L) increased [Ca2+]i in cells from all strains of all age groups. Responses were significantly lower (p < 0.05) in vascular smooth muscle cells from 9- and 17-week SHR compared with cells from age-matched Wistar and WKY rats. Concentration-response curves for IRL were blunted in cells from 17-week SHR versus cells from WKY rats. The selective ETA receptor antagonist BQ-123 (10(-7)-10(-5) mol/L) had no effect on IRL-induced [Ca2+]i but significantly reduced ET-1-induced [Ca2+]i by 135 +/- 4, 80 +/- 6, and 91 +/- 4 nmol/L in cells from 17-week SHR, WKY, and Wistar groups, respectively. The selective ETB receptor antagonist BQ-788 (10(-6) mol/L) significantly reduced ET-1-induced [Ca2+]i responses in 17-week rats. The Bmax for ET-1 binding was significantly lower in mesenteric artery membrane preparations from 17-week SHR (627 +/- 163 fmol/mg protein) compared with WKY and Wistar rats (1190 +/- 43 and 1059 +/- 55 fmol/mg protein, respectively). These data demonstrate the presence of both ETA and ETB receptors in rat mesenteric vascular smooth muscle cells. In adult SHR, reduced responses of vascular smooth muscle cells to IRL, which represents ETB-mediated effects, and to ET-1, may be partly due, as demonstrated in the binding studies, to lower ET receptor density than in normotensive rats.

Age Factors↗

PubMed2003

Contrasting regression of blood pressure and cardiovascular structure in declipped renovascular hypertensive rats.

We investigated the time relationship between changes in blood pressure and changes in the structure of the resistance vasculature. Blood pressure, heart/body weight ratio, and morphology and function of mesenteric resistance arteries from 1-kidney, 1-clip renovascular hypertensive rats were followed before and after declipping at age 14 weeks. The rats were divided into 5 groups, which were investigated 6 hours, 24 hours, 1 week, 4 weeks, and 8 weeks after declipping and compared with 2 normotensive and 2 renovascular hypertensive control groups at 14 weeks and 18 weeks. Systolic blood pressure was elevated 2 weeks after application of the clip and stabilized after 6 weeks. Declipping induced a prompt fall in blood pressure within 6 hours, and blood pressure was normalized within 1 week. Heart/body weight ratio was increased in renovascular hypertensive rats, and declipping induced a gradual decrease in the ratio, which was normalized within 4 weeks. Media/lumen ratio and media area of mesenteric resistance arteries were increased in renovascular hypertensive rats, and declipping did not affect media/lumen ratio and media area within 8 weeks, although there was a tendency for some regression of media/lumen ratio. There were no differences in response to high potassium, noradrenaline, or acetylcholine. Thus, these findings show definitively that declipping causes rapid reversal of renovascular hypertension in rats accompanied by gradual reduction of the heart/body weight ratio but lack of normalization in the mesenteric resistance vessels. This provides clear evidence that neither vascular nor cardiac structural changes are capable of keeping rats hypertensive.

Animals↗

PubMed1977

Dual effects of bradykinin on prostaglandin metabolism: relationship to the dissimilar vascular actions of kinins.

Generation of a prostaglandin of the F series by bovine mesenteric veins in response to bradykinin may depend on increased synthesis of PGE and conversion of the latter to PGF after activation of PGE 9-ketoreductase by the kinin. The prostaglandin then mediates the constrictor action of bradykinin on the bovine mesenteric vein. A high speed supernatant (HSS) fraction of bovine mesenteric blood vessels contains the highest activity of PGE 9-ketoreductase. Incubation of PGE2 with HSS at 37 degrees C in the presence of a NADPH generating system resulted in time-dependent conversion of PGE2 to PGF2alpha. Bradykin (0.01mM) more than doubled conversion of PGE2 to PGF2alpha by the PGE 9-ketoreductase obtained from mesenteric veins whereas the kinin had little effect on enzymic activity of the HSS fraction of mesenteric arteries. However, after inhibition of kininase catabolism, bradykinin increased PGE 9-ketoreductase activity of arteries and veins to the same degree. Prostaglandin release from veins by bradykinin appears essential to contraction of mesenteric venous strips evoked by the polypeptide as indomethacin treatment abolished this effect. PGE 9-ketoreductase may be an important prostaglandin regulatory mechanism of the vascular wall whereby the functional consequences of changes in rates of prostaglandin synthesis are governed by determining the ratio of PGE to PGF within vascular tissue. Constriction of bovine mesenteric veins evoked by bradykinin may, therefore, depend on increased prostaglandin synthesis and conversion of newly formed PGE to PGF, both steps being affected by the kinin.

Alcohol Oxidoreductases↗

PubMed1989

Metabolism of amines in the isolated perfused mesenteric arterial bed of the rat.

1. Semicarbazide-sensitive amine oxidase (SSAO) activity has been demonstrated in the isolated mesenteric arterial bed of the rat in vitro by studying the metabolism of benzylamine (Bz) and tyramine (Tyr) added to the perfusing fluid. 2. Pretreatment of rats with (E)-2-(3',4'-dimethoxyphenyl)-3-fluoroallylamine (MDL72145), a potent inhibitor of SSAO in rat mesenteric blood vessels, reduced the amount of metabolites, following the addition of Bz (25 microM) or Tyr (100 microM) to the perfusing fluid, by 83% and 52% respectively. Inactivation of monoamine oxidase type A (MAO-A) by the addition of clorgyline (10 microM) to the perfusing fluid, had little effect on the appearance of metabolites from Tyr. 3. The presence of 3 microM cocaine in the perfusing fluid increased the amount of metabolites produced from Tyr. 4. The metabolites of Tyr appearing in the perfusion fluid from control preparations were 85% p-hydroxyphenylacetic and the remainder consisted of a mixture of p-hydroxyphenylacetaldehyde and, possible, p-hydroxyphenylethanol. 5. The metabolism of Tyr by homogenates of the rat mesenteric vascular bed was carried out by SSAO (60%) and MAO-A (40%) with very little contribution from MAO-B. Homogenates from rats pretreated with MDL 72145 showed metabolism of Tyr by MAO-A only. 6. These data indicate that SSAO is capable of metabolizing amines present in the fluid perfusing blood vessels to metabolites that are readily released. Histochemical evidence has shown that whereas MAO-A is present in the mitochondria of smooth muscle cells and nerve endings, SSAO is located in the plasma membrane of the smooth muscle cells. This subcellular distribution may explain the differences found between metabolites released from intact vessels and the metabolism seen in homogenates. The identity of the Tyr metabolizing activity in intact vessels that is resistant to both MDL 72145 and clorgyline remains to be determined.

Animals↗

PubMed2000

A novel monoclonal antibody specific for lymphatic endothelium.

The difficulty of identifying and differentiating lymphatic and blood microvessels in tissue sections can be overcome by a monoclonal antibody specific for lymphatic endothelium. Unfortunately, the only known antibody also reacts with the endothelium of some blood vessels. The technique of double immunization (passive, with an antiserum to blood endothelium, and active, with a suspension of lymphatic endothelial cells) was, therefore, used to increase the chances of recognizing specific lymphatic antigens by the mouse immune system. The monoclonal antibody obtained, LyMAb, a G1 immunoglobulin, reacted strongly with the endothelium of bovine thoracic duct, mesenteric collecting vessels and lymphatic vessels of gallbladder and lymph nodes and moderately with those of the intestinal wall. Blood vessels (intercostal arteries, azygos vein and blood microvessels of all organs tested) were consistently negative. The antibody was species-specific and did not react with formalin-fixed, paraffin-embedded sections. Cross-reactivity was limited to some connective tissue fibres and scattered cells in the lymph node parenchyma, intestinal villi and hepatic lobules.

Animals↗