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PubMed2000

Bufokinin: immunoreactivity, receptor localization and actions in toad intestine and mesenteric circulation.

In this study, we have mapped the immunoreactivity and the binding sites for bufokinin, a tachykinin peptide from the toad intestine. Dense bufokinin-immunoreactive fibers were present at the myenteric plexus, but no cell bodies were stained, suggesting an extrinsic origin. Bufokinin nerve fibers were also associated with submucosal blood vessels and mesenteric arteries. Autoradiographic binding sites for [(125)I]Bolton-Hunter-bufokinin were densely localized over the intestinal circular and longitudinal muscle, submucosal blood vessels and the endothelium of mesenteric arteries. Mesenteric veins had minimal immunoreactivity and binding sites. In the anesthetized toad, topical application of bufokinin onto the mesentery caused a 2.7-fold increase in arterial blood flow, observed using intravital microscopy. This study supports a role for bufokinin as an endogenous spasmogen and hemodynamic regulator in the toad intestine.

Animals↗
PubMed2001

Spontaneous reanastomosis between lymphatic vessels following syngeneic transplantation of the small intestine in the rat.

Spontaneous lymphvascular reanastomosis (SLR) following small bowel transplantation in rats is of clinical relevance for the resorption of long chain fatty acids. Detailed morphological and molecular data concerning the process of lymphvascular reanastomosis are not available in the literature. In this study SLR was investigated using microradiology and scanning electron microscopy. Between the 8th and 21st postoperative days following transplantation SLR does not occur between the intestinal trunk of the transplant and the thoracic duct of the recipient. Instead, an indirect connection was observed between the inserted advential lymphatic vessels of the mesenteric artery and lymphatic vessels of the aorta or ductus deferens, which are connected with the thoracic duct.

Animals↗
PubMed2002

Effects of pregnancy and female sex steroid hormones on calcitonin gene-related peptide content of mesenteric artery in rats.

Calcitonin gene-related peptide (CGRP) levels in plasma and the dorsal root ganglia (DRG) are increased during pregnancy and in ovariectomized rats injected with ovarian hormones. Vasodilatory responses to CGRP are also increased in these animals. In the present study, we hypothesized that pregnancy and ovarian hormones elevate the contents of CGRP in perivascular nerves. We assessed CGRP-dependent mesenteric vascular relaxation induced by electrical field stimulation (EFS) and arterial content of CGRP. Because the mesenteric artery represents resistance vessels, segments of mesenteric arteries collected from female rats at different stages of the estrous cycle, pregnancy, or postpartum and from male rats were used in this study. The EFS-induced relaxation in the presence and absence of CGRP(8-37), an antagonist of CGRP, was used to measure CGRP-dependent relaxation, and radioimmunoassay (RIA) of tissue homogenates was used to assess changes in CGRP content in mesenteric branch arteries. The results show that CGRP-dependent, EFS-induced relaxation response was lower in female rats at diestrus and proestrus than in male rats, and no statistically significant differences were observed between Gestational Day 20 and Postpartum Day 2. The RIA revealed significantly lower mesenteric artery CGRP levels in female rats at proestrus, gestation, and postpartum than in female rats at diestrus or in male rats. We conclude that no correlation exists between CGRP-dependent, EFS-induced relaxation and CGRP content in the mesenteric arteries of these animal groups. Because both CGRP levels in DRG and serum are reported to be elevated, the reduced CGRP content in the vasculature during pregnancy and proestrus implicate enhanced basal release of CGRP at the nerve terminal in these animals.

Animals↗
PubMed1985

Cardiovascular pharmacology of nicardipine in animals.

The haemodynamic, antianginal and antihypertensive effects of nicardipine, a vascular selective calcium antagonist, were studied in experimental animals. In the canine isolated coronary artery, nicardipine relaxed potassium-induced contraction and suppressed 3,4-diaminopyridine-induced rhythmic contractions more effectively than nifedipine, verapamil or diltiazem. In anaesthetised rats, nicardipine prevented the elevation of ST segment induced by intracoronary injection of methacholine. In anaesthetised dogs, nicardipine produced a greater vasodilatation in vertebral, carotid, and coronary vessels than in mesenteric, femoral, and renal vessels and did not affect myocardial oxygen consumption. In conscious monkeys, nicardipine given intravenously lowered blood pressure and gave rise to reflex tachycardia but did not prolong the A-V conduction time. Nicardipine given orally lowered blood pressure in spontaneously hypertensive rats (SHR), renal hypertensive rats (RHR), and deoxycorticosterone acetate/salt hypertensive rats (DOCA/Salt), as well as in normotensive rats. Long-term treatment with nicardipine given orally for 12 weeks effectively lowered high blood pressure in the three types of hypertensive rats, reduced cardiac hypertrophy in SHR and DOCA/Salt rats, and prevented mortality from stroke in DOCA/Salt rats. Combined treatment with nicardipine and a beta-adrenoceptor blocking agent (indenolol) showed an antihypertensive effect similar to that obtained with nicardipine alone. Conscious renal hypertensive dogs given repeated oral administration of nicardipine for 14 days did not develop tolerance to the hypotensive activity of nicardipine. Under the same conditions, tolerance to hydralazine developed within 4 days.

Animals↗
PubMed1992

Structure of lymphatics in rat cecum with special reference to submucosal collecting lymphatics endowed with smooth muscle cells and valves. I. A scanning electron microscopic study.

The three-dimensional structure of lymphatic vessels in the rat cecum was studied by KOH-collagenase digestion/scanning electron microscopy (SEM), and corrosion casting/SEM. Abluminal surfaces of the lymphatic vessels show flat elliptical nuclear regions and flat cytoplasmic processes interdigitated with adjacent ones. The lymphatic capillaries closed by interdigitations of flat endothelial processes at their initial portion begin at the various levels of the mucosa. They descend and pass through the muscularis mucosa to connect with the lymphatic vessels in the submucosa. They form polygonal meshwork, the distances between intersections being about 0.2-0.5 mm. They also have valves, the distances between adjacent valves being about 0.1-0.6 mm. Most of the submucosal lymphatic vessels are surrounded by either periendothelial cells or typical smooth muscle cells. The polygonal meshworks made up of stellate periendothelial cells with many irregular processes embrace the initial segment of the collecting lymphatics. As they proceed proximally, the periendothelial cells become elongated and branch out by threes or fours, thus presenting the appearance of smooth muscle cells. These branches are connected side by side and run obliquely along the vessels, thus forming polygonal meshworks around the vessels. The more proximal collecting lymphatic vessels are surrounded by circularly oriented smooth muscle cells. Our results indicate that most of the lymphatic vessels in the submucosa are collecting ones and possess smooth muscle cells as well as valves. This suggests that the lymphatic vessels in the submucosa actively contract and propel the lymph towards the mesenteric lymphatic vessels.

Animals↗
PubMed1977

[Thormboembolisms and heart ruptures in myocardial infarct].

An analysis of the incidence of thromboembolism and heart ruptures with reference to different causative factors was conducted on the basis of 585 patients dying of myocardial infarction during the recent 30 years (autopsy data) and 1417 patients with myocardial infarction (298 mortality cases among them) hospitalized during the recent 10 years. A reduction of the incidence of thromboembolism and an increase of the incidence of heart ruptures in the recent years were revealed. Thromboembolism and heart ruptures play an important role among the causes of mortality in myocardial infarction. The development of thromboembolism in myocardial infarction is favoured by the macro-focal nature of the heart lesion, repeated necroses of the myocardium, localization of infarction in the posterior and posteriolateral zones, old age of the patients (over 60), presence of diabetes mellitus and acute cardiac aneurysm. Thromboembolism occurs with the same incidence rate within the initial 7 days, and later during the acute phase. Thrombi are most often found in the cardiac cavities, pulmonary, renal and splenic vessels, in the cerebral, mesenteric and other vessels. Heart ruptures are favoured by the macro-focal nature of the cardiac lesion, localization of the infarction in the anterior and anteriolateral zones, old age (over 60), presence of acute cardiac aneurysm. Most frequently the ruptures are observed in primary myocardial infarction within the initial 5--7 days of the disease. The use of anticoagulants in myocardial infarction decreases the incidence of thromboembolic complications and heart ruptures.

Aged↗
PubMed1998

Intracellular calcium stores modulation in lymph vessels depends on wall stretch.

We studied the effect of intracellular calcium stores modulation on the ability of lymph vessels to propel fluid in a preparation of actively contracting isolated bovine mesenteric lymph vessels. Vessels were cannulated at each end, placed in a temperature-controlled organ bath, and circulated with oxygenated Krebs solution. Vessel wall tension (transmural pressure) was changed by raising the height of the fluid-filled reservoir and outflow catheters appropriately. When transmural pressure was set and maintained at 6 cmH2O (1 cmH2O = 98.1 Pa), caffeine (10(-3) M), ryanodine (10(-7) M), and cyclopiazonic acid (CPA; 7 x 10(-6) M) inhibited lymphatic pumping. We also studied the effect of these agents on the relationship between lymph pump activity and transmural pressure, a relationship normally described by a bell-shaped curve. When transmural pressure was increased at 5-min intervals, the magnitude of inhibition by caffeine (10(-3) M) and CPA (7 x 10(-6) M) was greater than when transmural pressure was held constant. Ryanodine, on the other hand, had no effect on lymphatic contractility when transmural pressure was manipulated. The ryanodine results suggest the existence of an interaction between vessel wall stretch and intracellular calcium stores modulation that is not seen with caffeine or CPA.

Animals↗
PubMed1990

Possible mechanisms of abnormal norepinephrine sensitivity and reactivity of resistance vessels and the development of hypertension in spontaneously hypertensive rats. A hypothesis.

This study examined structural and functional changes of mesenteric resistance vessels in early, developing, and established stages of hypertension development in spontaneously hypertensive rats in an attempt to identify possible mechanisms of the development and maintenance of hypertension. Our results suggest that the development of hypertension in spontaneously hypertensive rats may be caused by genetic structural and functional abnormalities of resistance vessels. Both abnormalities may be caused by hyperreactivity to norepinephrine through an altered signal transduction process, including the regulation of protein kinase C in smooth muscle cells of resistance vessels in spontaneously hypertensive rats.

Animals↗
PubMed1989

The role of alpha- and beta-adrenoceptors in the response to noradrenaline of lymphatic vessels isolated from the bovine mesentery.

The role of postsynaptic adrenoceptors in the spontaneous activity of isolated bovine mesenteric lymphatic vessels was characterized. Low concentrations of noradrenaline (less than 10(-6) M) increased the amplitude and the frequency of the spontaneous contractions whereas high concentrations (less than 10(-6) M) depressed the activity. beta-Adrenoceptor blockade with propranolol enhanced the stimulation by noradrenaline and suppressed the inhibition. alpha 1-Blockade by prazosin or alpha 2-blockade by idazoxan antagonized the stimulation by noradrenaline and potentiated the inhibition. Activation of alpha 1-adrenoceptors by methoxamine, or of alpha 2-adrenoceptors by clonidine, stimulated lymphatic activity. The increases in the amplitude and frequency of the spontaneous contractions produced by each agonist were competitively antagonized by prazosin and idazoxan, respectively. Our results confirm the presence of postjunctional beta-, alpha 1-and alpha 2-adrenoceptors in lymphatic vessels and show that each of these receptors plays an important role in the adrenergic regulation of the spontaneous activity, with beta-adrenoceptors mediating inhibition, and alpha 1- and alpha 2-adrenoceptors mediating stimulation.

Animals↗
PubMed1993

Lymphatic drainage from the distal small intestine in sheep.

Lymphatic drainage from the wall of the distal small intestine, important especially in young sheep as a major site of gut-associated lymphoid tissue, begins with a series of longitudinally oriented subserosal vessels. These vessels convey lymph to the mesenteric border of the intestinal wall and unite to form larger vessels which course through the mesentery to the mesenteric lymph nodes. These nodes lie towards the periphery of a broad, fan-shaped mesentery, adjacent to major arteries and veins. Mesenteric vessels convey lymph from the jejunum and part of the proximal ileum to the jejunal nodes. Lymph from most of the ileum is conveyed to caecal nodes. The larger mesenteric lymphatics have well formed smooth muscle and connective tissue layers surrounding the endothelium. They are often adjacent to, but rarely within, the connective tissue band anchoring the major arteries and veins to one or both lamellae of mesentery. Few anastomoses occur between vessels from opposing sides of the gut wall or the mesentery. Afferent lymphatics enter the subcapsular and trabecular sinuses of the nodes over most surfaces apart from the hilar region. Lymph flows through cortical tissue to the medulla, which occupies most of the node. In the medulla, sinuses occur within medullary cords as well as between them. Initial efferent lymphatics occur throughout medullary tissue. Efferent vessels emerge at a hilus then coalesce and drain into the jejunal or ileal trunk. The hilus of the node varies from a flat, poorly defined area on the lesser curvature, to a depression or groove. The latter commonly occurs in elongated jejunal nodes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

The effects of extracellular pH and calcium change on force and intracellular calcium in rat vascular smooth muscle.

1. In order to investigate the mechanism whereby changes in external pH (pHo) alter tone in rat mesenteric resistance vessels, we have made simultaneous measurements of tension and intracellular Ca2+ [Ca2+]i. Strips of mesenteric artery were loaded with the Ca(2+)-sensitive indicator indo-1 and superfused with physiological salt solution at pH 7.4 and 37 degrees C. 2. An increase of pHo from 7.4 to 7.9 produced an increase in tension. This was accompanied by an increase in [Ca2+]i in resting and high-K(+)-depolarized vessels. Acidification to 6.9 reduced tension and was associated with a fall in [Ca2+]i. Over the pHi range examined, 6.6-7.9, parallel changes in [Ca2+]i and tension were found in K(+)-activated vessels. 3. In contrast to the relatively slow change in [Ca2+]i, pHi and tension with change of pHo, depolarization produced rapid changes in [Ca2+]i and tension, consistent with a more direct action on Ca2+ mobilization. 4. Reducing the external [Ca2+] below 1 mM produced a pronounced fall in [Ca2+]i and force. Changes in [Ca2+]i, produced by alteration of external [Ca2+] (Cao2+) were used to examine the relation between [Ca2+]i and tension. A linear relation was found. Alteration of pHo to 6.9 or 7.9 did not significantly change this relation. When the tension data were normalized to their own maxima, no shift in the tension-Ca2+ relation occurred, suggesting little or no effect of pH on the Ca2+ sensitivity of force production by the contractile proteins. 5. To determine further whether the changes in [Ca2+]i produced by alteration of pHo could account for all the changes observed in tension, [Ca2+]i was restored to control levels while maintaining an altered pHo. When this was done, restoration of [Ca2+]i led to restoration of force. Thus, in this preparation, the changes in [Ca2+]i produced by altering pHo in depolarized vessels can account for the changes in vascular tone.

Animals↗
PubMed2003

Myogenic responses and compliance of mesenteric and splenic vasculature in the rat.

In the rat, the spleen is a major site of fluid efflux out of the blood. By contrast, the mesenteric vasculature serves as a blood reservoir. We proposed that the compliance and myogenic responses of these vascular beds would reflect their different functional demands. Mesenteric and splenic arterioles ( approximately 150-200 microm) and venules (<250 microm) from rats anesthetized with pentobarbital sodium were mounted in a pressurized myograph. Mesenteric arterial diameter decreased from 146 +/- 6 to 133 +/- 6 microm on raising intraluminal pressures from 80 to 120 mmHg. This response was enhanced in the presence of N(omega)-nitro-l-arginine methyl ester (l-NAME; 139 +/- 6 to 112 +/- 7 microm). There was no such myogenic response in the splenic arterioles, except in the presence of l-NAME (194 +/- 4 to 164 +/- 4.2 microm). We propose that, whereas mesenteric arterioles exhibit myogenic responses, this is normally masked by NO-mediated dilation in the splenic vessels. The mesenteric venules were highly distensible (active, 184 +/- 15 to 320 +/- 30.9 microm; passive in Ca(2+)-free media, 209 +/- 31 to 344 +/- 27 microm; 4-8 mmHg) compared with the splenic vessels (active, 169 +/- 11 to 184 +/- 16 microm; passive, 187 +/- 12 to 207 +/- 17 microm). We conclude that, in response to an increase in perfusion pressure, mesenteric arterial diameter would decrease to limit the changes in flow and microvascular pressure. In addition, mesenteric venous capacitance would increase. By contrast, splenic arterial diameter would increase, while there would be little change in venous diameter. This would enhance the increase in intrasplenic microvascular pressure and increase fluid extravasation.

Animals↗
PubMed1983

Correlations and otherwise between blood pressure, cardiac mass and resistance vessel characteristics in hypertensive, normotensive and hypertensive/normotensive hybrid rats.

We have measured heart weight and properties of 150-200 microns mesenteric resistance vessels from spontaneously hypertensive (SHR), Wistar-Kyoto (WKY), two-kidney, one clip Goldblatt renal hypertensive (RHR) and outbred Wistar rats, as well as in SHR/WKY F2-hybrid rats. All rats were 14-weeks-old. In the SHRs, WKYs, RHRs and Wistars the mean blood pressures (measured intra-arterially) were, respectively: 136, 111, 164 and 100 mmHg. In the SHR/WKYs the systolic blood pressures (measured regularly over a two-week period by the tail cuff method) were normally distributed between the values obtained from control SHRs and WKYs. Relative heart weight and resistance vessel media thickness/lumen diameter ratio correlated (P less than 0.001) with blood pressure between SHRs, WKYs, RHRs and Wistars; however, no significant correlation was seen in SHR/WKYs. By contrast, the calcium sensitivity of the resistance vessel noradrenaline response did correlate (P less than 0.01) with blood pressure in the SHR/WKYs, but did not correlate between the pure strains (calcium sensitivity of the SHR and Wistar vessels was similar, but higher than that of the WKY vessels; induction of renal hypertension did not affect calcium sensitivity). The results suggest that although the cardiac enlargement and increased resistance vessel media/lumen ratio of 14-week SHRs may be advantageous for these animals, these structural abnormalities may not be primary causes of the hypertension. Furthermore, the results indicate that it is the WKYs which are abnormal in having a low calcium sensitivity of their resistance vessels, but suggest also that this reduced sensitivity may be associated with mechanisms which help to keep the WKYs normotensive.

Animals↗
PubMed1996

Effects of noradrenaline and neuropeptide Y on rat mesenteric microvessel contraction.

We have studied the contractile effects of the sympathetic transmitter noradrenaline and its cotransmitter neuropeptide Y (NPY) given alone and in combination on isolated rat mesenteric resistance vessels (200-300 microns diameter). Noradrenaline and NPY each concentration-dependently contracted rat mesenteric microvessels (EC50 approximately equal to 800 nM and 10 nM, respectively), but noradrenaline caused considerably greater maximal effects than NPY (14.3 mN vs. 3.5 mN). A low antagonistic potency of yohimbine indicated that the response to noradrenaline did not involve alpha 2-adrenoceptors, and the subtype-selective antagonists 5-methylurapidil, tamsulosin and chloroethylclonidine indicated mediation via an alpha 1A-adrenoceptor. Shallow Schild regressions for prazosin and 5-methylurapidil indicated that an alpha 1-adrenoceptor subtype with relatively low prazosin affinity might additionally be involved. Studies with the NPY analogues PYY, [Leu31, Pro34] NPY and NPY18-36 demonstrated that NPY acted via a Y1 NPY receptor. In addition to its direct vasoconstricting effects NPY also lowered the noradrenaline EC50 but did not appreciably affect maximal noradrenaline responses indicating possible potentiation. The potentiating NPY response occurred with similar agonist potency as the direct contractile NPY effects and also via a Y1 NPY receptor. The Ca2+ entry blocker nitrendipine (300 nM) reduced direct contractile responses to noradrenaline and NPY but did not affect the potentiation response to NPY.

Animals↗
PubMed1988

Calcium metabolism and structure in the peripheral vasculature: implications for hypertension.

This paper reviews in vitro investigations of resistance vessels taken from individuals with essential hypertension and from spontaneously hypertensive rats (SHRs). Unlike mesenteric resistance vessels from SHRs, the calcium sensitivity of subcutaneous resistance vessels from essential hypertensive patients is not increased, but decreased. However, like the resistance vessels from SHRs, the structure of the resistance vessels from the essential hypertensive patients (expressed in terms of their media thicknesses) was increased. In studies with SHRs, the increased media are found to be associated with cellular hyperplasia. If this also is true for the resistance vasculature of patients with essential hypertension, this may explain findings that antihypertensive treatment reduces blood pressure more readily than vascular structure. These findings could also be relevant as regards the rather limited effect of such treatment on hypertension-related diseases such as infarction.

Animals↗
PubMed2006

Distribution of lymphatic vessels in the neural plexuses surrounding the superior mesenteric artery.

OBJECTIVES: To investigate whether lymphatic vessels exist in the neural plexuses surrounding the superior mesenteric artery (SMA) and the ultrastructural relationship between neural plexuses and lymphatic vessels. METHODS: A total of 970 serial sections including the structure surrounding the SMA were obtained from 9 cadavers. They were subjected to conventional hematoxylin/eosin staining and immunostaining for the lymphatic marker D2-40. Epithelial membrane antigen and S100 were also immunostained to identify the perineurium and nerve bundles, respectively. RESULTS: Thin-walled, erythrocyte-free vessels staining with lymphatic markers (D2-40) were found in the neural plexuses surrounding the SMA along a full circumference. There seemed to be a distribution correlation between lymphatic vessels and neural plexuses. Lymphatic vessels were not identified within the nerve bundles. The plexuses contained no lymph nodes in any sections. CONCLUSIONS: To our knowledge we report the immunohistochemical visualization of lymphatic vessels in peri-SMA neural plexuses for the first time. Therefore, particular attention should be paid to the lymphatic vessels within neural plexuses as a possible route of invasion and the source of pancreatic cancer recurrence.

Aged↗
PubMed1989

Endothelium-dependent relaxation in resistance vessels from the spontaneously hypertensive rats.

The endothelium-dependent vasodilator acetylcholine was used to observe relaxation responses of noradrenaline-contracted mesenteric resistance vessels from 3-, 6-, 12- and 18-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Relaxation responses were greater than normal in the 3-week-old SHR but the pattern of response was different in the 6-18-week-old SHR compared with the WKY. In these older animals, low concentrations of acetylcholine relaxed SHR and WKY vessels to a similar extent, but high concentrations (greater than 10(-7) mol/l) caused the partially relaxed vessels to contract again. Indomethacin enhanced relaxation in the 12-week-old SHR and reduced the difference between the SHR and WKY. The reduction in acetylcholine-induced, endothelium-dependent relaxation in SHR suggested that a functional change occurred, causing the vessels to release a vasoconstrictor factor that opposes the action of endothelium-derived relaxing factor.

Acetylcholine↗
PubMed1986

Effects of calcium-antagonists on norepinephrine release from sympathetic nerve endings in rat mesenteric vasculature.

The present study was designed to investigate whether Ca-antagonists influence norepinephrine release from the sympathetic nerve endings in resistance vessels. Isolated mesenteric vascular preparations of rats, perfused with Ringer-Locke solution, were used to determine the effects of verapamil or diltiazem on norepinephrine release from sympathetic nerve terminals. Pressor responses to exogenous norepinephrine and electrical nerve stimulation were recorded, and the norepinephrine contents of the perfusate were measured before and after the electrical nerve stimulation, using high pressure liquid chromatography with an electrochemical detector. Pressor responses to exogenous norepinephrine and electrical nerve stimulation were depressed dose-dependently by verapamil and diltiazem. The inhibition of the pressor responses for nerve stimulation was greater than exogenous norepinephrine. Both verapamil and diltiazem reduced norepinephrine release from the mesenteric arterial beds after the electrical nerve stimulation. These results indicate that Ca++-antagonists, such as verapamil and diltiazem, have inhibitory effects on norepinephrine release from the sympathetic nerve endings, in addition to their direct actions on the vascular smooth muscle. It is also suggested that the presynaptic inhibitory action of Ca++-antagonists could be due to the blockade of Ca++-channels in nerve cell terminals, which may be important in the clinical use of Ca-antagonists.

Animals↗