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At least 343 records · Page 19Linked to original sources
PubMed1976

Release of prostaglandin E-like material from perfused mesenteric blood vessels of rabbits.

Infusions of noradrenaline (1-3 mug ml(-1) min(-1)) into the mesenteric vascular preparation of the rabbit caused a 2 to 5 fold rise in perfusion pressure and a release of prostaglandin E-like material (3.23 +/- 0.65 (s.e.) ng PGE2 equivalents ml(-1)). Indomethacin (3 mug ml(-1)) prevented whereas arachidonic acid (0.2 mug ml(-1)) augmented, the noradrenaline-evoked release of a prostaglandin E-like material. The walls of arterioles or precapillary vessels are the proposed site of prostaglandin generation.

Animals↗
PubMed1984

Extent of alpha 2-receptor-mediated autoinhibition of vasoconstrictor nerve responses in mesenteric resistance vessels from normotensive and hypertensive rats.

The authors have previously shown that vasoconstrictor nerve responses of mesenteric small arteries from spontaneously hypertensive rats (SHR) are increased compared with normotensive rats. In this paper, whether this is due to differences in the degree of negative feedback of the transmitter on its own release is investigated. Small (i.d. 200 microns) arteries from the mesenteric arcades of SHR and normotensive control rats (NCR) were mounted in a Mulvany-Halpern myograph. In both SHR and NCR, nerve stimulation and applied noradrenaline elicited maximal contractions of similar magnitude, although SHR vessels were somewhat stronger and more responsive to nerve stimulation. Blocking alpha 2-receptors with 10 nM RX 781094 reduced the frequency for half-maximal activation to 84% and 80%, respectively, but did not eliminate the difference between the strains. Presynaptic alpha 2-receptors thus do not seem to cause the enhanced vasoconstrictor responses in SHR vessels.

Adrenergic alpha-Antagonists↗
PubMed1992

Mesenteric vascular angiotensin-converting enzyme is increased in experimental diabetes mellitus.

1. Diabetes mellitus was induced by streptozotocin in male Wistar rats, and angiotensin-converting enzyme measured in plasma and mesenteric vessels 3 weeks later. 2. Diabetes was associated with increased mesenteric wet weight/bodyweight ratio (control 0.2 s.e.m. 0.02 mg/g, n = 21, vs diabetes 1.0 s.e.m. 0.3 mg/g, n = 27, P less than 0.01, ANOVA). 3. Plasma angiotensin-converting enzyme activity was increased in diabetic rats (98 s.e.m. 3 nmol HL/mL per min) compared with controls (64 s.e.m. 6 nmol HL/mL per min, P less than 0.01, ANOVA). 4. Mesenteric vessel angiotensin-converting enzyme was increased in diabetes mellitus estimated by radioligand binding site density (fmol/mg protein; 1407 s.e.m. 166 fmol/mg protein) compared with controls (890 s.e.m. 56 fmol/mg protein, P less than 0.05, ANOVA) and by enzyme kinetic assay (diabetes, 15.5 s.e.m. 1.5 nmol HL/mg protein per min, controls, 8.3 s.e.m. 0.7 nmol HL/mg protein per min, P less than 0.01, ANOVA). The equilibrium dissociation constant of ligand-angiotensin-converting enzyme interaction was unchanged. 5. Increased vascular angiotensin-converting enzyme concentration may contribute to vascular hypertrophy and diabetic vasculopathy by increased local synthesis of angiotensin II.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2004

A lower ratio of AT1/AT2 receptors of angiotensin II is found in female than in male spontaneously hypertensive rats.

OBJECTIVE: Sexual dimorphism has been observed in arterial hypertension. Blood pressure levels are lower in female than in male spontaneously hypertensive rats (SHR). Angiotensin II (Ang II) plays a major role in the regulation of blood pressure. The aim of this study was to compare Ang II vascular reactivity and AT(1) and AT(2) receptor gene expression in female and male SHR. METHODS: SHR animals were divided into four groups: (I) male, (II) female in physiological estrus, (III) ovariectomized and (IV) ovariectomized treated with estrogen. Arterial blood pressure, AT(1) and AT(2) mRNA expression were determined. Ang II responses in aorta and mesenteric vessels were also evaluated. RESULTS: In female SHR, aorta and mesenteric microvessels were hyporeactive to Ang II in comparison to male SHR. In ovariectomized females, Ang II vasoconstriction was similar to that of males. Estrogen treatment abolished this difference. The mRNA expression for AT(1) was higher in aorta and mesenteric vessels from males than in females. In ovariectomized SHR, mRNA expression for AT(1) was comparable to that of males. Treatment with estrogen reversed the over expression observed. Whereas AT(2) gene expression did not differ, a lower ratio AT(1)/AT(2) was found in female than in male vessels. A higher mRNA expression for AT(1) was observed in kidney from male than in female. Ovariectomy resulted in up-regulation of this subtype receptor. Treatment with estrogen reversed the overexpression. AT(2) gene expression was higher in kidney from female than male SHR. Ovariectomy reduced AT(2) gene expression and estrogen treatment reversed the alteration observed in kidney. CONCLUSION: There is sexual dimorphism in vascular reactivity and in receptor gene expression to Ang II in SHR. We conclude that estrogen modulates AT(1) and AT(2) receptor gene expression and that this might explain at least partially the lower blood pressure observed in female SHR.

Angiotensin II↗
PubMed2005

Congenital internal hernia as a cause of small bowel obstruction: CT findings in 11 adult patients.

The aim of this study is to report the CT findings in patients proved to have congenital internal hernia (CIH) as a cause of small bowel obstruction (SBO). The CT scans of 11 patients (9 men and 2 women, with ages ranging from 20 years to 95 years (mean 60.7 years), presenting with clinical symptoms and signs of SBO without previous abdominal surgery or trauma, were retrospectively reviewed. In all patients features of SBO were seen. In addition, in nine of them a saclike mass, containing dilated small bowel loops with mesenteric vessels converging toward its orifice was demonstrated and a pre-operative diagnosis of an incarcerated internal hernia was suggested. In the other two, a closed loop obstruction was seen without an identifiable cause. Mural thickening of the entrapped loops within the hernial sac was seen in five patients, with hypoperfusion in four of them, blurring of the mesenteric vessels with localized mesenteric fluid was demonstrated in seven and free peritoneal fluid in 10. All patients were operated on following the CT and an incarcerated CIH was confirmed. Gangrenous bowel was present at exploration in seven cases. One patient died. In conclusion, in patients with intact abdomen and SBO, CT may be the first imaging modality to discover a clinically unsuspected CIH, which requires prompt surgical intervention. Radiologists should be aware of the CT features suggestive of a SBO caused by CIH, i.e. a saclike mass of dilated small bowel loops, as a correct diagnosis will influence patient management and prognosis.

Adult↗
PubMed1988

Evidence for dopaminergic co-transmission in dog mesenteric arterial vessels.

1. The overflow of dopamine and noradrenaline (NA) from the main trunk of the dog mesenteric artery and its proximal branches during prolonged depolarization (120 min) by K+ (52 mM) was quantified by high performance liquid chromatography with electrochemical detection. 2. K+-induced depolarization resulted in release of both dopamine and NA. The amount of NA released from both blood vessels declined progressively throughout the experiment. In the main trunk the same pattern of release was observed for dopamine, whereas in the proximal branches the overflow of dopamine increased throughout the experiment. 3. The addition of phentolamine (0.2 microM) to the perifusion fluid increased the overflow of both amines. In the presence of sulpiride (1 microM) the overflow of dopamine and NA was found to be increased in the proximal branches, but not in the main trunk. The addition of phentolamine to sulpiride caused a further increase in amine overflow in proximal branches, but not in the main trunk. 4. The addition of alpha-methyl-p-tyrosine (50 microM) to the perifusion fluid caused a decrease in the amounts of dopamine and NA released from both preparations. In alpha-methyl-p-tyrosine-treated preparations phentolamine increased amine overflow to the same extent as in experiments without tyrosine hydroxylase inhibition. The increasing effect of sulpiride on the overflow of dopamine and NA from the proximal branches was completely abolished after alpha-methyl-p-tyrosine. 5. The results presented suggest that in the proximal branches of the dog mesenteric artery, dopamine beta-hydroxylase represents a rate limiting step in the synthesis of NA; dopamine, through activation of prejunctional dopamine receptors acts like a prejunctional co-transmitter in the control of transmitter release, but only newly-synthesized dopamine appears to be responsible for this effect.

Animals↗
PubMed1977

Effects of prolonged hemorrhagic hypotensive stress on catecholamine concentration of mesenteric blood vessels.

Norepinephrine (NE) and epinephrine (E) concentrations were determined fluorometrically as an index of functional adrenergic innervation in small mesenteric arteries, veins, and superior mesenteric arteries of dogs and rats subjected to a period of prolonged hemorrhage at a constant mean arterial pressure of 35 mm Hg. In nonhemorrhaged animals, highest catecholamine concentrations were found in the small principal arteries, next highest in the small veins, and least in superior mesenteric arteries. A significant decrease occurred in the NE and E concentrations of all three vessel types in the dog during the decompensatory phase of the hypotensive stress (defined as the hypotensive period beyond the time at which maximum bleedout volume occurred). In the rat significant decreases were detectable only in the NE concentrations of the small arteries and veins during this phase. It is concluded that the increase in neurogenic vascular tone accompanying severe hemorrhagic stress is lost simultaneously on the arterial and venous sides of compensatory vascular beds. Such loss is closely related to transmitter depletion at the adrenergic neuromuscular junction and, if allowed to continue uncorrected, can contribute significantly to irreversible cardiovascular collapse.

Animals↗
PubMed1988

Differential effects of 6-hydroxydopamine on the two types of nerve vesicles and dopamine and noradrenaline content in mesenteric arterial vessels.

1 6-hydroxydopamine (6-OHDA) reduced the noradrenaline content by 50% in the proximal branches of the canine mesenteric artery without significant change of dopamine content. For the main trunk from the same blood vessel a parallel depletion of dopamine and noradrenaline was found to occur. 2 In the proximal branches of control animals 43% of nerve profiles have a very high proportion of small dense cored vesicles (SDCV), whereas in the remaining nerve profiles the proportion of SDCV and large dense cored vesicles (LDCV) was about the same. In the main trunk 89% of nerve profiles have a similar proportion of both types of vesicles. 3 In the proximal branches, 6-OHDA drastically reduced the number of nerve profiles with a high proportion of SDCV, thus resulting in a preferential disappearance of SDCV. In the main trunk, 6-OHDA produced a parallel reduction of both SDCV and LDCV. 4 The results presented suggest that the 6-OHDA-insensitive dopamine pool found in the proximal branches of the mesenteric artery is mainly localized in LDCV, whereas SDCV appear to be the major store of noradrenaline.

Animals↗
PubMed1975

Adrenergic innervation of human mesenteric blood vessels.

A fluorescent histochemical technique has been applied to study the adrenergic innervation of human superior mesenteric arteries obtained at autopsy. Specific catecholamine fluorescence was demonstrated in the smaller branches of this artery taken from three infants and one child. No specific fluorescence was seen in arteries from three adult subjects.

Age Factors↗
PubMed1987

Dopamine released from nerve terminals activates prejunctional dopamine receptors in dog mesenteric arterial vessels.

The fractional release of dopamine and noradrenaline (NA) from the main trunk of the dog mesenteric artery and its proximal branches, when elicited by K+ (52 mM), was measured by high pressure liquid chromatography with electrochemical detection. K+-induced depolarization released both dopamine and NA. For the main trunk of the mesenteric artery, the fractional release of dopamine and NA were of the same order of magnitude, whereas for the proximal branches dopamine fractional release was significantly lower than that of NA. Phentolamine (0.2 microM) significantly increased dopamine and NA release in both segments of the mesenteric artery. However, for the proximal branches the effect of phentolamine on dopamine and NA release was greater than that observed in the main trunk. Sulpiride (1 microM) significantly increased dopamine and NA release in the proximal branches of the mesenteric artery, whereas in the main trunk sulpiride did not increase amine release. In the proximal branches of the mesenteric artery, sulpiride significantly enhanced dopamine and NA fractional release even after it had been augmented by phentolamine. Apomorphine (0.3 microM) significantly reduced dopamine and NA release in both segments of the mesenteric artery under study; this effect was abolished by sulpiride but not by phentolamine. These results suggest that dopamine and NA released during depolarization by K+ activate prejunctional dopamine and alpha-adrenoceptors, respectively, thereby playing a role in the control of transmitter release.

Animals↗
PubMed1998

Role of protein kinase C in the regulation of pumping activity in bovine mesenteric lymphatic vessels.

We investigated the role of protein kinase C (PKC) in regulating the lymphatic myogenic response. Bovine mesenteric lymphatics were suspended in an organ bath with inflow and outflow ends cannulated. Input was provided from a reservoir filled with Krebs solution. The PKC activator phorbol 12-myristate 13-acetate (PMA) inhibited pumping significantly whether tested at a fixed pressure or as pressures were raised in 2 cm H2O increments (50% inhibition achieved at 4.6 x 10(-8)M. The inactive phorbol ester (4-alpha-PMA) had no effect. The specific PKC inhibitors calphostin (10(-9) to 10(-7)M) or chelerythrine (10(-8) to 10(-6)M) had no significant effect on pumping. However, chelerythrine (10(-6)M) was capable of reversing the inhibitory effects of PMA (5 x 10(-8)M). PKC activation is believed to inhibit nitric oxide (NO) production in some blood vessels, and previous work from our laboratory has demonstrated that NO is important in facilitating pumping activity in bovine lymphatics. We observed that sodium nitroprusside (sNP, 10(-7)M) or L-arginine (10(-4)M), reversed the depressor effects of PMA. These results suggest that PKC may not be involved in regulating the vessel's contractile response to pressure-induced stretch. However, the data with PMA suggest that these ducts contain PKC. PKC activation depresses lymphatic pumping and this effect may be mediated in part, by inhibition of NO.

Alkaloids↗
PubMed1994

The influence of different amounts of n-3 polyunsaturated fatty acids on bleeding time and in vivo vascular reactivity.

Mesenteric bleeding time, mesenteric vascular reactivity, platelet and erythrocyte lipid fatty acid composition were measured at 2-3 weeks, 5-6 weeks and 11-22 weeks in normotensive Wistar rats, fed on high (6.5% energy) or moderate (1.6% energy) intakes of eicosapentaenoic acid (20:5n-3; EPA) as fish oil, compared with controls fed on a diet devoid of EPA. All diets contained the same level of linoleic acid (4% energy): the moderate- and high-EPA diets also contained 1.1 and 4.4% of the energy as docosahexaenoic acid (22:6n-3) respectively. Moderate, but not high, intakes of EPA increased mesenteric bleeding time. Similar reductions in erythrocyte and platelet arachidonic acid (20:4n-6) occurred in animals fed on either high or low amounts of EPA, but the proportion of EPA increased dose-dependently. At high intakes of EPA the proportion of oleic acid in platelets and erythrocytes was decreased. Blood pressure platelet counts, mesenteric vessel diameter and mesenteric vascular reactivity to vasopressin were unaffected by treatment. High intakes of fish oil led to a slight fall in packed cell volume. In a second experiment bleeding time and mesenteric vascular reactivity to noradrenaline were increased 2-4 weeks after receiving a moderate intake of EPA and these effects persisted 5-21 d after switching to a control diet. A similar increase in vascular reactivity to noradrenaline was observed in animals given indomethacin (6 mg/kg) but not in those given aspirin (20 mg/kg).

Animals↗
PubMed1997

Intracerebroventricular administration of NPY increases sympathetic tone selectively in vascular beds.

NPY is widely distributed and has broad regulatory actions in the peripheral and central nervous system (CNS) and is especially important in the regulation of cardiovascular responses. CNS administered NPY has been demonstrated to produce both increases and decreases in cardiovascular tone. In this study we evaluated the effect of intracerebroventricular (ICV) administered NPY on cardiovascular tone, regional blood flow dynamics, as well as the mechanism of this action in normal animals. Male rats were instrumented with ICV cannulas and allowed to recover. At the time of the experiment the rats were anesthetized with urethane/chloralose and the femoral artery cannulated for blood pressure determinations. The abdomen was opened and Doppler flow probes were placed around the iliac, renal, and superior mesenteric artery. Mean arterial pressure (MAP), heart rate (HR), iliac, renal, and superior mesenteric flow, as well as the calculated iliac, renal, and superior mesenteric conductance were determined. ICV administered NPY resulted in an increase in MAP and HR, which was associated with decreased flows in the iliac and superior mesenteric vessels while increasing renal flow. Conductance was decreased in the iliac and superior mesenteric vascular beds but not the renal artery. ICV administration of NPY in the presence of a systemically administered alpha1-adrenergic inhibitor, prazosin, attenuated the NPY-mediated effects on MAP as well as vascular conductance in the iliac and superior mesenteric vessels. Additionally, ICV administration of NPY in the presence of a systemically administered beta1-adrenergic inhibition, atenolol, also attenuated the NPY-mediated increase in HR and MAP. Blood flow responses and iliac and superior mesenteric vascular conductance were also attenuated by atenolol pretreatment. In these studies we conclude that lateral ventricular administration of NPY acts to increase systemic MAP and HR and the response is mediated by an increase in sympathetic tone to the heart and especially the splanchnic and skeletal muscle vasculature.

Animals↗
PubMed1996

Kinins or nitric oxide, or both, are involved in the antitrophic effects of angiotensin converting enzyme inhibitors on diabetes-associated mesenteric vascular hypertrophy in the rat.

OBJECTIVE: To determine the roles played by kinins/nitric oxide and angiotensin II in the antitrophic effects of angiotensin converting enzyme inhibitors on mesenteric arteries after 3 weeks of streptozotocin diabetes by using blockers both of the angiotensin II AT1 receptor and of the bradykinin B2 receptor. DESIGN: Male diabetic Wistar rats were randomly allocated to receive no treatment, the angiotensin converting enzyme inhibitors perindopril or ramipril, the AT1 receptor blocker ZD7155, the bradykinin B2 receptor blocker Hoe 140, the nitric oxide synthase inhibitor NG-nitro-L-arginine-methyl ester, concomitant administration of perindopril plus subcutaneous Hoe 140, perindopril plus NG-nitro-L-arginine, or ramipril plus Hoe 140 (Hoe 140 administered via an Alzet mini-osmotic pump). METHODS: After 3 weeks, the rats were killed, their blood collected and their mesenteric vessels removed. The mesenteric vascular weight was measured and the media wall: lumen area ratio was assessed using quantitative histomorphometric techniques. RESULTS: Diabetes was associated with an increase in mesenteric weight and media wall:lumen area ratio. The angiotensin converting enzyme inhibitors, perindopril and ramipril, and the AT1 receptor antagonist ZD7155 reduced blood pressure and attenuated vascular weight and media wall:lumen area ratio. Concomitant administration of an angiotensin converting enzyme inhibitor with the kinin antagonist Hoe 140, administered either subcutaneously or via a mini-osmotic pump, or of the nitric oxide synthase inhibitor NG-nitro-L-arginine attenuated the effect of the angiotensin converting enzyme inhibitor on the mesenteric vascular weight and wall:lumen area ratios. Treatment with Hoe 140 or NG-nitro-L-arginine alone affected none of these parameters. CONCLUSION: The antitrophic effect of angiotensin converting enzyme inhibitors on diabetic mesenteric arteries is mediated by inhibition of angiotensin II and by actions on the kinin-nitric oxide pathway.

Angiotensin II↗