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PubMed1989

Beta-adrenoceptor-mediated facilitation of [3H]-noradrenaline release from the intramural nerves of bovine mesenteric lymphatic vessels.

1. Isolated segments of bovine mesenteric lymphatic vessels were loaded with [3H]-noradrenaline and its efflux in response to field stimulation at 2 Hz (0.3 ms pulses, 1 min train) examined. 2. Isoprenaline (10(-6) M) increased evoked fractional 3H efflux (3H released as a percentage of total tissue 3H at the onset of stimulation) from its control value of 0.67 +/- 0.09 to 1.2 +/- 0.18% (s.e.mean; n = 5). 3. Propranolol (10(-6) M) alone had no effect on evoked fractional 3H efflux but blocked the increase in transmitter overflow induced by isoprenaline (10(-6) M). 4. In the presence of the alpha-adrenoceptor antagonist phentolamine (10(-6) M) the facilitatory effect of isoprenaline (10(-6) M) on transmitter efflux was enhanced. In 5 experiments isoprenaline increased evoked fractional 3H efflux from its control value of 1.07 +/- 0.17 to 2.5 +/- 0.37% when phentolamine was present. 5. Adrenaline (10(-8) M) increased evoked fractional 3H efflux from its control value of 0.76 +/- 0.09 to 1.13 +/- 0.17% (n = 7). 6. These findings are consistent with the presence of presynaptic beta-adrenoceptors in this preparation. There is no evidence that these receptors play any role in feedback regulation of transmitter release.

Animals↗

PubMed1978

Ultra-violet radiation and 8-methoxypsoralen have actions similar to those of known inhibitors of thromboxane A2 synthesis in rat mesenteric blood vessels.

In the rat mesenteric vascular bed three structurally different agents (imidazole, benzydamine and N-0164) which have been reported to be inhibitors of thromboxane (TX) A2 synthesis at certain concentrations, all have a characteristic spectrum of action. They inhibit pressor responses to noradrenaline and angiotensin with equal potency and the inhibition can be reversed by exogenous PGE2: they do not inhibit responses to potassium. Ultra-violet (UV) radiation has a similar spectrum of action. The main difference between the action of imidazole and that of UV radiation is that the former is rapidly reversible while the latter is not. However, irradiation administered to preparations inhibited by imidazole has no irreversible effect provided that the radiation is switched off before the imidazole is removed. The imidazole protects against radiation damage suggesting that the drug may stabilize the site affected by UV light. 8-methoxypsoralen, a light sensitizing agent used in treatment of psoriasis also inhibited noradrenaline and angiotensin but not potassium responses and seemed to make the preparation more sensitive to radiation damage. It is possible that UV radiation and 8-methoxypsoralen may inhibit TXA2 synthesis but this requires confirmation by direct methods.

Angiotensin II↗

PubMed1980

On the relation between contraction and prostaglandin release in rabbit mesenteric blood vessels.

The rabbit superior mesenteric artery and portal vein were used for a study of the effects of noradrenaline, high potassium, angiotensin II and bradykinin on both the contraction development and PG synthesis (PGE2 and PGF2 alpha) in tissue. Noradrenaline induced contractions but no PG release, high potassium evoked contractions and PG release, angiotensin II elicited contractions and PG release in the mesenteric artery but only PG release in the portal vein, and bradykinin initiated PG release and a small decrease in basal tone. The stimulus-evoked PG release was Ca2+-dependent. It is concluded that, at least in some tissues, stimulus-evoked PG release is completely independent from the contractile mechanism. The variable pattern in contractile responses and stimulus-evoked PG release in various tissue may depend on variations of the stimulus-induced accessibility of Ca2+ ions to either phospholipase A2 or the contractile apparatus.

Angiotensin II↗

PubMedDate not supplied

In vitro studies on responses to noradrenaline, serotonin, and potassium of intramyocardial and mesenteric resistance vessels from Wistar rats.

We compared the responses to noradrenaline, serotonin, and potassium of isolated intramyocardial (flow-regulating) coronary and mesenteric resistance vessels of similar internal diameter (approximately 200 microns) from Wistar rats. The coronary but not the mesenteric resistance vessels had spontaneous basal tone, which was reduced by elimination of extracellular calcium, by increasing the extracellular potassium concentration up to 22 mM, and by stimulation of coronary vessels with noradrenaline. Noradrenaline always caused contraction of mesenteric resistance vessels and in coronary vessels after incubation with propranolol (3 X 10(-6) M). The noradrenaline and potassium concentration-response characteristics of the mesenteric resistance vessels were modulated by perivascular adrenergic nerve terminals, whereas no influence of nerve terminals could be shown in the coronary resistance vessels. The sensitivity of mesenteric vascular smooth muscle to noradrenaline [concentration required to give half maximal response (EC50) approximately 0.4 X 10(-6) M] and serotonin (EC50 approximately 0.3 X 10(-6) M) was higher (p less than 0.001) than the sensitivity of coronary smooth muscle (EC50 values 1.6 X 10(-6) and 1.3 X 10(-6) M, respectively). The potassium sensitivity of the coronary smooth muscle (EC50 approximately 35 mM) was higher than that of the mesenteric smooth muscle (EC50 approximately 41 mM; p less than 0.01). The respective maximal noradrenaline and serotonin responses relative to the maximal potassium response were 35 and 55% in the coronary and 127 and 120% in the mesenteric resistance vessels (p less than 0.001).

Animals↗

PubMed2005

Internal hernia: computed tomography diagnosis and differentiation from adhesive small bowel obstruction.

BACKGROUND: The goals of this study were to evaluate the specific computed tomography (CT) features of internal hernia (IH), and to verify CT features useful for the differential diagnosis of IH from adhesive small bowel obstruction (ASBO), and for the early detection of intestinal strangulation. METHODS: CT findings for 28 patients with surgically proven IH were retrospectively reviewed and compared with those for 50 patients with surgically proven ASBO. RESULTS: CT features most suggestive of IH versus ASBO included the following: a cluster of small bowel segments (100% vs 4% of patients; p < 0.0001); crowding and convergence of mesenteric vessels (79% vs 4%; p < 0.0001); mesenteric vessel engorgement (79% vs 26%; p = 0.0002); and mass effect to the surrounding bowels (82% vs 44%; p = 0.002). In addition, intestinal strangulation, the most severe complication, occurred more in IH than ASBO (39% vs 10%; p = 0.002), whereas proximal small bowel dilation (46% vs 100%; p < 0.0001) and small-bowel feces sign (0% vs 26%; p = 0.0029) were less common in IH than ASBO. The CT features indicative of intestinal strangulation were localized mesenteric fluid (p < 0.0001), mesenteric infiltrates (p = 0.0005), bowel wall thickening (p = 0.003), intramural hemorrhage (p = 0.005), mesenteric vessel engorgement (p = 0.03), and abnormal bowel wall enhancement (p = 0.008); the first 4 of these features were noted more in patients with IH than ASBO. CONCLUSION: The most specific CT criteria for the diagnosis of IH, rather than ASBO, were engorged mesenteric vessels, mass effect to surrounding organs, and bowel wall thickening. When associated mesenteric infiltrates were found, intestinal strangulation was highly suspected.

Abdomen↗

PubMed1985

Differences in norepinephrine activation and diltiazem inhibition of calcium channels in isolated rabbit aorta and mesenteric resistance vessels.

The mechanisms of norepinephrine stimulation of calcium ion entry in isolated rabbit aorta and mesenteric resistance vessels were studied through measurements of effects on calcium-45 influx, tension, and membrane potential. The resistance vessels were considerably less sensitive to norepinephrine than the aorta. The aorta exhibited complex dose-response curves for norepinephrine-stimulated calcium influx and contraction, whereas these were simple in the arterioles. Both vessels were depolarized with increasing concentrations of potassium. Norepinephrine did not depolarize the aorta, whereas it did depolarize the mesenteric resistance vessels. This result supports the contention that norepinephrine opens receptor-operated channels to induce calcium entry in the aorta, while it may activate potential sensitive calcium channels in the mesenteric resistance vessels. However, the maximum depolarization with norepinephrine (10(-4) M) in the arterioles was completely blocked by 10(-5) M diltiazem, whereas that induced by 80 mM potassium was unaltered by the diltiazem. Furthermore, 10(-4) M norepinephrine was able to stimulate virtually the same contraction and calcium influx in 80 mM potassium-depolarized arterioles as in normal polarized tissues. These results are consistent with norepinephrine opening of receptor-operated channels to allow calcium entry in the rabbit mesenteric resistance vessels. That the behavior of norepinephrine-activated channels in the aorta is more complex than in the arterioles is further illustrated by a dramatically decreasing sensitivity of norepinephrine-stimulated calcium influx to diltiazem with increasing norepinephrine in the aorta but not in the arterioles.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1996

[An autopsy case of rheumatoid arthritis associated with proliferative endarteritis died of sudden severe melaena].

A 68-year-old male with a 2-year history of rheumatoid arthritis was hospitalized due to severe polyarthritis. Since level of rheumatoid factor was high, and subcutaneous nodules and cutaneous ulcers were present, the case was diagnosed as malignant rheumatoid arthritis (rheumatoid vasculitis). On 10th day after admission, severe dyspnea developed due to acute heart failure, followed by severe melaena. The patient did not respond to various treatments including steroid pulse therapy, and died 3 days later. Autopsy revealed widespread hemorrhagic infarction that was extended from the colon to the rectum. Proliferative endarteritis was recognized in mesenteric vessels, however neither necrosis nor inflammatory changes were observed. The melaena was caused by the interstinal infarction. The intestinal infarction was thought to be responsible for the circulatory disturbances due to heart failure in obstructive vessel lesion of mesenteric vessels.

Aged↗

PubMed1998

Proliferative effect of insulin on cultured smooth muscle cells from rat mesenteric resistance vessels.

The present study evaluates the growth promoting effect of insulin on the proliferative activity of cells from rat mesenteric arteries in culture in order to test the hypothesis that insulin may play a pathogenetic role in the hypertrophy of resistance vessels. The proliferative effect of insulin was studied in cultured vascular smooth muscle cells (SMC) obtained from two functionally different rat vessels: mesenteric arteries and aorta. Growth characteristics (cell number and growth rate) of mesenteric and aortic cells were determined after a quiescent period and followed-up for 24, 72, and 120 h after the addition of insulin. At all studied time intervals, aortic SMC exhibited a significatively higher cell number and specific growth rate than did mesenteric SMC. Aortic SMC also displayed a greater proliferation than did mesenteric SMC in the presence of 10% fetal calf serum (FCS). At a physiological concentration of 100 microU/mL, the proliferative effect of insulin, after a quiescent period, was seen only in aortic SMC, at 72 and 120 h. Higher insulin concentration (500 microU/mL) increased significantly the cell number in SMC of both arteries. The proliferative effect was significant at all studied periods for aortic SMC; however, in mesenteric SMC, insulin increased the cell number only at 72 and 120 h. The proliferative effect of insulin was observed on SMC obtained from functionally different arteries such as aorta and mesenteric, being greater in the former. The different behavior of these SMC in the presence not only of insulin, but also of 10% FCS, provides further evidence for the existence of intervascular heterogeneity. The mild stimulatory effect of insulin in vitro may contribute in this way to the vascular hypertrophy of pathological entities exhibiting hyperinsulinemia.

Animals↗

PubMed2004

Fructose overload modifies vascular morphology and prostaglandin production in rats.

1. A fructose (Fru)-enriched diet induces a mild increase in blood pressure associated with hyperglycaemia, hypertriglyceridaemia, and insulin resistance, resembling the human 'syndrome X', being an useful model to study hypertension and type 2 diabetes. 2. A sustained elevation of blood pressure is associated with cardiovascular structural modifications such as left ventricular hypertrophy and increased wall thickness:lumen diameter ratio in blood vessels. 3. Prostanoids (PR), metabolites of arachidonic acid through the cyclooxygenase pathway, include vasoactive substances synthesized and released by the vessel walls. 4. The aim of the present study was to analyse, in Fru-treated rats: (i) the morphology of mesenteric vessels and; (ii) the PR production in aorta and mesenteric vessels, in order to assess whether these parameters are related with the haemodynamic alterations observed in this experimental model. 5. Blood pressure, glycaemia and triglyceridaemia, were significantly elevated in both (4 and 22 weeks) Fru-treated groups. Meanwhile body and heart weight as well as insulinaemia were similar between experimental animals and controls. 6. The mesenteric vessels of Fru-treated rats (22 weeks) showed an increased thickness and area of the media when compared with the controls; meanwhile, the lumen diameter was similar in both groups. 7. The Fru treatment for 4 weeks did not modify PR production in aorta, whereas in the mesenteric bed it diminished prostaglandin (PG) E(2) release significantly compared with the controls. However, in the group treated for 22 weeks, Fru reduced PGI(2) production in the aorta, as assessed by 6-keto-PGF(1)alpha measurements. Meanwhile, in the mesenteric bed, the chronic Fru treatment decreased PGE(2) release but, rather surprisingly, increased the output of PGI(2) when compared with its corresponding controls. 8. In conclusion, the present study shows the existence of an alteration in the morphology of mesenteric vessels in Fru-treated rats, which could be related to an increase in peripheral resistance and the consequent mild hypertension observed in this model. However, a diminished release of vasodilator PRs, such as PGE(2) in mesenteric vessels at 4 and 22 weeks and PGI(2) in aorta at 22 weeks could further impair the vessel response. The increase in PGI(2) observed in the chronic group in mesenteric vessels could be attributed to a compensatory mechanism.

Animals↗

PubMed1988

Differences in Ca2+ handling along the arterial tree: an update including studies in human mesenteric resistance vessels.

The effects of noradrenaline (NA) on rat, rabbit, and human mesenteric resistance vessels (MRVs) in Ca2+-free medium have been compared. The maximum tension obtained in the absence of extracellular Ca2+ is least and is lost most rapidly with time in the MRVs from rabbit, followed by those from Wistar-Kyoto (WKY) rats, spontaneously hypertensive rats (SHR), Sprague-Dawley (SD) rats, and from humans. Hence, it seems that the utilization of intracellular Ca2+ during activation of human MRVs by NA may be more substantial than has been found in the animal models. Nonetheless, in studies of the effects of isradipine on NA-induced tension, the human MRVs are similarly sensitive to the effects of this Ca2+ antagonist as WKY rat MRVs have been shown to be. All these resistance vessels, therefore, present quite a contrast to large vessels from rabbit, such as aorta, wherein the utilization of intracellular Ca2+ for NA-induced contraction is far more substantial, and the sensitivity of NA-induced contractions to Ca2+ antagonists is orders of magnitude less than in the MRVs. The basis for high sensitivity of rat and rabbit MRVs to Ca2+ antagonists may lie, at least in part, in the fact that these vessels (from rabbit and rat) depolarize in response to NA from approximately -50 to -30 mV, while aorta (from rabbit) does not, and the affinities of Ca2+ antagonists for voltage-sensitive Ca2+ channels (VSCs) are known to be voltage-dependent. Finally, the effects of the putative K+ channel opener BRL 34915 in rat MRVs appear to involve two sites of action, one with a lower affinity (K1 approximately 0.1 microM), similar to that shown previously in rat aorta, and a second with a higher affinity (K1 approximately 0.01 nM). In summary, these studies provide further evidence that Ca2+ handling processes controlled by both intracellular organelles and by the plasma membrane differ in mesenteric resistance vessels from those in aorta and in other large arteries.

Animals↗

PubMed1988

Effects of ryanodine on tension development in rat aorta and mesenteric resistance vessels.

1. The effect of ryanodine on contractile responses dependent either on intracellular Ca2+ release or on extracellular Ca2+ influx were studied in aorta and mesenteric resistance vessels of the rat. 2. In aorta, in the presence of extracellular Ca2+, pretreatment with ryanodine (10(-5)M) did not modify contractile responses to noradrenaline (NA) (10(-6)M) whereas in the absence of Ca2+, pretreatment with ryanodine reduced to about 25% the contractile response to NA (10(-6)M) and totally abolished the transient contraction elicited by caffeine (5 x 10(-2)M). 3. In mesenteric resistance vessels, ryanodine (10(-5)M) had no effects on NA (10(-5)M)-induced tension in the presence of extracellular Ca2+ but totally abolished contractile responses to caffeine (10(-2)M) in the absence of Ca2+. 4. In K+ -depolarized mesenteric resistance vessels, pretreatment with ryanodine (10(-5)M) significantly enhanced contractile responses to Ca2+ concentrations higher than 10(-4)M and 10(-3)M for arteries depolarized with 30 mM and 40 mM K+ respectively. Concentrations of either diltiazem (6 x 10(-7)M) or nifedipine (10(-8)M) that abolished contractile responses to Ca2+ in depolarized arteries (K+, 40 mM) did not totally inhibit the enhancement of Ca2+ -induced contractions obtained in the presence of ryanodine. 5. Ryanodine did not modify the Ca2+ concentration-effect relationships in mesenteric resistance vessels exposed to NA or arginine vasopressin. 6. These data are consistent with the hypothesis that ryanodine induces a release of Ca2+ from intracellular stores, resulting in a subsequent reduction of the amplitude of contractions dependent upon intracellular Ca2+ liberation. Furthermore, the ability of sarcoplasmic reticulum to buffer rises in cytoplasmic Ca2+ may be reduced in the presence of ryanodine, thereby accounting for the potentiation of contractile responses to Ca2+ in K+-depolarized mesenteric resistance vessels.

Alkaloids↗

PubMed1983

Morphometric study of structural changes in the mesenteric blood vessels of spontaneously hypertensive rats.

Structural changes of three categories of mesenteric arteries (representing elastic, muscular and arteriolar vessels) from 10- to 12-week-old and 28-week-old spontaneously hypertensive rats (SHR) were studied morphometrically at the light microscope level, and the results compared with age-matched Wistar-Kyoto normotensive rats. In 10- to 12-week-old SHR, hypertrophy of the vessel wall occurred only in the muscular and arteriolar vessels. At 28 weeks, further thickening of the vessel wall occurred in the muscular and arteriolar vessels, and the superior mesenteric artery (elastic vessel) was also thickened in the SHR. There was no evidence that the wall of the relaxed hypertrophied vessels encroached upon the lumen of the vessel. The structural basis for the increase in the vessel wall thickness varied with vessel type. In the superior mesenteric artery, increase in the media at 28 weeks of age would be consistent with hypertrophy of the smooth muscle cells. In the large muscular arteries, at 10-12 weeks of age, increase in medial mass occurred with increase in the number of the smooth muscle cell layers whereas at 28 weeks further increase in media could be due to hypertrophy of the smooth muscle cells. In the small arteriolar vessels, medial enlargement was due at all ages to an increase in the number of smooth muscle layers. Our results show that in the SHR hypertrophy of the media occurs not only in the small arteriolar vessels, but also in large elastic and muscular arteries.

Animals↗

PubMed2000

[Function of dopamine in mesenteric blood vessels of rats poisoned with lead and cadmium].

The aim of this study was to evaluate the impact of combined exposure to lead and cadmium, used in hypertensive doses, on the reactivity of isolated mesenteric rat vessels to dopamine. Experiments were performed on 64 male Buffalo rats (195-245 g body weight) administered intragastrically with lead acetate (35 mg Pb/kg b.w.) and/or cadmium chloride (5 mg Cd/kg b.w.) once a week for seven weeks. The isolated mesenteric bed was prepared according to McGregor's method. Dopamine (800 micrograms) was injected before and during the infusion, one after the other, of angiotensin converting enzyme (0.0004 j/ml/min), ketoprofen (0.2 mg/ml/min), and losartan (0.05 mg/ml/min) or infusion of nitric oxide synthase blocker, N-omega-nitro-L-argine (22 micrograms/ml/min), verapamil (0.001 mg/ml/min), and then propranolol (0.3 mg/ml/min). The results show an unchanged, in comparison to controls, vascular effect of dopamine in lead and cadmium poisoned rats. However, these metals modified the reactivity of mesenteric vessels to endogenous angiotensin and prostaglandins mediated pressor action of dopamine.

Animals↗

PubMedDate not supplied

Substance P and gastrin releasing peptide in bovine mesenteric lymphatic vessels: chemical characterization and action.

Alcoholic extracts of bovine mesenteric lymphatic vessels were assayed for the presence of SP, GRP, VIP, PHI, GIP and NT using specific radioimmunoassays. SP and GRP immunoreactivities were detected at concentrations of 190 +/- 20 and 1,000 +/- 130 pg.g-1, respectively. No significant levels of immunoreactivity were detected for any of the other peptides. SP and GRP immunoreactivities coeluted with their synthetic counterparts from both Sephadex G-50 and reversed phase HPLC columns. Synthetic SP (10(-9)-10(-7) M) and the naturally occurring analogue of GRP, bombesin (10(-9)-10(-7) M), increased spontaneous contraction rate in isolated vessel segments. This excitatory effect was not blocked by the alpha-adrenoceptor antagonist phentolamine (3 x 10(-6) M).

Animals↗

PubMed1992

Midgut malrotation, the reliability of sonographic diagnosis.

We are unaware of any other anatomical study which deals with normal variations in the relationship between the superior mesenteric artery (SMA) and the superior mesenteric vein (SMV). In our investigation in the majority of cases, the SMV lies to the right of the SMA. It has been suggested that ultrasonographic demonstration of a left sided SMV, is characteristic of midgut malrotation so a prospective study was undertaken in order to try to correlate the position of the mesenteric vessels on Ultrasound with the radiological diagnosis of midgut malrotation on upper GI series. 427 children (95% infants) who were planned for upper GI investigation, have had color Doppler U.S. of the mesenteric vessels before the barium study. In 67 cases, the mesenteric vessels were obscured by intestinal gas. Among them, there were 2 cases of malrotation. Three different positions of the mesenteric vessels were found in the 360 remaining cases. 1) A left sided SMV was found in 4% of the cases, all had midgut malrotation on X-rays and at surgery. 2) A mesenteric vein anterior to the SMA was found in 5% of the cases, 28% had midgut malrotation. 3) A normal right sided SMV was found in 91% of the cases. However 3% of these had midgut malrotation. There are anatomical variations in the position of the mesenteric vessels and a normal relationship between SMA and SMV does not exclude the possibility of intestinal malrotation. Nevertheless, ultrasound remains a useful noninvasive screening technique for the diagnosis of midgut malrotation.

Cecal Diseases↗

PubMed1984

Induction of Ca++ influx and intracellular Ca++ release in isolated rat aorta and mesenteric resistance vessels by norepinephrine activation of alpha-1 receptors.

This study was undertaken to determine which alpha adrenoceptor subtype(s) is involved in the activation of isolated rat aorta and mesenteric resistance vessels by norepinephrine and to ascertain whether norepinephrine-induced Ca++ influx into the smooth muscle is activated by one alpha adrenoceptor subtype while intracellular Ca++ release is mediated by the other subtype. The concentration-response curves for prazosin and yohimbine inhibition of norepinephrine-induced 45Ca influx, intracellular Ca++ release (as judged from contractions in Ca++-free solution) and contraction in the rat aorta indicate that the norepinephrine activation of the alpha-1 adrenoceptor was responsible for both Ca++ mobilization processes leading to norepinephrine contraction of this tissue. Contractions induced by norepinephrine in the isolated rat mesenteric resistance vessels demonstrated a phasic component, which was shown to be primarily dependent on intracellular Ca++ release, and a tonic component, which was completely dependent on Ca++ influx. Prazosin was three orders of magnitude more potent than yohimbine in inhibiting both components of the norepinephrine contracture in these vessels. We conclude that norepinephrine activation of alpha-1 adrenoceptors is responsible for both Ca++ influx and intracellular Ca++ release in isolated rat aorta and mesenteric resistance vessels.

Animals↗

PubMed2004

Cyclopiazonic acid decreases spontaneous transient depolarizations in guinea pig mesenteric lymphatic vessels in endothelium-dependent and -independent manners.

Guinea pig mesenteric lymphatic vessels exhibit vasomotion through a pacemaker mechanism that involves intracellular Ca(2+) release and resultant spontaneous transient depolarizations (STDs) of the smooth muscle membrane potential. This study presents a detailed characterization of the effects of cyclopiazonic acid (CPA) on this pacemaker activity. Microelectrode recordings from smooth muscle in vessel segments revealed that application of CPA (1-10 microM) caused a hyperpolarization accompanied by a decrease in the frequency and amplitude of STDs. The CPA-induced hyperpolarization was abolished after destruction of the endothelium and in the presence of N(G)-nitro-L-arginine (100 microM) or 1H-[1,2,4]oxadiazolol-[4,3-a]quinoxaline-1-one (10 microM), which suggests a contribution of endothelium-derived nitric oxide (EDNO) in this response. In the absence of EDNO-induced effects, CPA decreased the frequency and amplitude of STDs recorded before and in the presence of the thromboxane A(2) mimetic U-46619, norepinephrine, or thimerosal. CPA abolished U-46619-induced vasomotion as determined by measurement of constriction-associated intracellular Ca2+ concentration using the ratiometric Ca2+ indicator fura-2. The endothelial actions of CPA were compared with those of ACh, which is known to cause EDNO release in this preparation. Although CPA and ACh both increased endothelial intracellular Ca2+ concentration and depolarized the membrane potential, the kinetics of action for both parameters were markedly slower for CPA than ACh. These results suggest that CPA first hyperpolarizes the lymphatic smooth muscle and decreases STD frequency and amplitude through endothelial release of EDNO, and second, consistent with the action of CPA to inhibit sarcoplasmic reticulum Ca2+-ATPase and deplete Ca2+ stores, it further reduces STD activity. Inhibition of the lymphatic smooth muscle pacemaker mechanism is thought to abolish agonist-induced vasomotion.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1993

Tone dependent nitric oxide production in ovine vessels in vitro.

We have determined the role of endogenous nitric oxide (NO) in regulation of vasomotor tone in ovine intrapulmonary and mesenteric vessels with resting tension and elevated vasomotor tone. Third generation intrapulmonary vessel rings and mesenteric vessel rings, 2-3 mm in diameter, were isolated from 20 sheep. NO production in the vessels was assessed by the change in tension induced by NG-nitro-L-arginine methyl ester (L-NAME), a competitive inhibitor of NO synthase. In vessels under resting tension, 10(-4) to 10(-3) M L-NAME induced a significant increase in tension only in veins but not in arteries. When tone was elevated with phenylephrine or U 46,619, a thromboxane A2 analogue, there was now a significant increase in tension in arteries with 10(-4) M L-NAME and in veins with 10(-5) M L-NAME. The increase in tension induced by L-NAME in veins was greater than that in arteries and greater when tone was elevated than under resting tension. Responses of pulmonary and mesenteric vessels were similar. Our data suggest that NO may play a role in regulating venous tone under baseline conditions and that the role of NO in regulation of vasomotor tone becomes more significant in the presence of nonspecific elevation of vasomotor tone in both arteries and veins. We speculate that endogenous NO production may be one mechanism by which pulmonary and systemic vessels counter the effects of vasoconstrictive agents.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗