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At least 73 records · Page 4Linked to original sources
PubMed1996

Effects of glibenclamide on the regional haemodynamic actions of alpha-trinositol and its influence on responses to vasodilators in conscious rats.

1. In conscious rats, alpha-trinositol (D-myo-inositol-1, 2, 6 triphosphate; 5-80 mg kg-1 h-1 infusion) caused dose-dependent hypotension, tachycardia and hyperaemic dilatation in renal, mesenteric and hindquarters vascular beds. These effects were accompanied by inhibition of the renal vasodilator effects of acetylcholine (ACh), and of the mesenteric vasodilator effects of sodium nitroprusside (SNP) and, particularly, of levcromakalim (LCK). 2. In the light of the latter finding, in a second experiment, we assessed the influence of the KATP channel inhibitor, glibenclamide (20 mg kg-1), on resting haemodynamics, on responses to ACh, bradykinin (BK), SNP and LCK, on the haemodynamic action of alpha-trinositol, and on the effects of the latter on responses to the vasodilators, over a period of 3 days. 3. In the presence of saline, glibenclamide caused a reproducible pressor effect, accompanied by renal, mesenteric, and hindquarters vasoconstrictions on all 3 experimental days; these effects were unrelated to changes in blood glucose. In the presence of glibenclamide, only the hindquarters vasodilator response to BK, and all the cardiovascular actions of LCK were inhibited. 4. On the first experimental day, the hindquarters vasodilator effect of alpha-trinositol was substantially inhibited by glibenclamide, the renal vasodilatation less so, and the mesenteric vasodilatation not at all. However, over the subsequent two days, the mesenteric vasodilator effect of alpha-trinositol became increasingly sensitive to glibenclamide. 5. In the presence of alpha-trinositol and glibenclamide, on the first experimental day, the inhibition of the renal vasodilator effect of ACh was no greater than with alpha-trinositol alone in the first experiment. Moreover, on the third experimental day, both before and after glibenclamide, the inhibition by alpha-trinositol of the renal vasodilator response to ACh was less than on the first experimental day. Similarly, the alpha-trinositol-induced inhibition of the mesenteric vasodilator effect of SNP, and of the hindquarters vasodilator action of BK, waned over the 3 experimental days. The inhibition of the cardiovascular effects of LCK were similar on all 3 experimental days, but no greater in the presence of alpha-trinositol and glibenclamide than with glibenclamide alone. 6. These results indicate that KATP channels are involved in the maintenance of resting vasodilator tone in renal, mesenteric and hindquarters vascular beds. However, although additional activation of KATP channels is responsible for all the haemodynamic effects of LCK, it contributes only to the hindquarters vasodilator action of BK and is not involved in any of the responses to ACh or SNP. The hindquarters, renal and mesenteric vasodilator effects of alpha-trinositol may involve (in the same rank order) activation of KATP channels, probably through an indirect mechanism. However, it is unlikely that direct or indirect interaction of alpha-trinositol with KATP channels explains the ability of the drug to inhibit the renal vasodilator action of ACh, or the mesenteric vasodilator effects of SNP or LCK.

Acetylcholine↗
PubMed1986

Selective hemoglobin inhibition of endothelium-dependent vasodilation of rabbit basilar artery.

The effect of hemoglobin on endothelium-dependent vasodilation of the isolated rabbit basilar artery was examined using an isometric tension recording method. Acetylcholine (ACh) (10(-7) - (10(-4) M) evoked a dose-dependent vasodilation of isolated rabbit basilar artery previously contracted by 10(-6) M serotonin. This vasodilating action disappeared after removal of the endothelium. The ACh-induced vasodilation of rabbit basilar artery is thought to be strictly endothelium-dependent. Hemoglobin (10(-7) - 10(-5) M) inhibited this ACh-induced endothelium-dependent vasodilation conditional upon the dose. Adenosine triphosphate (ATP, 10(-7) - 10(-4) M) also relaxed isolated rabbit basilar artery already contracted by 10(-6) M serotonin. This vasodilating action was slightly inhibited by adenosine antagonist, 8-phenyltheophylline (8-PT), and markedly attenuated by removal of the endothelium. This ATP-induced vasodilation is thought to be composed of ATP itself (endothelium-dependent) and ATP degradation products (endothelium-independent) such as adenosine monophosphate or adenosine. Hemoglobin markedly inhibited ATP-induced vasodilation, but there still remained a small vasodilation, which was blocked by 8-PT. Papaverine-induced vasodilation was not affected by removal of the endothelium, and hemoglobin did not inhibit the papaverine-induced vasodilation. These results suggest that rabbit basilar artery has endothelium-dependent vasodilating mechanisms induced by ACh and ATP, and that hemoglobin selectively blocks the endothelium-dependent vasodilation. This finding may relate to the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage: there is a possibility that the presence of hemoglobin released from lysed erythrocytes inhibits the endothelium-dependent vasodilation of cerebral arteries; furthermore, the endothelial degeneration following subarachnoid hemorrhage may impair the vasodilating mechanisms of cerebral artery smooth-muscle cells.

Acetylcholine↗
PubMed1996

Effects of oxygen tension on flow-induced vasodilation in porcine coronary resistance arterioles.

Vascular tone has been shown to be importantly influenced by flow-induced release of endothelium-derived vasodilators. The purpose of the present study was to test the hypothesis that in porcine coronary resistance-size arterioles, flow-induced vasodilation is sensitive to oxygen tension. Arterioles (55-150 mu m) were studied in vitro under conditions of constant intraluminal pressure to dynamically measure arteriolar diameter in response to changes in flow or, alternatively, in response to bradykinin under three conditions: hyperoxia (pO(2) 400 mm Hg), normoxia (pO(2) 160 mm Hg), and hypoxia (p0(2) 40 mm Hg). Under conditions of constant pressure and no flow, hypoxia alone resulted in vasodilation that was blocked by the nitric oxide synthase inhibitor omega-nitro-L-arginine methyl ester (L-NAME). Hypoxia did not alter the vasodilator response to bradykinin when compared to the vasodilator response to bradykinin during normoxia. During hyperoxia, flow-induced vasodilation was significantly reduced by either indomethacin, or L-NAME. Indomethacin and L-NAME combined completely abolished flow-induced vasodilation under conditions of hyperoxia. Under conditions of normoxia and hypoxia, indomethacin or L-NAME alone only partially blocked flow-induced vasodilation. No further inhibition was observed when indomethacin and L-NAME were combined. Glybenclamide failed to alter flow-induced vasodilation either alone or in combination with indomethacin and L-NAME. The results suggest that the mechanisms responsible for flow-induced vasodilation in coronary arterioles are complex and are different depending upon the oxygen tension. During hyperoxia, vasodilation is due to the combined actions of prostanoids and nitric oxide, while under conditions of normoxia and hypoxia, flow-induced vasodilation is the result of not only prostanoids and nitric oxide, but of another as of yet unidentified oxygen-sensitive endogenous vasodilator.

Animals↗
PubMed1999

Intravascular ATP and coronary vasodilation in the isolated working rat heart.

1. Adenosine-5'-triphosphate (ATP) is a potent coronary vasodilator. Because of the efficient hydrolysis of ATP, adenosine-5'-diphosphate (ADP) and adenosine-5'-monophosphate (AMP) by ectonucleotidases located in the coronary endothelium ATP-induced vasodilation may be mediated via both P1 (AMP and adenosine) and P2Y (ATP and ADP) receptors. We have used the change in total coronary resistance (TCR) induced by intravascular ATP in the isolated working rat heart to determine both the component of the vasodilation mediated via P2Y receptors and the identity of the subclass of receptor involved. 2. The dose response for ATP revealed a half maximal effect at an apparent ATP concentration of 0.08 +/- 0.009 microM. The response was saturated at apparent ATP concentrations greater than 0.23 microM. Contrary to much of the current literature, the perfusion of a 0.25 microM concentration of adenosine resulted in the identical response to an equimolar concentration of ATP suggesting a significant role for adenosine in coronary vasodilation. 3. The non-selective P1 receptor antagonist 8-(p-Sulfophenyl)theophylline (8-SPT) was used to show that the response to ATP was mediated via both P1 and P2Y receptors. Whilst 8-SPT abolished the effect of adenosine it reduced the effect of ATP by only 50%. Thus, at a saturating concentration of ATP, P1 and P2Y receptors were shown to contribute equally to the observed vasodilation. 4. Uridine-5'-triphosphate (UTP), ADP and adenosine-5'-O-thiotriphosphate (ATP gamma S) were used to characterize the component of coronary vasodilation that was mediated via P2Y receptors. UTP at 0.25 microM was ineffective and did not induce vasodilation. Perfusion with 0.25 microM ADP resulted in a vasodilation that was identical to 0.25 microM ATP. In the absence of 8-SPT the perfusion of 0.25 microM ATP gamma S produced a vasodilation that was significantly (P < 0.05) less than ATP. However, the vasodilation due to ATP gamma S, like that of adenosine, but unlike that of both ATP and ADP, was abolished in the presence of 8-SPT. The ability of ADP to induce vasodilation combined with both the lack of response to UTP and the ability of 8-SPT to abolish the vasodilation induced by ATP gamma S suggested very strongly that the component of ATP-induced coronary vasodilation in the isolated working rat heart that was mediated via P2Y receptors was achieved by the action of ADP (and not ATP) at P2Y1 receptors. 5. These results suggest that the vasodilatory action of intravascular ATP in the coronary circulation should be attributed to the dual and equal activities of adenosine and ADP acting at P1 and P2Y1 receptors respectively.

Adenosine Triphosphate↗
PubMed1998

Dipyridamole potentiates pulmonary vasodilation induced by acetylcholine and nitric oxide in the ovine fetus.

Nitric oxide (NO) modulates pulmonary vascular resistance (PVR) in the normal fetus by increasing the cyclic guanosine 3',5'-monophosphate (cGMP) content of pulmonary vascular smooth muscle cells. Although several vasodilator stimuli, including acetylcholine, decrease fetal PVR through the release of endogenous NO, fetal pulmonary vasodilation is often transient despite prolonged treatment. Because cGMP is hydrolyzed and inactivated by cGMP-specific (type 5) phosphodiesterases (PDE5), we hypothesized that PDE5 activity contributes to high fetal PVR and limits the capability of the fetal pulmonary circulation to dilate or sustain vasodilation in response to cGMP-dependent stimuli. To test this hypothesis, we studied the hemodynamic effects of dipyridamole in 19 late-gestation fetal lambs. To determine whether dipyridamole-induced vasodilation is dependent upon basal NO release, we measured the response to dipyridamole before and after pretreatment with the NO synthase antagonist nitro-L-arginine (L-NA) in five fetal lambs. L-NA completely blocked dipyridamole-induced pulmonary vasodilation. To evaluate the effect of dipyridamole on pulmonary vasodilation due to the stimulated release of NO, we studied effects of prolonged intrapulmonary acetylcholine infusions, with and without concomitant administration of low-dose dipyridamole, in six fetal lambs. During prolonged (2-h) infusions, acetylcholine and dipyridamole individually caused transient pulmonary vasodilation. When administered together, pulmonary vasodilation was of greater magnitude and was sustained for the entire study period. To determine the effects of dipyridamole on endothelium-independent pulmonary vasodilation, we investigated the hemodynamic effects of inhaled NO (5 and 20 ppm) alone and in combination with dipyridamole during mechanical ventilation with low FlO2. The combination of dipyridamole with inhaled NO resulted in a greater degree of pulmonary vasodilation than that achieved with inhaled NO alone. We conclude that dipyridamole-induced pulmonary vasodilation is dependent on endogenous (basal) NO production and that dipyridamole potentiates vasodilator responses to endothelium-dependent and -independent dilators in the ovine fetal pulmonary circulation. We speculate that PDES activity opposes vasodilation and maintains high PVR in the normal fetal lung.

Acetylcholine↗
PubMed2001

Albumin restores lysophosphatidylcholine-induced inhibition of vasodilation in rat aorta.

BACKGROUND: Impairment of vasodilation by oxidized low-density lipoprotein has been attributed to lysophosphatidylcholine (LPC). Albumin avidly binds LPC. Therefore, hypoalbuminemia may directly impair vasodilation and thus contribute to increased risk of atherosclerosis in nephrotic syndrome. The addition of albumin reduces LPC in erythrocytes and endothelial cells. We hypothesized that the addition of albumin will salvage vasodilation in aortic rings previously exposed to LPC. LPC increases superoxide production and disturbs L-arginine availability. Therefore, we also decreased superoxide with a superoxide dismutase mimic, MnCl(2), and supplemented L-arginine in an attempt to restore vasodilation. METHODS: Rat aorta rings, which had been incubated with various concentrations of LPC and human serum albumin (HSA), were mounted in organ chambers. Relaxation was studied with acetylcholine (0.01 to 100 micromol/L) after precontraction with phenylephrine (CON, 0.3 micromol/L; LPC, 0.03 micromol/L). In some studies MnCl(2) or L-arginine was added to the organ chamber. RESULTS: LPC had time- and dose-dependent inhibitory effects on acetylcholine-mediated vasodilation, but no effect on nitroprusside-mediated vasodilation. Preincubation with albumin (50 or 6 g/L) could protect vasodilation against very high levels of LPC. After preincubation with LPC, the addition of albumin to the incubation salvaged vasodilation. Albumin was more effective after short LPC incubation. MnCl(2) had no specific effect on the LPC-mediated disturbance in vasodilation. L-arginine completely salvaged vasodilation at low concentrations of LPC. However, even high concentrations of L-arginine (1 mmol/L) could not improve vasodilation at LPC levels at which vasodilation was restored by albumin. CONCLUSIONS: LPC affects several pathways that inhibit vasodilation, all of which are salvaged by addition of albumin.

Acetylcholine↗
PubMed2005

The response to inhaled nitric oxide in patients with pulmonary artery hypertension is not masked by baseline vasodilator use.

BACKGROUND: Assessment of pulmonary vasodilator responsiveness is important in determining the prognosis and management of patients with pulmonary hypertension. Many patients, however, are already on vasodilators at the time of testing. It is unclear if these agents should be temporarily discontinued to improve the sensitivity of testing. METHODS: We examined the hemodynamic effects of nitric oxide (NO) inhalation in 60 patients with pulmonary arterial hypertension. Thirty-one of these patients were receiving medications with vasodilating properties. Vasodilator testing was performed with invasive measurement of pressure of the right side of the heart at baseline and during inhalation of 40 ppm NO. RESULTS: No significant demographic differences were seen between patients receiving and not receiving vasodilators. Similar reductions in mean pulmonary artery pressure (19 +/- 12% vs 20 +/- 12%, P = .734) and pulmonary vascular resistance (31 +/- 18 vs 32 +/- 16, P = .967) were seen in patients receiving and not receiving vasodilators. Using the definition of positive vasodilator response (> or = 20% drop in mean pulmonary artery pressure), 55% (17/31) of patients in the baseline vasodilator group had a positive response compared with 62% (18/29) of the patients not on vasodilators (P = .570). CONCLUSIONS: Concurrent use of oral vasodilators does not appear to mask a significant response to inhaled NO on the pulmonary vasculature. Therefore, routine discontinuation of pulmonary vasodilators is likely unnecessary before vasodilator testing in patients with pulmonary arterial hypertension.

Administration, Inhalation↗
PubMed2005

Histamine-induced vasodilation and vasoconstriction in the mesenteric resistance artery of the rat.

The present study was designed to examine the vascular response to histamine in rat perfused mesenteric vascular beds with active tone. In preparations with intact endothelium, perfusion of histamine (1 nM-100 microM) produced a concentration-dependent vasodilation. Histamine-induced vasodilation was attenuated by L-NAME (nitric oxide (NO) synthase inhibitor, 100 microM) and olopatadine (histamine H(1) receptor antagonist, 1 microM) but not by lafutidine (histamine H(2) receptor antagonist, 1 microM). Cold-storage denervation (4 degrees C for 72 h) of the preparation with intact endothelium attenuated the histamine-induced vasodilation. In preparations without endothelium, histamine at low concentrations (1-100 nM) produced only a small and rapid vasodilation, whereas histamine at concentrations higher than 1 muM produced triphasic vascular responses: initial sharp vasodilation followed by transient vasoconstriction and subsequent gradual vasodilation. Lafutidine abolished only the histamine-induced initial vasodilation. Olopatadine abolished the histamine-induced second vasoconstriction and third vasodilation. Cold-storage denervation of the denuded preparation abolished the histamine-induced second vasoconstriction and third vasodilation. These findings suggest that histamine induced endothelium-dependent vasodilation via endothelium histamine H(1) receptors and endothelium-independent vasodilation via smooth muscle histamine H(2) receptors. It is also suggested that the histamine-induced endothelium-independent vasoconstriction and vasodilation are mediated by histamine H(1) receptors and perivascular nerves.

Animals↗
PubMed2000

Neurogenic vasodilation in human skeletal muscle: possible role in contraction-induced hyperaemia.

Whether or not neurally mediated vasodilation contributes to the rise in skeletal muscle blood flow during exercise in humans remains unknown. Such a mechanism might serve as an important 'feed-forward' regulatory signal causing blood flow to rise prior to the development of a metabolic demand. Research in animal species has identified three neurally mediated vasodilating mechanisms with the potential to increase skeletal muscle blood flow during exercise. These include sympathetic vasodilator nerves, the potential for substances released by motor nerves to evoke vasodilation and the possibility of an 'intrinsic' vasodilator nerve system within the walls of blood vessels. In humans, sympathetic vasodilator nerves are present in several vascular beds (e.g. cutaneous). However, more recent information suggests that the human skeletal muscle is not innervated by this class of nerves. Along these lines, the vasodilator response to exercise is unaffected by sympathectomy or by blockade of the traditional transmitters associated with neurally mediated vasodilation. The possibility that spillover of substances released from motor neurones evokes vasodilation is provocative. For example, acetylcholine could produce both skeletal muscle contraction via nicotinic receptors and vasodilation via endothelial muscarinic receptors. However, in many species including humans, atropine has no effect on exercise hyperaemia. While the concept of an 'intrinsic' vasodilator pathway within the walls of the skeletal muscle vascular bed is fascinating, limited information is available on this mechanism in animals and none is available in humans. Taken together, the current information suggests that neurally mediated vasodilating mechanisms may not exist in human skeletal muscle. Additionally, even if such mechanisms exist, they do not play an obligatory role in governing the rise in muscle blood flow during exercise in humans.

Humans↗