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PubMed1995

Histamine H2 receptor-mediated endothelium-dependent relaxation in canine spinal artery.

The mechanisms of histamine-induced relaxation were investigated in isolated canine spinal branches of intercostal artery (SBICA). Histamine (10(-7) to 10(-4)M) and dimaprit (3 x 10(-6) to 3 x 10(-4)M) produced concentration-dependent relaxation in the SBICA which had been contracted by 5 x 10(-6)M norepinephrine, whereas 2-pyridylethylamine caused only a very small relaxation. The histamine- and dimaprit-induced relaxation were inhibited by famotidine but not by diphenhydramine. In the SBICA without endothelium, histamine elicited very little relaxation. Aspirin (5 x 10(-5)M) and AA 861 (10(-5)M) did not affect the histamine-induced relaxation. Treatment with L-NMMA (3 x 10(-5)M) or methylene blue (10(-5)M) significantly suppressed the acetylcholine-induced relaxation of the SBICA but not the histamine-induced one. These results suggest that histamine produces relaxation in the isolated canine SBICA through stimulation of H2-receptors on the endothelium. The relaxing mediator(s) released by histamine seems to be neither endogenous prostaglandins, lipoxygenase products, nor nitric oxide.

Animals↗
PubMed1999

Inhibition of the endothelium-dependent relaxation by 18beta-glycyrrhetinic acid in the guinea-pig aorta.

The effect of 18beta-glycyrrhetinic acid (GA), an agent which interferes with gap junction conductivity, on endothelium-dependent relaxation produced by substance P was investigated in isolated aortic rings of the guinea-pig. In nor-adrenaline (NA)-contracted aortic rings, substance P (10(-7) M) induced an endothelium-dependent, transient relaxation. The relaxation was only slightly reduced by the co-application of nitroarginine and diclofenac. When GA (2x10(-5) M) was applied first, it slightly reduced substance P-induced relaxation, and a subsequent co-application of nitroarginine and diclofenac strongly reduced the relaxation. In aortic rings contracted with high-K solution ([K(+)](o) = 29.4 mM), substance P-induced relaxation was reduced by the simultaneous application of GA, nitroarginine and diclofenac, but not by GA alone. In endothelium-denuded aortic rings, GA reduced the threshold concentration of NA required to produce contractions and increased the amplitude of NA-induced contractions. GA increased the amplitude of contraction produced by small increases of [K(+)](o) (<30 mM) but reduced those produced by higher concentrations of [K(+)](o) (>54 mM). In NA-contracted aortic rings, Y-26763, a K(+)-channel opener, could relax muscles with reduced amplitude in the presence of GA. It is concluded that in guinea-pig aortic rings, GA inhibits mainly the EDHF-induced components of endothelium-dependent relaxation. GA also modulated contractions produced by NA or high-K solutions. The possible effects of inhibition of gap junctions by GA on endothelium-dependent relaxation were discussed.

Administration, Topical↗
PubMedDate not supplied

Longitudinal (T1) and transverse (T2) relaxation times of tissue water protons in mouse developing sarcoma 180-A: effect of hyperthermia.

In vitro studies on Swiss mice, inoculated with dead or live sarcoma 180-A ascites cells, were carried out to monitor the changes, if any, in the longitudinal (T1) and transverse (T2) relaxation times of tissue water protons following hyperthermic treatment and subsequent thermotolerance. Both relaxation processes exhibited biexponential relaxation curves. With increasing size of the tumours, the longitudinal relaxation behaviour changed from bi- to mono-exponential. This was not observed for the transverse relaxation phenomenon. Inoculation with either dead or live cells caused an immediate increase in the both relaxation times. In the case of dead cell inoculation, the increase lasted for only 24 h after which the relaxation times became the same as for the uninoculated controls. The transverse relaxation time increased as a result of exposure to hyperthermia. During development of thermotolerance, both the relaxation times decreased.

Animals↗
PubMed1999

Arterial relaxation mediated by endothelium-derived hyperpolarizing factor in hypertension induced by chronic inhibition of nitric oxide synthesis.

The aim of this study was to evaluate arterial relaxation mediated by endothelium-derived hyperpolarizing factor (EDHF) during chronic inhibition of nitric oxide (NO) synthase. We measured the isometric tension of isolated mesenteric arteries of Wistar rats administered Nomega-nitro-L-arginine methyl ester (L-NAME, 100 mg/Kg/day) for 3 weeks. Relaxation to acetylcholine (ACh) was reduced in L-NAME treated rats (maximum relaxation, 52% versus 79% ). After acute superfusion of 1x10(-4) M L-NAME, half the relaxation was inhibited in controls, while the relaxation was not changed in L-NAME treated rats. In contrast, relaxation to nitroprusside was normal in L-NAME treated rats. Superfusion of 1x10(-6) M apamin, which inhibits the effects of EDHF, reduced the relaxation. The relaxation inhibited by apamin was not significantly different between the two groups. These findings suggested that in endothelial cells, the synthesis of EDHF is unchanged during a chronic deficiency of relaxation influence of NO.

Acetylcholine↗
PubMed1989

The effect of atherosclerosis on endothelium-dependent relaxation in the aorta and intracranial arteries of rabbits.

The effect of hypercholesterolemia on vascular responsiveness was studied in isolated rabbit arteries. The arteries of animals maintained on a cholesterol-rich (1%) diet for 6 months had more pronounced intimal lesion than those receiving the diet for 3 months. The aortas were more severely damaged than the carotid or basilar arteries. Segments of the arteries were mounted in organ chambers for isometric tension recording or for measurement of the endothelium-derived relaxing factor. Endothelium-independent relaxation induced by glyceryl trinitrate was not affected even in the most severely damaged arteries; endothelium-dependent relaxation in response to acetylcholine (ACh) and A23187 was progressively inhibited as the degree of fatty streak formation increased. In the carotid arteries, mean (+/- standard deviation) relaxation induced by 10(-5) M of ACh (expressed as a percentage of the maximum relaxation induced by 10(-4) M of papaverine) decreased from 87.33% +/- 6.30% in control tissues to 60.90% +/- 4.64% in vessels from animals subjected to 6 months of hypercholesterolemia (p less than 0.01); in the aortas, mean relaxation due to 10(-5) M of ACh was 85.08% +/- 8.03% in control tissues and 41.35% +/- 13.68% in hypercholesterolemic tissues (p less than 0.01). In the carotid arteries, mean relaxation induced by 10(-7) M of A23187 decreased from 95.81% +/- 3.58% in control tissues to 55.95% +/- 2.81% in hypercholesterolemic tissues (p less than 0.01); in the aortas, relaxation in response to 10(-7) M of A23187 was 73.73% +/- 4.35% in control tissues and 29.35% +/- 6.77% in hypercholesterolemic tissues (p less than 0.01). Intimal lesions were not produced in the basilar arteries even in rabbits with 12 months of hypercholesterolemia, and endothelium-dependent relaxation was preserved.

Animals↗
PubMedDate not supplied

Clinical assessment of left ventricular relaxation.

Ventricular relaxation is altered in a number of cardiac disorders affecting domestic animals. Clinical determination of the ventricular relaxation rate can provide useful information regarding disease severity and response to therapy. We believe that the current gold standard for assessing left ventricular relaxation requires measurement of ventricular luminal pressure at end-expiration using a high-fidelity catheter. Ventricular pressure should be digitized at > or = 200 Hz for the period of pressure fall between the minimum rate of change of ventricular pressure and 10 mm Hg above left ventricular end-diastolic pressure of the preceding beat. The rate of relaxation then should be determined from the digitized data by Marquardt nonlinear least squares parameter estimation using an exponential decay model with nonzero asymptote. The major disadvantage in using an invasive method for evaluating left ventricular relaxation is that it requires general anesthesia in animals that frequently are categorized as high-risk anesthetic patients. Noninvasive estimates of ventricular relaxation using echocardiographic parameters such as isovolumic relaxation time, peak early filling rate, and time from end-systole to peak filling rate provide a crude and nonspecific assessment of ventricular relaxation that can be obtained from conscious animals. Determinations of these echocardiographic indices are of limited usefulness in assessing changes in ventricular relaxation associated with disease progression or therapeutic intervention, unless concurrent estimates of left atrial pressure, mitral valve characteristics, and left ventricular compliance are available.

Animals↗
PubMed1999

Androgen deprivation facilitates acetylcholine-induced relaxation by superoxide anion generation.

The aim of the present study was to assess the role of superoxide anions in the relaxation induced by acetylcholine (ACh) in aortic segments from male rats, and to investigate if their production is altered by sex hormone deprivation. In segments precontracted with 10 nmol/l noradrenaline, ACh (0.1 nmol/l-10 micromol/l) induced concentration-dependent relaxation, which was greater in segments from castrated compared with control animals. ACh-induced relaxation was abolished in segments from control rats, and reduced in those from castrated rats, by 0.1 mmol/l N(G)-nitro-L-arginine methyl ester (L-NAME; a nitric oxide synthase inhibitor). Indomethacin (1 micromol/l; a cyclo-oxygenase blocker) decreased the ACh-induced relaxation in arteries from control males only. Incubation of segments with superoxide dismutase (SOD; 100 units/ml; a superoxide anion scavenger) enhanced and reduced relaxation in segments from control and castrated animals respectively. For arteries from castrated animals, the presence of SOD plus L-NAME abolished such responses. In these arteries, incubation with L-NAME abolished the relaxation caused by ACh when the segments were precontracted with 30 mmol/l KCl. In segments obtained from castrated rats and pretreated with L-NAME, 1 mmol/l tetraethylammonium or 0.4 micromol/l charybdotoxin [blockers of Ca(2+)-sensitive and large-conductance Ca(2+)-sensitive (BK(Ca)) K(+) channels respectively] abolished the relaxation induced by ACh. These results suggest that ACh generates endothelial NO and superoxide anions from the arterial wall in both control and castrated animals; these agents negatively modulate ACh-induced relaxation in control rats by destruction of NO, and positively modulate ACh-induced relaxation in castrated rats by activation of BK(Ca) channels.

Acetylcholine↗
PubMed1992

[Early isovolumetric relaxation: correlation with the densitometric analysis of coronary stenosis].

Early relaxation is characterized by a segmental outward wall movement during isovolumic relaxation. There is still no general agreement as to its significance. Some Authors have considered the phenomenon to be a specific marker of isolated coronary narrowing, others have regarded it as a normal variation of left ventricular relaxation and still others concluded that it is a compensatory phenomenon to local ischemia in another region. We used a method of quantitative assessment of regional left ventricular function and a videodensitometric analysis of coronary stenosis. In our study we didn't observe an improved systolic function of the regions that presented early relaxation, but a slight non significant reduction. We did neither observe any correlation between early relaxation and ischemia provoked by stress test nor between early relaxation and coronary artery disease. The amplitude of early relaxation was not statistically different between patients with and without stenosis of left anterior descending artery. We conclude that early relaxation is a normal variation of left ventricular relaxation.

Constriction, Pathologic↗
PubMed2006

Mathematical description of stress relaxation of bovine femoral cortical bone.

In 1993 we proposed an empirical formula for describing the relaxation modulus of cortical bone based on the results of stress relaxation experiments performed for 1 x 10(5) sec: [E(t) = E0{A exp[ -(t/tau1)beta] + (1 - A) exp(-t/tau2)}, (0 < A, beta <1 and tau1 << tau2) where E0 is the initial value of the relaxation modulus, A is the portion of the first term, tau1 and tau2 are characteristic relaxation times, and beta is a shape factor [Sasaki et al., J. Biomechanics 26 (1993), 1369]. Although the relaxation properties of bone under various external conditions were described well by the above equation, recent experimental results have indicated some limitations in its application. In order to construct an empirical formula for the relaxation modulus of cortical bone that has a high degree of completeness, stress relaxation experiments were performed for 6 x 10(5) seconds. The second term in the equation was determined as an apparently linear portion in a log E(t) vs t plot at t>1 x 10(4) sec. The same plot for experiments performed for 6 x 10(5) seconds revealed that the linear portion corresponding to the second term was in fact a curve with a large radius of curvature. On the basis of this fact, we proposed a second improved empirical equation E(t) = E0{A exp [ -(t/tau1)beta] + (1 - A) exp[-(t/tau2)gamma]}, (0<A, beta, gamma <1) to describe the stress relaxation of cortical bone. The early stage of the stress relaxation process, which could not be expressed by the first, is well described by the second equation.

Animals↗
PubMed1976

Decreased vascular relaxation in hypertension.

Relaxation of spirally cut aortic strips was diminished in vessels from both spontaneously hypertensive rats and renal hypertensive rats. Aortic relaxation was decreased in response to the cyclic nucleotides and the beta adrenergic stimulant, isoproterenol, in both models, of hypertension. Defective aortic relaxation also occurred with two other vasodilators, nitroglycerin and adenosine. Further evidence for a reduced relaxant ability of blood vessels from hypertensive rats was obtained by measuring aortic relaxation after exposure and subsequent removal of vascular contractile agonists. The time for aortic preparations from spontaneously hypertensive rats to relax to base-line tension after maximum contraction with norepinephrine, serotonin and potassium chloride was significantly prolonged compared to recovery time for vessels from Kyoto Wistar normotensive rats. Treatment of the spontaneously hypertensive rat with reserpine, but not hydralazine, resulted in an improved ability of aortic preparations to relax. Based on these data, we propose that defects in vascular relaxation may contribute to hypertension and that some antihypertensive drugs may improve or facilitate vascular relaxation.

Adenosine↗
PubMed1991

Production of endothelium-dependent relaxation responses by saphenous vein grafts in the canine arterial circulation.

To determine if venous endothelium can acquire the ability to elicit endothelium-dependent relaxation responses, five dogs underwent femoral artery bypass with autogenous saphenous vein. The veins were harvested 15 to 17 months later. Endothelium-dependent relaxation was determined by measuring tension of deendothelialized coronary arteries mounted on a tensiometer and superfused with the effluent of the vein grafts. These grafts were perfused with acetylcholine and calcium ionophore A23187, which cause case vascular smooth muscle relaxation by means of endothelium-dependent relaxing factor production. Control arteries and veins were obtained from other dogs for comparison. In response to acetylcholine from 10(-9) to 10(-4) mol/L, the final cumulative relaxation produced in the detector coronary artery (mean +/- SD) was 64.2% +/- 25.7% by the control arteries, 14.2% +/- 5.5% by the vein bypass graft, and 5.3% +/- 5.6% by the control veins. In response to A23187 from 10(-8) to 10(-4) mol/L, the final cumulative relaxation was 66.2% +/- 19.0% by the control arteries, 30.6% +/- 8.9% by the vein bypass grafts, and 5.3% +/- 5.6% by the control veins. The differences were significant between the vein bypass grafts and the control arteries (p less than 0.04 for acetylcholine; p less than 0.04 for A23187) and the control veins (p less than 0.03 for acetylcholine; p less than 0.02 for A23187). Perfusion of saphenous veins used as chronic arterial bypass grafts with either acetylcholine or A23187 produced detector vessel relaxation, consistent with endothelium-dependent relaxing factor production. The magnitude of the relaxation response did not approach that from perfusion of control arteries.

Animals↗
PubMed1989

Relaxant effect of N-formyl-methionyl-leucyl-phenylalanine on rabbit vascular strips.

Some types of rabbit isolated blood vessels precontracted with phenylephrine relaxed when exposed to the chemotactic peptide N-formyl-Met-Leu-Phe (FMLP). The thoracic aorta was unresponsive whereas the portal vein and pulmonary artery exhibited concentration-dependent relaxing responses to FMLP (1-100 nM). FMLP-induced relaxations developed over several minutes and occurred after a latency of 30 to 40 sec. An inconsistent, brief and small contractile phase preceded the relaxations in some tissues. Stable responses to FMLP could be obtained repeatedly at 1.5-hr intervals. On both the portal vein and the pulmonary artery, the structure-activity relationship of peptides related to FMLP was similar to the one reported for activating phagocytic leukocytes. The peptide Boc-Phe-D-Leu-Phe-D-Leu-Phe behaved as a competitive antagonist of FMLP-induced relaxations with a calculated pA2 of 7.5 on both types of responsive vessels. Indomethacin inhibited the relaxations completely on the pulmonary artery and partially on the portal vein. FMLP-induced vasorelaxations were unaffected by a platelet-activating factor antagonist, BN 52021, or a 5-lipoxygenase inhibitor, L-651,392. Removal of the endothelium did not prevent the relaxant response to FMLP. The release of 6-keto-prostaglandin F1 alpha in the bathing fluid of portal vein and pulmonary artery exposed to FMLP was demonstrated using a radioimmunoassay. FMLP relaxed rabbit vascular strips in a blood-free environment by releasing secondary mediators tentatively identified as prostaglandins; however, a component of the relaxation in the portal vein was not mediated by cyclooxygenase products.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Endothelium-dependent relaxing factors do not affect the smooth muscle of portal-mesenteric veins.

Experiments were designed to analyze the difference in endothelium-dependent responsiveness to acetylcholine between arteries and veins. The effect of endothelium-derived relaxing factor(s) released from femoral arteries of the dog was compared on the coronary artery of the dog, the aorta of the rat, and portal-mesenteric veins of both species. Endothelium-derived relaxing factor(s) released by canine femoral arteries induced comparable relaxation of the canine coronary artery and the aorta of the rat. However, neither the canine nor the rat portal vein relaxed when exposed to endothelium-derived relaxing factor(s) released by the femoral arterial segments. Endothelium-derived relaxing factor(s) did not affect the action potentials and the spontaneous activity of the rat portal vein. Sodium nitroprusside induced complete relaxation of the canine coronary artery but failed to abolish the spontaneously evoked contractions of the portal veins. These experiments suggest that the longitudinal smooth muscle of portal veins is insensitive to endothelium-derived relaxing factor(s), presumably because of a different sensitivity of guanylate cyclase. Endothelium-derived relaxing factor does not possess calcium-entry blocking properties.

Acetylcholine↗
PubMed1989

Nonneurogenic relaxation to field stimulation in coronary arteries.

Coronary artery strips of cattle hearts in vitro respond to transmural stimulation with two potent but distinctly different responses. A neurogenic constriction, attributable to the endogenous release of acetylcholine, is predominant under conditions of minimal and moderate tone. During a high degree of spontaneous tone, and in the presence of near maximal contractions induced by 5-hydroxytryptamine, the response to field stimulation is relaxation rather than constriction. This process was studied more clearly after blockade of the cholinergic effects with atropine. The relaxation response elicited by 5 Hz stimulation for 2 min consisted of two components, one occurring during stimulation and the other promptly after its cessation. The overall relaxation was sufficient to almost obliterate a spontaneous contraction or a near-maximal contraction to 5-hydroxytryptamine. The relaxation to transmural stimulation was unaltered by tetrodotoxin, adrenergic blockade, indomethacin or 5 days cold storage of tissue. Relaxation was elicitable even by a single pulse. With a few pulses, the maximal effect was achieved at 0.5 Hz. Repeated application of three pulses, in strips with spontaneous tone, led to substantial but transient relaxations, which simulated spontaneous rhythm. Removal of the endothelium was without effect on the relaxations, and they were unaltered by inhibition of guanylate cyclase. In the presence of elevated potassium (30 mM), contractions to 5-hydroxytryptamine and those generated spontaneously did not relax to field stimulation. Inhibition of Na+-K+-ATPase with ouabain (5 microM) partially antagonized both components of the relaxation response.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Selective blockade of endothelium-dependent and glyceryl trinitrate-induced relaxation by hemoglobin and by methylene blue in the rabbit aorta.

Hemoglobin at 1 microM reduced and at 10 microM abolished the endothelium-dependent relaxation induced by acetylcholine or by A23187 in rabbit aortic rings. Similarly, methylene blue at 10 microM reduced and at 50 microM abolished relaxation induced by acetylcholine and by A23187. Furthermore, hemoglobin (1-10 microM) and methylene blue (10-50 microM) each induced a dose-dependent inhibition of the endothelium-independent relaxation produced by glyceryl trinitrate, but neither had any effect on the relaxation produced by isoproterenol. The inhibitory effects of hemoglobin and methylene blue may be due to blockade of guanylate cyclase, as the rises in cyclic GMP content which accompany relaxation induced by acetylcholine, A23187 or glyceryl trinitrate were abolished. Isoproterenol-induced relaxation took place with no change in cyclic GMP content. Hemoglobin and methylene blue appear therefore to inhibit selectively vaso-relaxation induced by agents which increase cyclic GMP levels. Hemoglobin and methylene blue augment tone in aortic rings, particularly when endothelial cells are present, suggesting that the endothelium-derived relaxing factor (EDRF) might be released spontaneously in low concentrations. The possibility that hemoglobin inhibits endothelium-dependent and glyceryl trinitrate-induced relaxation by binding EDRF and nitric oxide, respectively, is discussed together with the proposal that methylene blue might produce its effects by oxidizing a component of guanylate cyclase, possibly a ferrous heme group linked to the enzyme molecule. Methylene blue might, in addition, interact directly with EDRF.

Acetylcholine↗
PubMed1985

Differences in responsiveness of intrapulmonary artery and vein to arachidonic acid: mechanism of arterial relaxation involves cyclic guanosine 3':5'-monophosphate and cyclic adenosine 3':5'-monophosphate.

The objective of this study was to examine the relationship between responses of bovine intrapulmonary artery and vein to arachidonic acid and cyclic nucleotide levels in order to better understand the mechanism of relaxation elicited by arachidonic acid and acetylcholine. Arachidonic acid relaxed phenylephrine-precontracted arterial rings and elevated both cyclic GMP and cyclic AMP levels in arteries with intact endothelium. In contrast, endothelium-damaged arterial rings contracted to arachidonic acid without demonstrating significant changes in cyclic nucleotide levels. Indomethacin partially inhibited endothelium-dependent relaxation and abolished cyclic AMP accumulation whereas methylene blue, a guanylate cyclase inhibitor, partially inhibited relaxation and abolished cyclic GMP accumulation in response to arachidonic acid. All vessel responses were blocked by a combination of the two inhibitors. Prostaglandin (PG) I2 relaxed arterial rings and elevated cyclic AMP levels whereas PGE2 and PGF2 alpha caused contraction, suggesting that the indomethacin-sensitive component of arachidonic acid-elicited relaxation is due to PGI2 formation and cyclic AMP accumulation. The methylene blue-sensitive component is attributed to an endothelium-dependent but cyclooxygenase-independent generation of a substance causing cyclic GMP accumulation. Intrapulmonary veins contracted to arachidonic acid with no changes in cyclic nucleotide levels and PGI2 was without effect. Homogenates of intrapulmonary artery and vein formed 6-keto-PGF1 alpha, PGF2 alpha and PGE2 from [14C]arachidonic acid, which was inhibited by indomethacin. Thus, bovine intrapulmonary vein may not possess receptors for PGI2. The failure of endothelium-intact vein to relax to acetylcholine may be related to the lack of a relaxant effect by arachidonic acid, perhaps attributed to the absence of generation of an endothelium-derived relaxing factor.

Acetylcholine↗
PubMed1986

[Effect of age on left ventricular relaxation: pulsed Doppler echocardiographic evaluation].

There is no noninvasive index to assess the left ventricular relaxation property during the isovolumic relaxation period except for the isovolumic relaxation time, which is derived from M-mode echocardiography or phonocardiography. The intracardiac blood flow can now be precisely observed using pulsed Doppler echocardiography. We evaluated the left ventricular relaxation property and studied the effect of age on the relaxation property using this method. Cardiac catheterization and pulsed Doppler echocardiography were performed for 27 patients with various heart diseases, none of whom had wall motion abnormalities on left ventriculography, to determine the relationships between invasive and noninvasive parameters. The effects of age were examined in 25 normal healthy persons ranging in age from 26 to 69 years. In all cases, the intracardiac blood flow during the isovolumic relaxation period (isovolumic relaxation flow) as obtained by pulsed Doppler echocardiography was laminar, and directed from the base toward the apex of the left ventricle. The duration of this flow (the time interval from the beginning to the end of this flow; IRT), the acceleration time (the time interval from the beginning to the peak velocity; ACT) and the acceleration rate (the slope of the beginning to the peak velocity; AcR) were measured, and IRT, ln AcT (natural logarithm of AcT) and ln AcR (natural logarithm of AcR) were compared with the parameters obtained by cardiac catheterization. The time constant T of the fall in left ventricular pressure during the isovolumic relaxation period, which was proposed as an index of the left ventricular relaxation property, correlated well with IRT (r = 0.82, p less than 0.001), ln AcT (r = 0.69, p less than 0.001) and ln AcR (r = -0.77, p less than 0.001), but there were no significant correlations with maximum blood pressure, left ventricular ejection fraction, maximal positive dp/dt or the left ventricular end-diastolic volume index. Age and these three Doppler indexes in normal healthy persons correlated significantly as follows; IRT (r = 0.80, p less than 0.001), ln AcT (r = 0.60, p less than 0.001) and ln AcR (r = -0.61, p less than 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1984

Adenosine-mediated relaxation and activation of cyclic AMP-dependent protein kinase in coronary arterial smooth muscle.

Conflicting evidence exists regarding the participation of cyclic AMP (cAMP) in adenosine-induced relaxation of the coronary vasculature. Because the mechanism of action of cAMP is thought to involve activation of its dependent protein kinase, the purpose of this study was to determine if cytosolic cAMP protein kinase was activated in response to adenosine stimulation and to determine if such activation was correlated to the extent of relaxation in intact coronary arterial strips. Adenosine produced increases in cAMP protein kinase activity in both main trunk and branch circumflex bovine arterial strips. However, both the relaxant and kinase effects were greater in branch strips. Concentration and time-dependent increases in adenosine-induced relaxation of contracted branch strips were tightly coupled to concomitant increases in cAMP protein kinase activity (r = 0.93). Moreover, this increase in kinase activity was ascribable to the cAMP-dependent kinase, as the specific inhibitor of the cAMP protein kinase attenuated these increases. In contrast, relaxation produced by sodium nitroprusside was associated with an increase in a cAMP-independent kinase. In additional experiments, cumulative dose-response curves (10(-7) to 10(-3) M) for relaxation by adenosine and nine of its analogs showed that all agents were more effective in branch strips. Adenine-9-beta-D-arabinofuranoside, the least potent analog, did not produce relaxation or increase kinase activity. In contrast, 2-chloroadenosine, the most effective relaxant analog, also increased cAMP protein kinase activity. These findings suggest that adenosine-induced relaxation may involve cAMP and activation of cAMP protein kinase in coronary arterial smooth muscle.

Adenosine↗