Endothelium-dependent relaxation induced by sodium fluoride in the rabbit ear artery

Sodium fluoride (NaF) produced concentration-dependent relaxation of isolated rabbit ear artery precontracted with norepinephrine. In contrast, an arterial preparation with the endothelium rubbed off did not relax, but contracted in response to NaF. NaF-induced relaxation was not influenced by indomethacin but was inhibited by methylene blue or NG-monomethyl-L-arginine. The results indicate that NaF relaxes the artery by releasing a so-called EDRF.     

Endothelium-dependent relaxation induced by sodium fluoride in the rabbit ear artery

Summary Sodium fluoride (NaF) produced concentration-dependent relaxation of isolated rabbit ear artery precontracted with norepinephrine. In contrast, an arterial preparation with the endothelium rubbed off did not relax, but contracted in response to NaF. NaF-induced relaxation was not influenced by indomethacin but was inhibited by methylene blue or N^G-monomethyl-L-arginine. The results indicate that NaF relaxes the artery by releasing a so-called EDRF.     

Mediation by nitric oxide of neurally-induced human cerebral artery relaxation

Human cerebral artery strips relaxed in response to non-adrenergic, non-cholinergic vasodilator nerve stimulation by electrical pulses or nicotine. The relaxation response was abolished by treatment with N^G-nitro-L-arginine, a nitric oxide synthase inhibitor; the inhibitory effect was reversed by L-, but not D-, arginine. Nitric oxide-induced relaxation was unaffected. These findings support the hypothesis that nitric oxide plays a crucial role, possibly as neurotransmitter, in transmitting information from vasodilator nerve to smooth muscle in human cerebral arteries.     

The endothelium-dependent relaxation of human middle cerebral artery: effects of activated neutrophils.

Neutrophils, activated by 4 beta-phorbol-12 beta-myristate-13 alpha-acetate, decreased acetylcholine-induced relaxation of strips of human middle cerebral artery precontracted with noradrenaline. This effect was prevented by catalase, but not by superoxide dismutase. Nifedipine, propranolol and, less markedly, captopril reduced the decrease in acetylcholine-induced relaxation. Aspirin and dipyridamole did not reduce it.     

Blood pressure and impairment of endothelium-dependent relaxation in spontaneously hypertensive rats

Summary Correlation between hypertension and impairment of endothelium-dependent relaxation was demonstrated using aortae from certain strains of rats with various levels of spontaneous hypertension. It was also observed that the impairment of endothelium-dependent relaxation is the secondary change due to hypertension, and the level and duration of hypertension is the determinant factor of the impairment.     

Blood pressure and impairment of endothelium-dependent relaxation in spontaneously hypertensive rats

Correlation between hypertension and impairment of endothelium-dependent relaxation was demonstrated using aortae from certain strains of rats with various levels of spontaneous hypertension. It was also observed that the impairment of endothelium-dependent relaxation is the secondary change due to hypertension, and the level and duration of hypertension is the determinant factor of the impairment.     

Influences of temperature change on the relaxation and amplitude inhibition by noradrenaline in the rabbit jejunum.

In the rabbit jejunum, the elevation of temperature within the range of 25-37 degrees C diminished the sensitivity to noradrenaline (NA) for both the relaxation and amplitude inhibition. The relaxation by NA was mainly mediated via adrenergic beta-receptors at 25, 30 or 37 degrees C. The amplitude inhibition was mediated via alpha-receptors at 37 degrees C, and both alpha- and beta-receptors at 30 or 25 degrees C.     

Acetylcholine induced endothelial-dependent vasodilation increases as artery diameter decreases in the rabbit ear

Isolated resistance vessels in the rabbit ear preconstricted with histamine were relaxed by acetylcholine by a proportionately greater amount than the central ear artery. The relaxation was antagonized by atropine and also by endothelium removal. Our studies represent the first direct evidence that endothelium-dependent dilation can occur in resistance vessels.     

Responses of monkey, rabbit and dog internal carotid arteries to atrial natriuretic factor

Effects of atrial natriuretic factor (ANF) on monkey, rabbit and dog internal carotid arteries were investigated. ANF caused a concentration-dependent relaxation in arterial strips submaximally precontracted with noradrenaline, 5-hydroxytryptamine, or high-potassium solution (10-30 mM). The response was greatest in the monkey arteries and least in the dog arteries. These results suggest that there is a marked species difference in the ANF-induced relaxation of the internal carotid arteries.     

Responses of monkey,rabbit and dog internal carotid arteries to atrial natriuretic factor

Summary Effects of atrial natriuretic factor (ANF) on monkey, rabbit and dog internal carotid arteries were investigated. ANF caused a concentration-dependent relaxation in arterial strips submaximally precontracted with noradrenaline, 5-hydroxytryptamine, or high-potassium solution (10–30 mM). The response was greatest in the monkey arteries and least in the dog arteries. These results suggest that there is a marked species difference in the ANF-induced relaxation of the internal carotid arteries.     

Relationship between action potential, contraction-relaxation pattern, and intracellular Ca2+ transient in cardiomyocytes of dogs with chronic heart failure

Abnormalities of contractile function have been identified in cardiomyocytes isolated from failed human hearts and from hearts of animals with experimentally induced heart failure (HF). The mechanism(s) responsible for these functional abnormalities are not fully understood. In the present study, we examined the relationship between action potential duration, pattern of contraction and relaxation, and associated intracellular Ca²⁺ transients in single cardiomyocytes isolated from the left ventricle (LV) of dogs (n = 7) with HF produced by multiple sequential intracoronary microembolizations. Comparisons were made with LV cardiomyocytes isolated from normal dogs. Action potentials were measured in isolated LV cardiomyocytes by perforated patch clamp, Ca²⁺ transients by fluo 3 probe fluorescence, and cardiomyocyte contraction and relaxation by edge movement detector. HF cardiomyocytes exhibited an abnormal pattern of contraction and relaxation characterized by an attenuated initial twitch (spike) followed by a sustained contracture ('dome') of 1 to 8 s in duration and subsequent delayed relaxation. This pattern was more prominent at low stimulation rates (58% at 0.2 Hz, n = 211, 21% at 0.5 Hz, n = 185). Measurements of Ca²⁺ transients in HF cardiomyocytes at 0.2 Hz manifested a similar spike and dome configuration. The dome phase of both the contraction/relaxation pattern and Ca²⁺ transients seen in HF cardiomyocytes coincided with a sustained plateau of the action potential. Shortening of the action potential duration by administration of saxitoxin (100 nM) or lidocaine (30 μM) reduced the duration of the dome phase of both the contraction/relaxation profile as well as that of the Ca²⁺ transient profile. An increase of stimulation rate up to 1 Hz caused shortening of the action potential and disappearance of the spike-dome profile in the majority of HF cardiomyocytes. In HF cardiomyocytes, the action potential and Ca²⁺ transient duration were not significantly different from those measured in normal cells. However, the contraction-relaxation cycle was significantly longer in HF cells (314 ± 67 ms, n = 21, vs. 221 ± 38 ms, n = 46, mean ± SD), indicating impaired excitation-contraction uncou pling in HF cardiomyocytes. The results show that, in cardiomyocytes isolated from dogs with HF, contractile abnormalities and abnormalities of intracellular Ca²⁺ transients at low stimulation rates are characterized by a spike-dome configuration. This abnormal pattern appears to result from prolongation of the action potential. Received 22 January 1998; received after revision 16 March 1998; accepted 27 March 1998     

13C NMR-study of flexibilide,an anti-inflammatory agent from a soft cora

Summary The use of¹³C spin-lattice relaxation measurements as a probe of structure in solution is illustrated for flexibilide. Analysis of quaternary carbon relaxation behaviour indicates that the structure in solution differs from the crystal structure. The effects of lanthanide shift and relaxation reagents on¹³C spectral parameters are also reported.Acknowledgment. We thank R.J. Wells, RRIMP, for helpful discussions.     

Isometric relaxation in rat myocardium: load dependence and influence of caffeine

When caffeine plus calcium is added to the perfusing medium, isometric relaxation of rat myocardium is no longer affected by length changes occurring during the twitch. The dependence of isometric relaxation on the initial muscle length is still present and more pronounced after caffeine addition.     

Isometric relaxation in rat myocardium: Load dependence and influence of caffeine

Summary When caffeine plus calcium is added to the perfusing medium, isometric relaxation of rat myocardium is no longer affected by length changes occurring during the twitch. The dependence of isometric relaxation on the initial muscle length is still present and more pronounced after caffeine addition.     

On the biomechanical function of the liver capsule

Summary We have carried out histomechanical studies on the human and bovine liver capsule under tension loading. Results: Nonlinear force-time curve under extension with constant speed, initial upper and lower summit decrease of the dynamic relaxation curve, amplitude diminution phenomenon of the dynamic relaxation in the lower nonlinear part of the extension-time curve, dynamic (cyclic) force recovery.Acknowledgments. We are grateful for helpful suggestions to Dr P. Freyer. The authors are indebted to Mrs C. Beckers and Mr W. Graulich — The experimental study was supported by the DFG (Deutsche Forschungsgemeinschaft).     

Characterization of the rat basilar artery in vitro

Summary Segments of the rat basilar artery were examined in vitro for their mechanical responsiveness to a variety of vasoactive substances. Serotonin was the most potent agonist while norepinephrine elicited a dose-dependent relaxation. The findings lend support to the concept that there exists a marked heterogeneity amongst species in cerebrovascular responsiveness.This work was supported by grants from the National Institutes of Health (NIHLBI-06080, 18575).     

Relaxation of isolated rabbit veins mediated by latent histamine H2-receptors

Summary Isolated rabbit veins preconstricted by either norepinephrine, methoxamine or potassium were relaxed by histamine in the presence of mepyramine, a histamine H₁-antagonist. The relaxation was not antagonized by atropine, propranolol and indomethacin but by an H₂-antagonist cimetidine. It is likely that histamine relaxes the rabbit veins through H₂-receptors.     

Effect of potassium on isolated bovine facial and human saphenous veins

Summary A moderate elevation of external (K ₀ ⁺ ) (5–10 mM) induces relaxation in bovine facial and human saphenous veins. A further increase of (K ₀ ⁺ ) leads to biphasic reactions (relaxation followed by contraction). Concentrations of (K ₀ ⁺ ) higher than about 15 mM cause contractions only. The potassium-induced relaxation may be explained by the stimulation of an electrogenic sodium pump.     

The endothelium-dependent relaxation of human middle cerebral artery: Effects of activated neutrophils

Neutrophils, activated by 4-phorbol-12-myristate-13-acetate, decreased acetylcholine-induced relaxation of strips of human middle cerebral artery precontracted with noradrenaline. This effect was prevented by catalase, but not by superoxide dismutase. Nifedipine, propranolol and, less markedly, captopril reduced the decrease in acetylcholine-induced relaxation. Aspirin and dipyridamole did not reduce it.     

Acetylcholine induced endothelial-dependent vasodilation increases as artery diameter decreases in the rabbit ear

Summary Isolated resistance vessels in the rabbit ear preconstricted with histamine were relaxed by acetylcholine by a proportionately greater amount than the central ear artery. The relaxation was antagonized by atropine and also by endothelium removal. Our studies represent the first direct evidence that endothelium-dependent dilation can occur in resistance vessels.Acknowledgments. We thank Christine Quinn for her careful technical assistance in the use of the myographs and Daniel Netto for construction of the small vessel myographs. The tungsten wire used for mounting the vessels was given by Westinghouse Corporation Lamp Division. This work was supported by American Heart Association Fellowship 608 and National Heart, Lung, and Blood Institute Grant HL-32985.