摘要:

Sialic acids are negatively charged groups in the carbohydrate side chains of glycolipids and glycoproteins which line the external membrane surface. The goal of this study was to characterize the effect of neuraminidase, which selectively cleaves sialic acids, on contractile activity in vascular smooth muscle. Helically cut strips of rat tail artery were mounted in an organ chamber and isometric contractions were recorded. Following treatment with neuraminidase (0.2 U/ml, 1 h), contractile responses to norepinephrine were significantly greater than control responses. Phasic contractions to norepinephrine in calcium-free medium were not altered by neuraminidase, whereas following calcium depletion with EGTA, contractile responses to added calcium were greater in enzyme-treated strips than in control when activated with norepinephrine. The augmentation of norepinephrine-induced contractions following neuraminidase treatment was reversed by incubation of the arterial strips with N-acetylneuraminic acid (10-4M). Neuraminidase had no effect on contractile responses to potassium chloride, angiotensin II, and caffeine. Biochemical assay indicated that approximately 63% of the total sialic acid residues were removed from the arterial strips during incubation with the enzyme. It is concluded that a component for the control of the transmembrane calcium movement in response to norepinephrine is dependent on the presence of sialic acid residues.

ISSN:1018-1172    

DOI:10.1159/000158489

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

Alpha-thrombin was applied in cumulative concentrations of 0.001, 0.01, 0.1, 1.0, 10, and/or 100 U/ml to determine peak responses in isolated canine arterial rings. Alpha-thrombin failed to elicit contraction in the mesenteric artery, produced inconsistent effects in the renal artery, and produced biphasic effects (relaxation superseded by contraction) in the coronary and basilar arteries. In the basilar artery the relaxation induced by alpha-thrombin was blocked and the maximal contractions enhanced by reaming the vessel or by substituting heated thrombin for alpha-thrombin. The results support the hypotheses that alpha-thrombin acts on two distinct receptors in the basilar artery and that it is involved in the pathogenesis of cerebral vasospasm.

ISSN:1018-1172    

DOI:10.1159/000158490

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

The dependence of norepinephrine-(NE-) and high potassium (80 mMK) depolarization-induced contractions on extracellular versus intracellular calcium (Ca2+) pools was studied in strips of rabbit superior mesenteric artery and its branches, and in perfused mesenteric resistance vessels. 80 mM K contractions were abolished in the presence of 0 Ca2+ 2 mM EGTA in all arteries studied, whereas 10-5M NE-induced contractions and stimulated 45Ca efflux in 0 Ca2+ 2 mM EGTA decreased in a graded fashion from proximal to distal arteries. These data indicate a decreasing release of intracellular Ca2+ and an increasing dependence on extracellular Ca2+ for NE-induced contractions as one proceeds from proximal to distal arteries. This pattern was paralleled by increasing sensitivity of NE-induced contractions to inhibition by diltiazem (10-9 10-4M) from proximal to distal arteries, while inhibition of 80 mM K contractions was similar in all vessels. 45Ca influx induced by 10-5M NE in the resistance vessels, wherein the NE does not release intracellular Ca2+, is approximately 10,000-fold more sensitive to the action of diltiazem than that in the aorta. However, when the aorta is activated by 10-8 MNE, it becomes more sensitive to inhibition by diltiazem than when it is activated by 10-5 MNE. The former NE concentration does not release intracellular Ca2+ in the aorta, whereas the latter does. Thus, it appears that NE-induced 45Ca influx is most susceptible to inhibition by diltiazem when the NE has not also released intracellular Ca2+. We suggest that the release of intracellular Ca2+ by NE may make its stimulated Ca2+ influx less susceptible to inhibition by diltiazem.

ISSN:1018-1172    

DOI:10.1159/000158491

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

Atrial homografts from newborn hamsters, transplanted into cheek pouches of adult Syrian golden hamsters, were studied using intravital and electron microscopy. Half of the transplants survived up to 1 year, performing spontaneous pulsatile activity. The transplants could be influenced by β-receptor activating or blocking substances applied intravenously to the host animal. For morphological analysis homografts were taken 3, 6, and 12 months after transplantation. Irregular arrangement of the myofibers occurred, and the T system was seen to be replaced by plasmalemmal and sub-plasmalemmal vesiculations. There was some evidence for hypoxia in the grafts. Dedifferentiation of atrial cardiocytes, somehow resembling smooth muscle cells, is discussed. Despite these morphological changes the specific contractile function of the grafts was preserved

ISSN:1018-1172    

DOI:10.1159/000158492

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

A comparison was made between the properties of the norepinephrine- and caffeine-sensitive Ca2+ store in both intact and skinned smooth muscle of the rabbit mesenteric artery. After a first application of 10-5M norepinephrine, reapplication of norepinephrine did not induce a second contraction in Ca2+-free medium. However, following this sequence 25 mM caffeine still induced a large contraction. The rates of Ca2+ leakage and Ca2+ filling of the norepinephrine-sensitive store were much faster than those of the caffeine-sensitive one. The amplitude of the norepinephrine-induced contraction in Ca2+-free medium also depended on the amount of Ca2+ present in the caffeine-sensitive store. In the saponin-treated skinned muscle caffeine induced a Ca2+ release only after loading with Ca2+, whereas norepinephrine was unable to induce Ca2+ release in the skinned preparation even after loading with Ca2+. The release of Ca2+ from the caffeine-sensitive store could be activated by Ca2+ itself when the skinned muscle was loaded with Ca2+ above 10-6M. These results suggest that the norepinephrine-sensitive Ca2+ store is distinct from a large fraction of the caffeine-sensitive one, and that the norepinephrine-sensitive store is close to the cell membrane. In vascular smooth muscle, under physiological conditions, Ca2+ released from the norepinephrine-sensitive store by norepinephrine may induce Ca2+ release from the caffeine-sensitive Ca2+ store which may be comprised of the sarcoplasmic reticulum.

ISSN:1018-1172    

DOI:10.1159/000158493

出版商:S. Karger AG    

年代:1984

数据来源: Karger

ISSN:1018-1172    

DOI:10.1159/000158494

出版商:S. Karger AG    

年代:1984

数据来源: Karger