摘要:

To determine the effects of copper deficiency on the vascular wall, female rats of the Wistar King A strain were fed a copper-deficient diet (0.58 ppm), and all delivered pups were kept on the same diet. The copper level of sera of all copper-deficient animals was significantly lower (10.6 fig/ dl) than that of the controls (141.4 jug/dl). The body weight of copper-deficient rats was about 40% of the controls at 12 weeks of age. Copper deficiency produced a reduction in norepinephrine (NE) content in aortic tissue (40%), but not in portal veins. There was an increase in sensitivity of aortic tissue to NE. Depolarization of the muscle membrane of pulmonary arteries in response to NE decreased at high NE concentrations. The tensile strength of the aortas decreased, and there was an increase in the active contraction and a shift of the maximum amplitude to the right in the aortic length-tension curve. A reduction in aortic elastin and collagen contents was observed on electron micrographs. There also was a prolongation of relaxation times after contraction produced by NE, in a manner similar to that observed after 6-hydroxydopamine (6-OHDA) treatment. Also, in aortas, copper deficiency produced a resistance to NE depletion by chemical sympathectomy (6-OHDA), whereas in portal veins, there was no reduction in NE content after treatment with 6-OHDA (50 mg/kg, ip). These results suggest that rupture of copper-deficient aortas is due mainly to a decrease in elasticity of the aortic wall, probably as a result of reduction in elastin and collagen. The changes observed in the membrane and contractile properties of elastic arterial smooth muscle cells under conditions of copper deficiency probably are compensatory mechanisms which serve to protect the vascular wall.Circ Res 46: 681-689, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We studied the developmental sequence of transmitter synthesis and neurotransmission by parasympathetic neurons in rat heart. Measurements of atrial and ventricular choline acetyltrans- ferase activity were used as indicators of acetylcholine synthesis, and negative chronotropic effects of neuronal stimulation were used to demonstrate neuroeffector transmission. Activity of the mitochon- dria! enzyme, carnitine acetyltransferase, was measured separately to avoid spuriously high apparent choline acetyltransferase activity. Activity of the acetylcholine synthetic enzyme, choline acetyltrans- ferase, first was detected in rat hearts on embryonic day 19, and the levels of the enzyme activity increased during the first and third weeks after birth, with levels in the atria always appearing higher than in the ventricles. In contrast, carnitine acetyltransferase activity was higher in the ventricles than in the atria, and the activity levels increased continuously from embryonic day 18 to postnatal day 21, the last day measured. Neuroeffector transmission first appeared in the rat heart on embryonic day 21, the day of birth, and was blocked by atropine. Newborn and adult hearts had similar acetylcholine sensitivity (ED50of 100 DM). Embryonic rat hearts showed slightly higher acetylcholine sensitivity. The avian class was used for comparison, and choline acetyltransferase activity first appeared in embryonic chicks on day 11. The pattern of neurotransmitter synthesis and function was identical in the avian and mammalian species, although the mammal is less mature at birth. Our studies have established the time course for development of the synthetic enzyme for acetylcholine and subsequent neurotransmis- sion in the rat heart. Circ Res 46: 690-695, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We studied: (1) the effects of an abrupt, moderate increase in arterial pressure on total and regional cerebral blood flow (CBF) and (2) whether sympathetic stimulation attenuates the transient hyperemia that occurs during a sudden increase in pressure within the physiological range of pressure. Abrupt increases in arterial pressure were produced by occlusion of the descending aorta. Cerebral blood flow was determined in dogs and cats using radioactive microspheres. In dogs, blood flow to all regions of the brain increased by 35-55% at the onset of hypertension and returned to normal by 60 seconds. Electrical stimulation of sympathetic nerves did not attenuate the transient rise in CBF in dogs. In cats, blood flow increased by 40-60% in cerebrum (cortical grey matter), cerebellum, and brainstem at the onset of hypertension and was still moderately elevated after 2.5 minutes. Electrical stimulation of sympathetic nerves in cats attenuated the initial rise in CBF. At the onset of hypertension in cats, the increase in blood flow to the unstimulated cerebrum was 42% greater than on the stimulated side. Blood flow to cortical grey matter was 71% and 65% greater on the unstimulated side than on the stimulated side at the onset and after 20 seconds of hypertension, respectively. We conclude that an abrupt, moderate increase in arterial pressure within the physiological range produces a transient increase in CBF and, furthermore, that stimulation of sympathetic nerves attenuates the increase in flow in cats. Circ Res 46: 696-702, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We studied the influence of inotropic factors on the shape of the relation between tension and sarcomere length.Tension measurements were performed on thin trabeculae dissected from the right ventricle of the rat heart. Sarcomere length was measured by laser diffraction techniques and controlled by a servomotor system. The relations between tension and sarcomere length were derived from contractions at various extracellular calcium concentrations [Ca2+]o. The time course of tension development was dependent on both sarcomere length and [Ca2+]o. At all [Ca2+]o, the tension attained during contraction was zero at sarcomere lengths of 1.55-1.60 pm and maximal at a sarcomere length of 2.35 /im. Neither a summit nor a descending limb was found in the sarcomere length-tension relation. At [Ca2+]o= 0.5 mM, tension increased linearly with sarcomere length, whereas at [Ca2+]o= 2.5 mM, it approached maximal tension exponentially with sarcomere length. The relations between tension and sarcomere length derived from isometric contractions of the muscle and of sarcomeres were identical, and this suggests that shortening of sarcomeres does not contribute significantly to the effect of [Ca2+]o. The relations between tension and sarcomere length obtained at [Ca2+]o= 0.5 mM from contractions 30 seconds after a potentiating burst of stimuli (4 seconds at 4 Hz) were identical to the relation between tension and sarcomere length at [Ca2+]o= 2.5mm. Our results are consistent with the hypothesis that cardiac muscle length affects contractile performance by its influence on excitation contraction coupling.CircRes 46: 703-714, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We explored the hypothesis that postaglandin-induced vasodilation is caused by activa- tion of the electrogenic sodium-potassium pump which results in membrane hyperpolarization and relaxation of vascular smooth muscle. Helical strips of rat tail artery relax in response to potassium after norepinephrine-induced contractions in physiological salt solution containing a low-potassium concentration. The amplitude of this potassium-induced relaxation is used as an index of sodium- potassium ATPase activity. It was observed that PGAi, PGE2, and PGF2o(10∼6g/ml) significantly enhanced the magnitude of potassium-induced relaxation. PGA2and PGEi (10∼6g/ml) had no significant effect. PGE2caused relaxation of contractions induced by either 25 mM KC1 or norepinephrine (10∼9g/ ml), and these relaxations were inhibited by 10∼4M ouabain. Indomethacin (5.3 × 10"" g/ml) and meclofenamate (10∼6g/ml) reduced the magnitude of potassium-induced relaxation by more than 30% of control. PGF2a(10∼sg/ml) reversed the inhibition of potassium relaxation by meclofenamate. These observations suggest that prostaglandins induce vascular smooth muscle relaxation by stimulation of the sodium pump and that endogenous prostaglandins normally potentiate potassium relaxation. Circ Res 46: 714-720, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

The synthesis of an angiotensin II (A II) antagonist, 8arcosyl1-cy8teinyl(S-methyl)8-angio- tensin II [Sar1-Cys(Me)8-A II], showing partial organ selectivity and properties of a noncompetitive antagonist, is described. The compound was found to be an extremely potent antagonist on vascular smooth muscle both in vitro (pA2for rabbit aorta s 9.2) and in vivo on rat blood pressure (dose ratio of 103 for ED25mm Hg during 1 fig/kg per min infusion of antagonist). It was without effect on norepinephrine responses in both assay systems. In contrast, it was a considerably weaker antagonist on visceral smooth muscle (pA2for guinea pig ileum = 8.5; pA2for rat uterus = 7.9). Interestingly, in the vascular smooth muscle preparations, the compound also exhibited elements of a noncompetitive antagonist in that both the slope and maximum of the A II dose-response curves were reduced markedly. Qualitatively similar results were obtained with sarcosyl1-alanyl8-angiotensin II (Saralasin) on rabbit aorta. Moderate depression of maximum response was seen in guinea pig ileum but not in rat uterus. These effects on vascular smooth muscle were reversible in vitro but only partially reversible in vivo. Circ Res 46: 720-725, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

We characterized the influence of high pressure and low pressure intra vascular receptors on renal nerve activity in the pentobarbital sodium-anesthetized nonhuman primate Macaca fascicu- laris. Epinephrine-induced increases in arterial pressure were used to stimulate high pressure recep- tors, and intravascular volume expansion was used to stimulate both high and low pressure receptors. In addition, the intravascular mechanoreceptors were stimulated directly by intravenous veratrine administration. All interventions produced large decreases in renal nerve activity in the intact state. Denervation of the carotid sinus or bilateral cervical vagal section diminished, whereas sino-aortic denervation with vagotomy completely abolished all responses of renal nerve activity to these inter- ventions. We conclude that the nonhuman primate possesses very sensitive renal nerve sympathetic reflexes that are modulated by intravascular mechanoreceptors whose afferents traverse the carotid sinus nerves and the vago-aortic trunks. The carotid sinus nerves and the vago-aortic trunks appear to be equally effective in inhibiting renal nerve activity in response to increases in arterial pressure. In addition, there are no afferent pathways mediating intravascular mechanoreceptor modulation of renal nerve activity outside the carotid sinus nerves and the vago-aortic trunks. Circ Res 46: 726-730, 1980

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1980

数据来源: OVID