bluuebunny/crossref_metadata_2025 huggingface dataset:
Ischemia of the dog heart induces the appearance of a cardiac mRNA coding for a protein with migration characteristics similar to heat-shock/stress protein 71.
Authors: Dillmann W H , Mehta H B , Barrieux A , Guth B D , Neeley W E , Ross J
Published: June 2012

Recent evidence indicates that different forms of stress, including hypoxia, can induce specific proteins called heat-shock or stress proteins in various types of mammalian cells. These studies examined whether myocardial ischemia can result in increased levels of proteins with molecular weight and isoelectric point characteristics similar to those described for heat-shock or stress proteins. The left anterior descending coronary artery of the dog heart was completely occluded; normal and ischemic myocardial samples were obtained 6 hours after occlusion; and total cardiac proteins and RNA were prepared. Ribonucleic acid was translated in vitro in a modified rabbit reticulocyte lysate system, and [35S]-methionine-labelled translational products as well as unlabelled cardiac proteins were separated by two-dimensional gel electrophoresis. Total proteins were visualized by silver staining and in vitro translation products quantified by fluorometry. A translatable mRNA coding for a 71,000 dalton peptide with an isoelectric point of 5.8 was markedly increased in the ischemic myocardium after 6 hours of ischemia. A protein with similar migration characteristics was detected in ischemic myocardium but not in normal myocardium. These results indicate that an mRNA coding for a translational product with similar migration characteristics of heat-shock protein 71 is induced by ischemia in the dog heart.
Myosin isozymes in rabbit and human smooth muscles.
Authors: Lema M J , Pagani E D , Shemin R , Julian F J
Published: June 2012

Although multiple forms of myosin in cardiac and skeletal muscles have been identified, it has not been firmly established that myosin isozymes are present in adult smooth muscle. Myosin, extracted from human thoracic aorta and lower saphenous vein and rabbit aorta and uterus, was analyzed by pyrophosphate gel electrophoresis to determine if myosin isozymes are present in these tissues. In all smooth muscle tissues studied, two myosin isozymes were detected and labelled as smooth muscle 1 and smooth muscle 2, smooth muscle 2 being the faster migrating isozyme. Bovine cultured smooth muscle cells from the media of thoracic aorta also contained two forms of myosin. However, cultured fibroblasts contained only one form of myosin. Extracting myosin from either relaxed or contracting rabbit aortic smooth muscle did not influence the mobilities of smooth muscle 1 and smooth muscle 2 on pyrophosphate gels, suggesting that the degree of light chain phosphorylation did not significantly alter the electrophoretic mobility under our conditions. Smooth muscle 1 and smooth muscle 2 myosins each contain heavy chains (200,000 daltons) and light chains (20,000 and 17,000 daltons) in addition to filamin (235,000 daltons), which is closely associated with the native protein. Myosin peptide maps of rabbit aorta and uterus revealed areas of substantially different banding patterns between smooth muscle 1 and smooth muscle 2 from the same tissue. Similar peptide maps of smooth muscle 1 bands were produced from the different tissues, but the smooth muscle 2 maps were dissimilar.(ABSTRACT TRUNCATED AT 250 WORDS)
Renal and systemic hemodynamic effects of synthetic atrial natriuretic peptide in the anesthetized rat.
Authors: Dunn B R , Ichikawa I , Pfeffer J M , Troy J L , Brenner B M
Published: June 2012

To characterize the hemodynamic events responsible for alterations in renal function during administration of atrial natriuretic peptide, we studied the systemic, renal, and glomerular circulatory effects of intravenous rANP[126-149], administered as a 4 micrograms/kg prime and 0.5 microgram/kg per minute continuous infusion in anesthetized, euvolemic rats. With this protocol, a small decline in mean systemic arterial blood pressure occurred in the context of markedly enhanced urinary sodium excretion, hemoconcentration, and reduced left ventricular end-diastolic pressure and +dP/dt. However, despite a significant decrement in renal vascular resistance, total peripheral resistance remained constant, thereby denoting a preferential renal vasodilatory effect of this peptide in vivo. Whole kidney and single nephron GFR increased by approximately 20%, while effective renal and glomerular plasma flow rates remained stable, resulting in a substantial rise in filtration fraction. Of all the parameters potentially capable of augmenting single nephron GFR, only glomerular capillary hydraulic pressure increased significantly and therefore accounted entirely for the hyperfiltration observed during ANP infusion. This rise in glomerular capillary pressure, in turn, resulted from afferent arteriolar vasodilatation and concurrent efferent arteriolar vasoconstriction, findings that proved independent of both endogenous angiotensin II activity and ANP-induced reductions in renal perfusion pressure. These renal hemodynamic effects are unique when compared with actions of previously studied renal vasodilatory agents.
Ascending aortic impedance patterns in the kangaroo: their explanation and relation to pressure waveforms.
Authors: Nichols W W , Avolio A P , O'Rourke M F
Published: June 2012

This study seeks to explain mechanisms responsible for the peculiar ascending aortic pressure waveform and impedance spectral pattern in kangaroos. Pulsatile pressure and blood flow velocity were measured and input impedance calculated in the ascending aorta, descending thoracic aorta, and brachiocephalic artery of 15 rock kangaroos. Pressure and velocity waveforms and impedance spectral patterns were interpreted with the aid of an asymmetric uniform T-tube model of the systemic arterial tree. The ascending aortic pressure waveform displayed a very large secondary wave that began in late systole or early diastole and continued throughout most of diastole. The peak of this secondary wave (which almost always occurred in diastole) was often greater than peak systolic pressure and results from apparently intense wave reflections from peripheral vascular beds. This contention is supported by the configuration of the impedance spectral pattern that is explained on the basis of a single (or dominant) functionally discrete reflecting site in the lower part of the body. These findings are explicable on the basis of body size and shape and the extreme eccentric location of the heart within the body. Wave reflections from the diminutive upper body are so small that they are totally dominated by intensive wave reflections from the large muscular lower body. These conclusions are supported by results obtained from the asymmetric T-tube model.
Porcine heart valves produce a protein that induces cell-mediated connective tissue degradation: I. Biological properties.
Authors: Henney A M , Dingle J T , Decker R S
Published: June 2012

Cultured porcine heart valves secrete a factor that induces cells to degrade their extracellular matrix. This activity was routinely monitored by measuring the release of glycosaminoglycans from proteoglycan in cultured bovine nasal cartilage. It was observed that factor-mediated matrix degradation was dose dependent and required live target cells, while factor production by valves was inhibited by cycloheximide and declined with reduced cell viability. The effect of various steroidal and nonsteroidal anti-inflammatory drugs on the production and activity of the factor is discussed with reference to similar cytokines. It is concluded that there is a close similarity between the cardiac catabolic factor described here and catabolin, a protein isolated from porcine synovia and leukocytes, as shown by the neutralization of biological activity with antisera raised to porcine catabolin (interleukin-1).
Centrally infused atrial natriuretic polypeptide attenuates exaggerated salt appetite in spontaneously hypertensive rats.
Authors: Itoh H , Nakao K , Katsuura G , Morii N , Shiono S , Sakamoto M , Sugawara A , Yamada T , Saito Y , Matsushita A
Published: June 2012

We have previously shown that atrial natriuretic polypeptide is present in the brain with the highest concentration in the hypothalamus and septum and that intracerebroventricular injection of atrial natriuretic polypeptide inhibits water drinking induced by centrally injected angiotensin II or 24-hour water deprivation in rats. To study further the role of brain atrial natriuretic polypeptide in the control of water and electrolyte balance, the effect of chronic intracerebroventricular infusion of atrial natriuretic polypeptide on salt appetite in spontaneously hypertensive rats and normotensive Wistar-Kyoto rats was examined with a free-choice, two-bottle preference test. The intracerebroventricular infusion of 100 ng/hour and 500 ng/hour of alpha-human atrial natriuretic polypeptide preferentially suppressed the intake of 0.30 M NaCl solution and attenuated the elevated preference for the hypertonic saline in spontaneously hypertensive rats while centrally infused alpha-human atrial natriuretic polypeptide had no significant effects on drinking behavior in Wistar-Kyoto rats. Blood pressure did not change significantly throughout the experiment in either rat strain. It is concluded that the exaggerated salt appetite in spontaneously hypertensive rats is blunted by centrally administered atrial natriuretic polypeptide. Such an effect of atrial natriuretic polypeptide along with its antidipsogenic effect suggests that brain atrial natriuretic polypeptide plays a role in water and electrolyte homeostasis and in blood pressure control.
Voltage-tension relations in single frog atrial cardiac cells.
Authors: Tarr M , Trank J W , Goertz K K
Published: June 2012

Voltage-clamp experiments were performed on isolated single frog (Rana catesbeiana or Rana pipiens) atrial cells to determine the voltage-contraction relations of the single cardiac cell. The contractile responses of the single cell associated with long duration (3 second) depolarizing steps consisted of a rise to peak (phasic) followed by a decay to a sustained contraction (tonic). These phasic-tonic type contractile responses could be obtained under conditions where membrane potential was well controlled along the entire length of the cell. Thus, the data obtained on the single cell indicate that the phasic-tonic contractile response is the characteristic contractile response of frog atrial tissue. The voltage dependence of the extent of relaxation to the tonic component following the peak of the contraction was affected dramatically by the intracellular sodium concentration. This result indicates that both the relaxation following peak contraction as well as the tonic contraction are related to calcium control via the sodium-calcium exchanger. The data also indicate that calcium entry via the inward calcium current is required for the contractile response to have a phasic component. These data indicate that calcium entry via the inward calcium current followed by the sodium-calcium exchanger first reducing and then maintaining the intracellular calcium level produces the characteristic phasic-tonic contractile response.
Myosin isoenzymes of vascular smooth and cardiac muscle in the spontaneously hypertensive and normotensive male and female rat: a comparative study.
Authors: Morano I , Gagelmann M , Arner A , Ganten U , Rüegg J C
Published: June 2012

Cardiac hypertrophy in hypertensive subjects, its biochemical markers, and functional consequences are of great clinical importance but still unclear. We observed a shift of the ventricular isomyosin of adult spontaneously hypertensive (H) rats of both sexes to the V3 form and a decreased myofibrillar ATPase activity in the H animals when compared to normotensive (N) controls. Compared to the male H rats, age-matched female H animals revealed a lower blood pressure, the same or even an elevated magnitude of cardiac hypertrophy, a different ventricular isomyosin pattern, and a higher myofibrillar ATPase activity. In female H rats the V1 and V3 isomyosins were equally distributed (35% V1 and 35% V3), but in male H animals the V3 was predominant (24% V1 and 45% V3). The Ca2+-regulated Mg2+-dependent myofibrillar ATPase of the rat ventricle correlated positively with the amount of V1 when measured at pCa 5 (maximum activation). At submaximum Ca2+-concentrations (pCa 6.9-5.9) the myofibrillar ATPase activities were not changed with the proportion of V1. The cooperativity of the Ca2+-activation of the myofibrillar ATPase increased with increasing amount of V1 (Hill-coefficient 3.7 with 100% V1) and decreased with increased proportion of V3 (Hill-coefficient 1.3 at 45% V3). Two myosin isoenzymes were detected in the aorta of rats, a slow migrating (S2) and a fast migrating (S1) form having both a higher mobility than the ventricular isomyosins. Only one band was observed in the portal vein, which revealed the same mobility as S2. Hypertension did not change the appearance of these vascular smooth muscle isomyosins neither in male nor in female animals.
Dopamine attenuates the contractile response to angiotensin II in isolated rat glomeruli and cultured mesangial cells.
Authors: Barnett R , Singhal P C , Scharschmidt L A , Schlondorff D
Published: June 2012

Recent evidence suggests that dopamine may alter kidney function by actions not only in the renal vasculature but also at the glomerular-mesangial level. We studied this phenomenon by examining the ability of dopamine to antagonize the contractile properties of angiotensin II in isolated rat glomeruli and cultured mesangial cells. In isolated rat glomeruli angiotensin II caused a decrease in the planar surface area, indicating glomerular contraction, an effect that was abolished by coincubation with dopamine. Angiotensin II also mediated shape changes in cultured mesangial cells, which resulted in a decline in their planar areas. Simultaneous addition of dopamine prevented these decreases in cell size. In mesangial cells grown on a flexible silicone rubber support, angiotensin II addition enhanced wrinkling of the mobile surface. This indicated that the angiotensin-II-induced decrease in cell size observed in cells grown on conventional substrata represented contraction. Conversely, dopamine caused a rapid reduction in wrinkling of the surfaces from control cells as well as those previously treated with angiotensin II, actions consistent with cell relaxation. The prostaglandin inhibitor indomethacin did not alter the ability of dopamine to attenuate angiotensin-II-associated reductions in mesangial cell surface area. Direct determination of mesangial cell prostaglandin-E2 production showed that dopamine did not change either basal synthesis or angiotensin-II-stimulated synthesis of prostaglandin. The results demonstrate that dopamine antagonizes the constrictor effect of angiotensin II at the glomerular-mesangial level. This action of dopamine is prostaglandin independent. These findings support a role for dopamine in the regulation of glomerular filtration and may provide a rationale for its use during states of renal vasoconstriction.
Coordination of mural elements and myofilaments during arteriolar constriction.
Authors: Sleek G E , Duling B R
Published: June 2012

Arterioles undergo major morphological changes during vasoconstriction. We used transmission electron microscopy to study wall morphology in both dilated and constricted microvessels to understand the cellular basis of these changes. The relation between the orientation and density of myofilaments and the distribution of dense bodies was analyzed with respect to the level of microvessel tone. The data show a strong correlation between the degree of arteriolar constriction and both the orientation and density of myofilaments. In dilated arterioles, myofilament orientation was predominantly circumferential across the entire smooth muscle cell, averaging 84 +/- 2 degrees (SEM) relative to a radial reference line. In vessels constricted to 50% of their maximal diameter, myofilament orientation was dependent upon the location within the cell, being largely circumferential at the adventitial border (77 +/- 4 degrees) and shifting to a radial arrangement at the intimal border (36 +/- 5 degrees). The reorganization of myofilaments during constriction was associated with a decrease in myofilament density at the intimal-medial border of the smooth muscle cells. The decrease in myofilament density resulted from a selective withdrawal of myofilaments from periluminal areas where "ridges" had formed. Our observations suggest that an ordered distribution of membrane-associated dense bodies along the periluminal aspect of the smooth muscle cells is responsible for both the myofilament reorganization and ridge formation during vasoconstriction. Results of the present study are incorporated into a hypothetical model of arteriolar ultrastructure compatible with the mural reorganization observed during vasoconstriction.
Three forms of xanthine: acceptor oxidoreductase in rat heart.
Authors: Kaminski Z W , Pohorecki R , Ballast C L , Domino E F
Published: June 2012

The enzyme xanthine: acceptor oxidoreductase found in rat heart equilibrates between three forms differing in electron acceptor specificity. Form D transfers electrons exclusively to NAD+ and accounts for 85% of total oxidoreductase activity. Form O transfers electrons to molecular oxygen and accounts for 8%. The D/O form prefers NAD+, but without NAD+ transfers electrons to oxygen. Interconversion from D to O and O to D forms is catalyzed by sulfhydryl group-modifying reagents: Cd2+, Cu2+, disulfiram, and heating with dithiothreitol. This suggests that sulfhydryl groups participate in the first stage of enzyme conversion. The NADH/NAD+ concentration ratio may regulate the dehydrogenase activity of xanthine:acceptor oxidoreductase (NAD+-dependent activity of D and D/O forms). Accumulating NADH inhibits hypoxanthine hydroxylation. The amount of form O increases during cardiac ischemia, facilitating superoxide radical-ion generation. Also, NADH/NAD+ does not regulate form O, promoting adenylate nucleotide pool depletion, especially in the heart which has low de novo purine nucleotide synthesis.
Effects of High Carbohydrate or Protein Diets on Blood Pressure of Normotensive and Hypertensive Dogs
Authors: WILHELMJ C. M. , MEYERS V. W. , MCCARTHY H. H.
Published: June 2012

The effects of diets high in carbohydrate or protein were studied on four dogs when normotensive and later when hypertensive. The results suggest that under certain conditions a cardiovascular homeostatic relationship may exist between diet, VEM-VDM and the sympathicoadrenal system.
Significance of Homologous Donor Blood to the Toxic Reaction in Dogs Undergoing Extracorporeal Hemodialysis
Authors: MAHER FRANK T. , WATKINS LEE C. , BROADBENT JAMES C. , BOLLMAN JESSE L.
Published: June 2012

Application of hemodialysis to dogs has been complicated by an acute reaction consisting of hypotension, bradycardia and respiratory depression followed by instability and a mortality rate of about 30 per cent. This reaction appears to be a response to homologous blood used to fill the dialyzers. Sensitization occurs in survivors, and accentuated reactions with marked hemolysis are noted on subsequent challenge. Cross matching the donor and recipient bloods has not permitted an adequate determination of compatibility under the conditions of hemodialysis. Satisfactory hemodialysis may be accomplished in dogs by using autogenous blood or blood substitutes to fill the dialyzers.
Inotropic Action of Hexamethonium
Authors: LEE WOO CHOO , SHIDEMAN F. E.
Published: June 2012

The positive inotropic action of hexamethonium in hypodynamic and freshly prepared papillary muscles of the eat and the hypodynamic heart-lung preparation of the dog has been demonstrated. Within certain limits, there exists a proportionality between the concentration of hexamethonium and the magnitude of the inotropic response. In both preparations results have been obtained which indicate that a state of partial refractoriness to the positive inotropic action of hexamethonium may be produced.
Hemodynamic Effects of Hypervolemia with and without Anemia
Authors: FOWLER NOBLE O. , BLOOM WALTER L. , WARD JOHN A.
Published: June 2012

Hypervolemia was produced in dogs by infusion of matched whole blood or of red cells suspended in dextran. In the dogs which had received matched whole blood, bleeding with simultaneous volume replacement with dextran produced acute hypervolemic anemia. This was associated with increased cardiac output, whereas no increase of cardiac output was seen in the same animals with a comparable amount of hypervolemia without anemia. The results suggest that anemia rather than hypervolemia was the important factor in causing an increase of cardiac output in these experiments.
Effects of Dietary Protein and Carbohydrate Level on Cholesterolemia and Atherogenesis in Cockerels on a High-Fat, High-Cholesterol Mash
Authors: STAME JEREMIAH , PICK RUTH , KATZ LOUIS N.
Published: June 2012

Decreased protein intake in the presence of a high-fat, high-cholesterol diet was found to produce marked aggravation of hypercholesterolemia and atherogenesis in cockerels. Sucrose was substituted for protein in this low protein diet. The effect of this diet is not due to sucrose since restoring the protein to a high level, while keeping the sucrose in the ration constant, had no such effect.
Critical Closing Pressure of Vessels Supplying the Capillary Loops of the Nailfold
Authors: GASKELL PETER , KRISMAN ASHLEY M.
Published: June 2012

The critical closing pressure (CCP) of vessels supplying the capillary loops of the nailfold was estimated as the digital systolic pressure minus the air pressure required on the finger to just prevent flow of blood in the capillary loops. The digital blood pressure was estimated by an auscultatory method and the presence or absence of flow in the loops was detected by direct microscopic examination. It was shown that the method is valid and does not simply measure a local intravascular pressure or some rheological factor. The CCP was lower after body heating than after body cooling and was markedly reduced by anesthetization of the digital nerves. In hypertensive patients the CCP was higher than in normal subjects.
Dynamics of the Normal Aorta
Authors: SPENCER MERRILL P. , JOHNSTON FRANK R. , DENISON ADAM B.
Published: June 2012

The contour of the flow pulse along the normal unopened aorta of human subjects and dogs was established by recording with the surgical probe type, square-wave magnetic flowmeter. The contour at a given vessel segment was found to be the result of the transforming action of the arterial system on the ventricular ejection pulse. The characteristics of the aorta and its branches were found to be analagous to a low-pass electric tuned circuit, which resonates at 3 to 6 c.p.s. The resonant frequency, apparent from midsystole throughout diastole, was independent of heart rate, damped to extinction during diastole and renewed with each systole. New terms for elastic hydraulics are proposed and defined.
Effects of Temperature, Na and K Concentration and Quinidine on Transmembrane Flux of K
42
and Incidence of Atrial Fibrillation
Authors: HOLLAND W. C. , KLEIN R. L.
Published: June 2012

Experimental data is presented and discussed on the effects of temperature, K and Na concentration, and quinidine on transmembrane ion fluxes and the incidence of fibrillation in isolated rabbit atria.
Statistical Properties of Pulsatile Pressure and Flow in the Femoral Artery of the Dog
Authors: RANDALL JAMES E.
Published: June 2012

Femoral pulsatile pressure and flow in anesthetized dogs were measured as time series. The computed cross products of pressure and flow were also expressed as time series. The statistical variance (ó
2
) of each of these was analyzed into a frequency spectrum. The spectral magnitudes at each frequency were used to compute the pressure-flow coherence, impedance magnitude and phase angle as a function of frequency. The high coherency between pressure and flow at most frequencies indicated that a linear deterministic model may suffice to express the opposition to flow pulsations. The impedance variation with frequency indicated that the model may be frequency dependent. Computed autocorrelation and cross correlation functions measured the statistical nature of the observed time series.
Inhibition of Levarterenol by Intra-Arterial Phenoxybenzamine in Man
Authors: GINSBURG JEAN , DUFF ROBERT S.
Published: June 2012

The infusion of 1.2 mg. phenoxybenzamine into the brachial artery of healthy adults was followed by a marked reduction in constrictor responses in the corresponding hands to infused levarterenol and to sympathetic stimuli.
Diverse Distribution of Red Cells and Albumin in the Dog Kidney
Authors: LILIENFIELD LAWRENCE S. , ROSE JOHN C. , LASSEN NIELS A.
Published: June 2012

Cr
31
labeled red cells and I
131
human serum albumin were injected intravenously into 8 mongrel dogs. After 1 hour kidneys were removed and frozen rapidly with dry ice. Sections of outer cortex, inner cortex, outer medulla, inner medulla, outer papilla and inner papilla were removed and analyzed for Cr
51
and I
131
radioactivity. Tissue radioactivity was compared with that of arterial blood and concentrations of labeled red cells and albumin were calculated. No significant difference was found in relative red cell and albumin content between outer and inner cortex. The magnitude of the I
131
albumin content in the cortex is interpreted to indicate a sizeable
extnivascular
exchangeable albumin pool. The renal papillae were extraordinarily deficient in red cells, but contained per 100 Gm., albumin equivalent to that of 39 ml. of plasma.
Do Ganglion-Blocking Agents and Reserpine Affect Central Vasomotor Activity?
Authors: MCCUBBIN JAMES W. , PAGE IRVINE H.
Published: June 2012

In a majority of experiments on both dogs and cats, hypotensive doses of tetraethylam-monium chloride or mecamylamine caused no change or moderate increase in efferent electric activity in the largely preganglionic thoracic portion of the splanchnic nerve, and caused complete and prolonged elimination of efferent activity in the postganglionic inferior cardiac and renal nerves. Both drugs failed to suppress changes in splanchnic nerve activity that were elicited refiexly. These results imply strongly that both ganglion-blocking drugs, in dosage used intravenously to induce hypotension, act mainly through their peripheral effects rather than through one on central vasomotor synapses. In both dogs and cats, reserpine caused slowly progressive and marked diminution in efferent splanchnic nerve activity, which supports the hypothesis that the central action of this agent contributes to its hypotensive effect.
Microtubules and desmin filaments during onset of heart hypertrophy in rat: a double immunoelectron microscope study.
Authors: Watkins S C , Samuel J L , Marotte F , Bertier-Savalle B , Rappaport L
Published: June 2012

The distribution of tubulin and desmin, the constituent proteins of microtubules and intermediate filaments, respectively, were studied in normal and hypertrophied rat myocardium by high-resolution immunofluorescence and immunoelectron microscopy. Cardiac hypertrophy was induced in 25-day-old rats by aortic stenosis. In the normal heart, double immunolabelling of ultrathin frozen sections of papillary muscle using gold-labelled probes for tubulin and desmin showed that microtubules ran primarily in a longitudinal direction through the intermyofibrillar spaces, perpendicularly to the desmin filaments. Microtubules were present near nuclei, mitochondria, and plasma membranes, while desmin filaments formed transverse connections between adjacent Z disks. No tubulin was observed near the intercalated disks, which were rich in desmin filaments. In hypertrophied hearts, myocytes exhibited the typical morphological features of developing hypertrophy. While there was little difference in the distribution of the microtubules around mitochondria and at the plasma membrane, considerable increases were seen near the nuclei and along the myofibrils. Desmin labelling was distributed transversely as in the controls; however, sometimes it was longitudinally oriented either in the intermyofibrillar space linking 2 Z disks out of register or along digitations of the intercalated disks connecting neighboring desmosomes. The unique rearrangement of desmin and tubulin filaments in hypertrophied cardiac myocytes emphasizes their distinct role in myocyte organization. We suggest that, during the development of cardiac hypertrophy, desmin filaments are mainly involved in maintaining the myofibrils in register, whereas the degree of assembly of microtubules is correlated with the rate of protein synthesis and with myofibrillogenesis.
Centripetal spread of arterial collateral endothelial cell hyperplasia after renal artery stenosis in the rat.
Authors: Hollenberg N K , Odori T
Published: June 2012

The factors responsible for collateral arterial growth after major artery occlusion remain obscure, despite their importance for tissue survival. An increase in endothelial cell labelling with tritiated thymidine, as an index of collateral arterial growth, occurs early after renal artery occlusion. Our working premise was that an increase in endothelial cell labelling would occur simultaneously throughout the length of the collateral arteries if biophysical factors related to blood flow were the responsible mechanism, because blood flow must be increased simultaneously throughout the length of the small, preformed collateral arterial vessels. On the other hand, if the information spread from the ischemic zone, one would anticipate centripetal spread of the endothelial cell hyperplasia in a retrograde direction from the ischemic zone. With the periureteric collateral arterial supply as the model, we performed serial studies of tritiated thymidine labelling following renal artery stenosis in the rat. As anticipated, endothelial cell labelling rose sharply within 24 to 48 hours, first evident in the area immediately adjacent to the renal hilum. Thereafter, a progressive, time-related centripetal gradient in endothelial cell tritiated thymidine labelling occurred (p less than 0.01). These findings indicate that the factors responsible for endothelial cell hyperplasia are less related to blood flow in the lumen than to downstream, ischemic events. Although the mechanism responsible for the centripetal spread remains speculative, the communication system is likely to involve cell-to-cell contact in the vessel wall.
Maximal rates of activation in electrically stimulated swine carotid media.
Authors: Singer H A , Murphy R A
Published: June 2012

The kinetics of crossbridge phosphorylation and cellular activation rates in arterial smooth muscle are unknown, and the response rates are usually limited by agonist diffusion rates. In this study, electrical field stimulation (10-20 V AC, 60 Hz) was used to activate strips of swine carotid artery smooth muscle. Pretreatment with 0.5 microM phenoxybenzamine (PBZ) for 30 minutes significantly inhibited field stimulated stress due to norepinephrine released from adrenergic nerves. Addition of 1-10 mM tetraethylammonium ion (TEA) to PBZ-pretreated tissues allowed direct stimulation of muscle cells and significantly potentiated the response to field stimulation. Activation in field stimulated tissues pretreated with PBZ and TEA was strongly inhibited by the Ca2+-channel antagonist verapamil (0.5 microM for 15 minutes). Activation was rapid with myosin light chain (MLC)-phosphorylation values rising to greater than 50% of total MLC, with a half-time of approximately 1 second. Stress and stiffness development was biphasic and lagged with an estimated half-time for the first phase of 3 seconds. Stress and stiffness continued to slowly rise after 5 seconds of stimulation, while MLC phosphorylation declined significantly between 5 and 10 seconds to a nearly constant value of 35-40% for up to 60 seconds. Unloaded shortening velocity was maximal (0.067 Lo/sec) at the earliest time point examined (0.5 second), prior to significant stress development and at submaximal phosphorylation. Significant decreases in unloaded shortening velocity were observed after 10 seconds. These results show that the kinetics of phosphorylation and dephosphorylation and the rates of activation are very rapid in this arterial smooth muscle.
Force, velocity, and power changes during normal and potentiated contractions of cat papillary muscle.
Authors: Chiu Y C , Ballou E W , Ford L E
Published: June 2012

The instantaneous force-velocity relations of cat papillary muscles were studied at different times in the twitch in normal and in postextrasystolic potentiated contractions. Fourteen to sixteen different loads were used to define each of the force-velocity curves. The curves were fitted by a least-squares procedure to the hyperbolic (Hill equation). The hyperbolae were extrapolated to obtain maximum velocity and isometric force and interpolated to obtain maximum power. All three of these values rose more quickly than developed force. Maximum velocity reached 77% of its peak at the earliest time studied, 20-25% of the time to peak force. Developed force achieved 22% of its final value at this time, while extrapolated isometric force and maximum power both reached 44% of their peak values. Postextrasystolic potentiation sufficient to produce a 1.5 to twofold increase in peak developed force produced less than a 20% increase in extrapolated maximum velocity. The results can be interpreted in terms of a model in which the maximum velocity of the contractile elements remains constant during the twitch. Variation in maximum velocity is attributed to a small internal load, equivalent to 6% of twitch force. Since maximum velocity is relatively constant, it does not give a good measure of changes in the force-velocity curves. By contrast, the extrapolated isometric force and maximum power are much more sensitive to changes in the force-velocity curves, and they vary in proportion to each other. The advantage of using interpolated maximum power rather than isometric force to define changes in the curves is that it can be normalized to muscle mass.
Effects of anoxia on kinetics of [13N] glutamate and 13NH3 metabolism in rabbit myocardium.
Authors: Krivokapich J , Keen R E , Phelps M E , Shine K I , Barrio J R
Published: June 2012

Positron emission tomography is a unique noninvasive imaging technique that provides cross-sectional images of radiotracer concentrations in myocardium and permits measurement of blood flow as well as metabolism. Ammonia and glutamate have been labeled with the positron-emitter 13N (half-life 10 minutes) for use with positron emission tomography as tracers of flow and metabolism, respectively. In order to characterize the fate of these 13N-labelled compounds in myocardium, isolated rabbit interventricular septa were used to study the kinetics of [13N] glutamate ([13N]glu) and 13NH3 under aerobic and anoxic conditions. Tissue analyses 6 minutes after injection of a [13N]glu bolus into myocardium revealed that 70% of the 13N-label was present in [13N]glu 12%, 11%, and 4% in [13N]alanine ([13N]ala), [13N]aspartate ([13N]asp), and [13N]glutamine ([13N]gln), respectively. The corresponding relative specific activities were 1.0:0.4:0.5:0.01. Anoxia resulted in a significant increase in [13N]ala with a reduction in [13N]glu. This was consistent with increased pyruvate production due to increased anaerobic glycolysis and transamination of pyruvate with [13N]glu to yield [13N]ala. In support of this, addition of 2 mM pyruvate to the perfusate under control conditions produced a tissue distribution of 13N similar to that with anoxia. Six minutes after a bolus of 13NH3 during both control and anoxic conditions, 60% of the tissue 13N-label was in [13N]gln with no detectable amounts in other amino acids. The rest of the 13N-label was in 13NH3. Time-activity curve analyses demonstrated that anoxia significantly reduced the tissue retention of 13N-label from 13NH3 but not from [13N]glu. Thus, 13N from 13NH3 and [13N]glu was retained in tissue by different mechanisms involving glutamate, which were affected differentially by anoxia. These results suggest that positron emission tomography imaging with 13NH3 and [13N]glu in combination may be useful in identifying ischemic myocardium.
Catecholamine-induced myocardial potassium uptake mediated by beta 1-adrenoceptors and adenylate cyclase activation in the pig.
Authors: Ellingsen O , Sejersted O M , Leraand S , Ilebekk A
Published: June 2012

The myocardial potassium uptake during intracoronary isoproterenol stimulation was characterized in 12 anesthetized pigs. The beta-receptor subtype specificity and the effect of adenylate cyclase activation were determined. Potassium concentrations were continuously recorded by PVC-valinomycin minielectrodes in the left atrial cavity and in coronary sinus blood diverted through a shunt to the right atrium. The difference in potassium concentration between the left atrial cavity and coronary sinus, and the accumulated myocardial potassium uptake were calculated after computerized data sampling. By intracoronary drug infusion, changes in heart rate and systemic effects were minimized. Isoproterenol (0.6-0.8 microgram/min), a nonspecific beta-agonist, reduced coronary sinus potassium concentration transiently to a nadir of 0.28 (0.15-0.43) mM (median and 95% confidence interval) below control values (n = 12). The potassium uptake, which amounted to 140 (79-202) mumol/100 g tissue, corresponding to an intracellular potassium increase of about 3 mM, was abolished after selective beta 1-blockade by pafenolol. The specific beta 1-agonist dobutamine (40 micrograms/min) caused a similar potassium uptake before and after selective beta 2-blockade by ICI 118, 551. Salbutamol (2 micrograms/min), a specific beta 2-agonist, induced a minor potassium uptake of 4 (1-20) mumol/100 g, blocked by pafenolol. After nonselective beta-blockade by propranolol the adenylate cyclase stimulator forskolin caused a myocardial potassium uptake of similar magnitude to that of isoproterenol before beta-blockade. We conclude that a myocardial potassium uptake ensues during beta 1-adrenoceptor stimulation and adenylate cyclase activation.
Regulation of angiotensin II in rat adrenal gland.
Authors: Husain A , DeSilva P , Speth R C , Bumpus F M
Published: June 2012

Levels of angiotensin II immunoreactivity in the rat adrenal gland are over one hundredfold higher than those in plasma. It is unclear, however, whether the major source of adrenal angiotensin II immunoreactivity is intracellular synthesis by a local renin-angiotensin system, uptake by angiotensin II receptors, or both. Our studies show that angiotensin II immunoreactivity in the adrenal gland is predominantly attributable to angiotensin II (greater than 75%). Angiotensin III (16%) and other angiotensin II fragments are also present. The majority of angiotensin II immunoreactivity (73%), renin activity (73%), and angiotensin II receptor binding activity (66%) in the adrenal gland is located in the capsular glomerulosa cell layers. Dehydration produced by 2% NaCl imbibition decreased these activities in the capsular-glomerulosa. In the fasciculata-medullary regions of the adrenal gland, dehydration decreased renin activity but not angiotensin II immunoreactivity or angiotensin II receptor binding activity. Combined data from control and dehydrated rats showed a close correlation of the capsular-glomerulosa angiotensin II immunoreactivity with angiotensin II receptor binding activity (r = 0.94, p less than 0.001) and a weaker, nonsignificant correlation with renin activity (r = 0.66, p less than 0.1). In the fasciculata-medullary cell layers, no significant correlations were found between angiotensin II immunoreactivity and either renin or angiotensin II receptor binding activity. These data demonstrate that functionally distinct layers of the rat adrenal gland differentially regulate angiotensin II receptors and the renin-angiotensin system.(ABSTRACT TRUNCATED AT 250 WORDS)
Release of adenosine and cyclic AMP from coronary endothelium in isolated guinea pig hearts: relation to coronary flow.
Authors: Kroll K , Schrader J , Piper H M , Henrich M
Published: June 2012

The coronary efflux of radioactive 3',5'-cyclic adenosine monophosphate (cAMP) and adenosine from isolated guinea pig hearts was measured following selective prelabelling of coronary endothelial adenine nucleotides with 10 nM [2,8,5'-3H] adenosine. Intracoronary infusion of adenosine and its derivatives 5'-N-ethyl-carboxamide-adenosine (NECA), (-)-N6-(R-phenyl-isopropyl)-adenosine (R-PIA), and (+)-N6-(S-phenyl-isopropyl)-adenosine (S-PIA) caused dose-dependent parallel increases in both coronary flow and the coronary efflux of radioactive cAMP with a rank order of potency: NECA greater than R-PIA greater than adenosine greater than S-PIA. In contrast, adenosine receptor stimulation of isolated cardiomyocytes in primary culture decreased the cellular release of cAMP below control levels with a rank order of potency: R-PIA greater than NECA. Under control conditions, coronary efflux of adenosine and cAMP was 34.3 +/- 2.3 and 3.9 +/- 0.8 pmol/min (mean +/- SEM, n = 6), respectively. NECA (12 microM) caused an increase in cardiac cAMP release of 3.8 times and elevated the specific radioactivity of cAMP 5 times to 63.7 +/- 6.0 Ci/mol, a value 11 times greater than the specific radioactivity of tissue ATP. Based on these findings, it was concluded that the coronary endothelium possesses adenosine A2 receptors linked to adenylate cyclase, which are activated in parallel with increases in coronary flow and that cardiomyocyte adenosine receptors are predominantly of the A1 subtype. In addition, the contribution of the coronary endothelium to total cardiac adenosine release was calculated to be 14% using the specific radioactivities of adenosine and cAMP released into the effluent perfusate.
Molecular cloning of human angiotensinogen cDNA and evidence for the presence of its mRNA in rat heart.
Authors: Kunapuli S P , Kumar A
Published: June 2012

Human angiotensinogen cDNA clone was isolated from a liver cDNA library using a 32-nucleotide-long, synthetic oligonucleotide. The cDNA insert was 1,030 bp long and coded for the secretory and biologically active angiotensin II regions of the angiotensinogen molecule. The RNA from rat liver, brain, and heart was analyzed by the Northern hybridization procedure using nick translated angiotensinogen cDNA as a probe. In addition to liver, the angiotensinogen mRNA is present in the brain and the heart. The angiotensinogen mRNA in the heart is at least fourfold to fivefold more abundant as compared with the liver. We also provide evidence that angiotensinogen mRNA is present in the rat atria and right ventricle but not detectable in the left ventricle. The size of the angiotensinogen mRNA is the same from all three of the tissues, as judged by their electrophoretic mobilities.
Relation between membrane potential and contractile force in smooth muscle of the rat tail artery during stimulation by norepinephrine, 5-hydroxytryptamine, and potassium.
Authors: Neild T O , Kotecha N
Published: June 2012

The relation between smooth muscle membrane potential and contractile force was investigated in the rat tail artery to assess the importance of smooth muscle depolarization in the control of smooth muscle tone. Smooth muscle membrane potential and contractile force were measured simultaneously in isolated pieces of rat tail artery exposed to a range of concentrations of norepinephrine, 5-hydroxy-tryptamine, or raised external potassium. Potassium caused depolarization and contraction when the membrane was depolarized beyond -40 mV. Maximum contraction occurred at -19 mV, and further depolarization gave no increase in contraction. Both norepinephrine and 5-hydroxytryptamine caused contraction and depolarization, but the relation between depolarization and contraction was not the same as when potassium was used. There was significant contraction when the membrane potential was more negative than -50 mV, and the membrane potential was around -30 mV during maximal contractions. Although they acted on pharmacologically different membrane receptors, the relation between membrane potential and contraction was the same for norepinephrine and 5-hydroxytryptamine. Prazosin reduced the responses to norepinephrine but did not change the relation between membrane potential and contractile force. These results indicated that norepinephrine and 5-hydroxytryptamine binding to their respective receptors might activate the same sets of intracellular processes that subsequently caused both depolarization and contraction.
Relation between reversal of diastolic creep and recovery of systolic function after ischemic myocardial injury in conscious dogs.
Authors: Glower D D , Schaper J , Kabas J S , Hoffmeister H M , Schaper W , Spratt J A , Davis J W , Rankin J S
Published: June 2012

Although prolonged functional abnormalities after transient myocardial ischemia have been well described, the interrelationship between postischemic systolic and diastolic alterations remains controversial. Therefore, 24 chronically instrumented conscious dogs were studied with left ventricular and pleural micromanometers, ultrasonic dimension transducers in the left anterior descending (LAD) coronary distribution, and vena caval and coronary artery occluders. The LAD was occluded for 15 minutes and reperfused for 24 hours while vena caval occlusions were performed at intervals to measure myocardial segment length at 0 mm Hg transmural diastolic left ventricular pressure (L0). Coronary occlusion produced an immediate fall in systolic function as assessed by ejection shortening and stroke work and also induced a 16 +/- 4% increase in L0, which was termed diastolic creep. Throughout reperfusion, reversal of diastolic abnormalities correlated strongly with recovery of segmental shortening and stroke work (p less than 0.001). Correlation between systolic dysfunction and diastolic creep was also observed during alteration of inotropic state by dopamine, during initial reperfusion hyperfunction, and during pharmacologic manipulation of afterload. In 5 additional dog hearts fixed in diastole by rapid glutaraldehyde infusion after coronary occlusion, myocardial creep measured by the segment length transducers paralleled sarcomere elongation measured by electron microscopy. Thus, the direct correlation between diastolic creep and systolic dysfunction throughout reperfusion and during hemodynamic alterations suggests that diastolic properties of postischemic myocardium may not be entirely passive and that systolic and diastolic dysfunction induced by ischemia may have a common basis at the cellular level.