bluuebunny/crossref_metadata_2025 huggingface dataset:
Cardiac performance in relation to oxygen supply varies with dietary lipid composition in sturgeon
Authors: Agnisola C. , McKenzie D. J. , Taylor E. W. , Bolis C. L. , Tota B.
Published: December 2017

Dietary polyunsaturated fatty acids (PUFA) of the n-3 series that have beneficial effects on mammalian heart function are typically found at high levels in fish tissues. The effects of dietary fatty acid composition on cardiac function were investigated in the sturgeon. When compared with sturgeon maintained for 1 yr on a diet enriched with saturated fatty acids (SFA) (the coconut oil-supplemented diet, COD), sturgeon maintained on a diet enriched with n-3 PUFA (the fish oil-supplemented diet, FOD) had higher myocardial 20:5(n-3) and lower 20:4(n-6) content with a consequent decrease in the n-6-to-n-3 ratio (from 0.86 to 0.25) and a lower intrinsic in vitro heart rate (22.0 +/- 1.5 vs. 29.9 +/- 1.0 beats/min) and cardiac power output (PO) (0.33 +/- 0.08 vs. 0.48 +/- 0.03 mW/g), but had a greater in vitro scope for cardiac work (almost twice the maximal-to-basal PO ratio). Reducing the oxygen supply to the hearts significantly decreased, by approximately 40%, the maximal in vitro PO in the COD group of animals but had no effect in the FOD group. These differences in performance were not reflected in heart rate or blood pressure in vivo, either in normoxia or hypoxia. Addition of vitamin E as an antioxidant to the diets reduced intrinsic heart rate by approximately 25% but did not influence the effects (dietary fatty acid composition on in vitro cardiac performance. The results indicate that dietary n-3 PUFA can have beneficial effects on the resistance of the fish heart to environmental stressors such as hypoxia.
Atrial natriuretic hormone inhibits angiotensin II-stimulated sympathetic nerve activity in humans
Authors: Matsukawa T. , Mano T.
Published: December 2017

We examined the effect of intravenous infusion of atrial natriuretic hormone (ANH) on the response of muscle sympathetic nerve activity (MSNA) to infused angiotensin II (ANG II) in humans. Infusion of saline alone or ANH (10 ng.kg-1.min-1) alone produced no significant change in MSNA, whereas the infusion of ANG II (5 ng.kg-1.min-1) alone caused a decrease in MSNA. Because elevations in arterial pressure (AP) and central venous pressure (CVP) also occurred due to ANG II, such elevations in AP and CVP could inhibit MSNA via baroreflexes. Then, the effect of ANG II on AP and CVP was inhibited by the simultaneous infusion of nitroprusside (N). Infusion of ANG II (5 ng.kg-1.min-1) produced significant increases in MSNA when ANG II was infused along with N. However, the simultaneously infused ANH (10 ng.kg-1.min-1) abolished the increases in MSNA induced by ANG II when the elevation in AP and CVP was inhibited by N. Thus ANH inhibits ANG II-induced sympathetic activation in humans. The results suggest that ANH may modulate sympathetic nerve activity at least in part by antagonizing the action of ANG II.
Spectral analysis of arterial blood pressure and raphe magnus neuronal activity in anesthetized rats
Authors: Leung C. G. , Mason P.
Published: December 2017

Recent evidence suggests that nociceptive modulatory cells in the nucleus raphe magnus (RM) and adjacent nucleus reticularis magnocellularis (NRMC) may participate in the modulation of autonomic processing. Therefore, spectral analyses were used to determine component frequencies common to both arterial blood pressure and the activity of RM/NRMC neurons in rats lightly anesthetized with isoflurane. These analyses detected powerful, extremely low frequency (period length: 6.4-18.5 min) oscillations in arterial blood pressure and in the activity of two classes of RM/NRMC neurons, ON and OFF cells. All ON cells discharged during periods of low blood pressure, whereas all OFF cells discharged during periods of high blood pressure. In contrast, the discharge of NEUTRAL and REGULAR cells did not have a consistent relationship to blood pressure. The role of these cells in nociceptive modulation is also unclear. The results presented indicate that ON and OFF cells may participate in the modulation of both autonomic and nociceptive processing.
Conscious obese rats have impaired reflex bradycardia and enhanced norepinephrine sensitivity
Authors: Bunag R. D. , Meyer M. , Vansell N. , Kerecsen L.
Published: December 2017

Male Sprague-Dawley rats fed a condensed milk diet were classified as either "obesity susceptible" (OS) or "obesity resistant" (OR) based on body weight increases attained after 12 wk. Overall caloric intake in OS rats was higher than in chow-fed controls, and OS rats were heavier than chow-fed controls or OR rats. There were no significant differences in blood glucose, serum insulin, ventricular weight, basal blood pressure, or heart rate. Pressor responses recorded after combined blockade with atropine and propranolol to eliminate reflex effects were identical for vasopressin, but those to norepinephrine were larger in OS than in OR rats, whereas those to angiotensin were larger in OS than in control rats. When baroreflex sensitivity was assessed using intravenously infused sodium nitroprusside or phenylephrine to alter systemic arterial pressure, differences in reflex tachycardia were equivocal, but reflex bradycardia was clearly inhibited in OS rats. These results show that, although basal blood pressure was unaffected in OS rats, their impaired reflex bradycardia along with enhanced pressor responsiveness to norepinephrine could predispose them to subsequent development of hypertension.
Cardiac force and high-energy phosphates under metabolic inhibition in four ectothermic vertebrates
Authors: Hartmund T. , Gesser H.
Published: December 2017

Isometric twitch tension of ventricular preparations stimulated at 0.2 Hz fell over 30 min of anoxia by a fraction decreasing in the order rainbow trout, cod, eel, and freshwater turtle. Drops in the estimated cytoplasmic energy state were related to larger tension losses for trout than for the other species, possibly due to larger changes in free phosphate. Anoxic energy degradation was slower for turtle than for the other species. Anoxia combined with glycolytic inhibition (1 mmol/l iodoacetate) enhanced the decrease in twitch tension for a drop in energy state and enlarged the increase in ADP/ATP relative to that in creatine/phosphocreatine to an extent inversely related to the creatine kinase activity. Furthermore, it increased resting tension to an extent possibly related to myosin-adenosinetriphosphatase (ATPase) activity and lowered the content of phosphorylated adenylates in trout and turtle myocardium. The results indicate that species differences in performance of the metabolically challenged myocardium depend on energy-degrading processes, e.g., myosin-ATPase activity, phosphate release, creatine kinase activity, and efflux/degradation of ADP and AMP, and that glycolysis offers protection due to its cytoplasmic localization.
Dissociation of temperature changes and anorexia after experimental colitis and LPS administration in rats
Authors: Larson S. J. , Collins S. M. , Weingarten H. P.
Published: December 2017

The acute phase of inflammation induces both anorexia and fever. Because several analyses suggest a linkage between the meal size and body temperature, we assessed whether temperature changes were causal to anorexia in situations involving acute inflammation. Specifically, we evaluated whether elevations of body temperature could account for the reduced food intake after induction of experimental colitis [via intrarectal infusions of trinitrobenzene sulfonic acid (TNB)] or injection of 100 micrograms/kg lipopolysaccharide (LPS). Temperature was monitored telemetrically in rats via implanted temperature transmitters. TNB-treated rats demonstrated a 5-day anorexia that resulted specifically from a decrease in meal size. Although TNB-treated rats were hypothermic on the day of treatment, no other body temperature changes were noted. LPS reduced food intake and elevated temperature, but these two effects were uncorrelated temporally. Although these results do not identify the mechanisms of anorexia, the findings indicate clearly that the anorexia associated with the acute inflammatory response is not secondary to fever.
Norepinephrine-mediated hypoxic stimulation of embryonic red cell carbonic anhydrase and 2,3-DPG synthesis
Authors: Dragon S. , Glombitza S. , Gotz R. , Baumann R.
Published: December 2017

Hypoxia is the stimulus for activation of red cell carbonic anhydrase II (CAII) and 2,3-diphosphoglycerate (2,3-DPG) synthesis of chick red blood cells during late embryonic development. We have tested whether plasma catecholamines are involved as hormonal mediators, because hypoxia is a well-known stimulus for catecholamine release in mammalian fetuses. Plasma catecholamines were measured in 8- to 16-day-old chick embryos. Plasma levels of norepinephrine (NE) were initially low, but its concentration increased rapidly from 2.7 nM (day 12) to 13.4 nM at day 13 and 25.5 nM at day 16. Epinephrine (E) was not detectable before day 13. Short-term hypoxic exposure of day 11 embryos (1-h incubation at 13.5% O2) increased plasma NE concentration fivefold compared with the controls but had no effect on E. During 15-h in vitro incubation of red blood cells from day 11, addition of 1 microM NE to the incubation medium increased the red cell 2,3-DPG concentration nearly threefold and CAII activity sixfold compared with the control. The CAII activity and 2,3-DPG concentration were also increased when cells were incubated with plasma from late chick embryos. The activation was induced by beta-adrenergic stimulation of adenylyl cyclase. Atenolol and propranolol blocked the effects of NE and embryonic chick plasma. Analysis of de novo protein synthesis ([35S]methionine incorporation) demonstrated that catecholamines stimulate the synthesis of several proteins besides CAII. The results indicate that developmental changes of plasma NE concentration are instrumental in the adenosine 3',5'-cyclic monophosphate-dependent activation of CAII and 2,3-DPG synthesis of red blood cells from late chick embryos.
High plasma cholesterol, but low triglycerides and plaque-free arteries, in Mexican free-tailed bats
Authors: Widmaier E. P. , Gornstein E. R. , Hennessey J. L. , Bloss J. M. , Greenberg J. A. , Kunz T. H.
Published: December 2017

Female mammals typically become hyperphagic from mid- to late pregnancy and during lactation. Mexican free-tailed bats, Tadarida brasiliensis mexicana, double their nightly food intake from late pregnancy to peak lactation and consume an insect diet that is exceptionally high in fat. During late pregnancy and throughout lactation, fasting plasma levels of cholesterol in this insectivorous bat are high (215 +/- 8 mg/dl) and are nearly 10-fold higher than in three species of Old World frugivorous bats. Fasting triglycerides were unexpectedly low in T. brasiliensis (25 +/- 2 mg/dl), despite evidence of high fat intake during nightly feeding bouts (postprandial cholesterol and triglycerides, 268 +/- 18 and 122 +/- 20 mg/dl, respectively). High-density lipoprotein (HDL) cholesterol levels were extraordinarily high (124 +/- 5 mg/dl) and unaffected by feeding. Low-density lipoprotein cholesterol levels were correspondingly low (86 +/- 7 mg/dl). This unusual plasma lipid profile was not associated with coronary or aortic atherosclerosis, nor was there evidence of hyperglycemia or hyperinsulinemia. A high-fat diet and high levels of cholesterol in T. brasiliensis are not correlated with cardiovascular disease or (possibly) insulin resistance. Among several possible factors that might account for these observations, nightly bouts of powered flight (commuting and foraging for food) may contribute to elevated HDL cholesterol, which may protect this species from developing atherosclerosis.
Relationship between cold-induced thermoregulation and spontaneous rapid body weight loss of aging F344 rats
Authors: McDonald R. B. , Florez-Duquet M. , Murtagh-Mark C. , Horwitz B. A.
Published: December 2017

We previously showed that, although cold-induced thermoregulation is attenuated in 26-mo-old male Fischer 344 (F344) rats, not all rats this age exhibit the same degree of cold-exposed hypothermia or diminished brown adipose tissue nonshivering thermogenic capacity. Examination of this heterogeneity suggested the hypothesis that it was associated with a difference in the physiological state between aged rats that were maintaining stable body weight versus those showing the rapid weight loss often occurring near the end of the rat's natural life span. To test this, we acutely exposed male F344 rats to cold (4 h at 6 degrees C) beginning at 24 mo of age. This exposure was weekly for the first 2 wk and then on alternate weeks as long as the rat's body weight was stable. If body weight progressively declined for 3-5 consecutive days, the rat's response to the acute cold exposure was again measured, as was that of two additional rats not displaying this rapid loss in body weight. If body temperature decreased during the cold exposure to intraperitoneal temperatures < or = 32.5 degrees C, the rat was killed with pentobarbital sodium and interscapular brown adipose tissue was removed. One of the age-matched controls was also killed at this time. The age at which body weight showed a spontaneous rapid decline ranged from 24.5 to 29 mos. All eight rats displaying spontaneous rapid weight loss had significant hypothermia during the acute cold exposure, whereas none of the eight weight-stable rats did. The development of hypothermia in the spontaneous rapid weight loss group was not, in general, observed before their weight loss. The weight loss and hypothermia were associated with lower levels of brown fat uncoupling protein and significant changes in body fat and protein. These data suggest that the development of senescence-related hypothermia occurs rapidly and is not a simple function of chronological age or the median life span of the animals. Furthermore, these data imply that the rate of aging in terms of maintenance of thermoregulatory homeostasis has both a gradual and rapid component, the latter being associated with a different physiological state than the former.
Relationship between basal NO release and cyclooxygenase products in the normal rat kidney
Authors: Baylis C. , Slangen B. , Hussain S. , Weaver C.
Published: December 2017

We investigated the physiological regulation of renal function by nitric oxide (NO) and its interactions with the endothelial cyclooxygenase products in the conscious, chronically catheterized rat. A subpressor dose of NO inhibitor nitro-L-arginine methyl ester (L-NAME) produced renal vasoconstriction that was unaffected by cyclooxygenase inhibition with indomethacin (Indo). Acute, high-dose L-NAME produced a pressor response of approximately 40 mmHg and marked renal vasoconstriction. Indo selectively amplified the renal vasoconstriction, whereas inhibition of the thromboxane-endoperoxide receptor had no effect. Chronic NO inhibition for 5 wk led to sustained hypertension and renal vasoconstriction; the latter was amplified by acute Indo. These data suggest that in the normal, conscious rat the kidney is under important NO-dependent tone. There is no obvious interaction between NO and the cyclooxygenase products in control of basal renal function. When systemic NO inhibition is produced with either acute or chronic high-dose L-NAME, the kidney is severely vasoconstricted. The renal vasoconstriction is not ameliorated by thromboxane-endoperoxide antagonism but is exacerbated by cyclooxygenase blockade, suggesting that vasodilator cyclooxygenase products compensate for the renal hypoperfusion because of severe NO deficiency.
Application of acute maximal exercise to protect orthostatic tolerance after simulated microgravity
Authors: Engelke K. A. , Doerr D. F. , Convertino V. A.
Published: December 2017

Pages R837–R847: K. A. Engelke, D. F. Doerr, and V. A. Convertino. “Application of acute maximal exercise to protect orthostatic tolerance after simulated microgravity.” On p. 837, the author line of the article and abstract and the affiliation line should read as follows:

KEITH A. ENGELKE, DONALD F. DOERR, CRAIG G. CRANDALL, AND VICTOR A. CONVERTINO

Department of Physiology, University of Florida, Gainesville, Florida 32610; National Aeronautics and Space Administration-Kennedy Space Center, Cape Canaveral, Florida 32899; Department of Physiology, University of North Texas Health Science Center, Ft. Worth, Texas 76107; and Physiology Research Branch, Clinical Science Division, Brooks Air Force Base, Texas 78235
Stimulation of Na(+)-K(+)-2Cl- cotransport in rat medullary thick ascending limb by dopamine
Authors: Aoki Y. , Albrecht F. E. , Bergman K. R. , Jose P. A.
Published: December 2017

Dopamine receptors are present in the medullary thick ascending limb (mTAL) of Henle, but their effect on ion transport in this nephron segment has not been tested. Therefore, we studied the short-term effects of dopamine on Na(+)-K(+)-2Cl- cotransport (assessed by 100 microM bumetanide-sensitive 86Rb uptake) in rat mTAL tubular suspensions. Dopamine (1 microM) stimulated bumetanide-sensitive 86Rb uptake (72.1 +/- 10.6% vs. control, n = 5) by increasing total 86Rb uptake and by decreasing bumetanide-insensitive 86Rb uptake; this effect was concentration dependent. The dopamine-induced stimulation of Na(+)-K(+)-2Cl- cotransport activity was mimicked by calyculin A, a protein phosphatase (PP) inhibitor, and Sp isomer of adenosine 3',5'-cyclic monophosphothioate (Sp-cAMP[S]), a protein kinase A (PKA) agonist, and blocked by Rp isomer of 8-(4-chlorophenylthio)-cAMP[S] (Rp-8-CPT-cAMP[S]), a PKA inhibitor (n = 5). Dopamine did not increase the stimulatory effect of the PP inhibitor. However, the stimulatory effect of the PP inhibitor and PKA agonist was additive and approached the stimulatory effect of dopamine. The stimulatory effects of dopamine, PP inhibitor, and PKA agonist persisted even when intracellular sodium was clamped by 5 microM monensin. When K+ channels were blocked by 1 mM BaCl2, the effects of dopamine and calyculin A on the cotransport were no longer apparent, although the stimulatory effect of the PKA agonist was attenuated. We conclude that dopamine stimulates Na(+)-K(+)-2Cl- cotransport activity. This action is mediated mainly by PKA-dependent phosphorylation/dephosphorylation processes and modulated by dopamine actions on K+ channels.
Responses of fetal sheep to reduced maternal renal blood flow and maternal hypertension
Authors: Lumbers E. R. , Burrell J. H. , Stevens A. D. , Bernasconi C.
Published: December 2017

In 16 chronically catheterized fetal sheep the effects of reducing and restoring maternal renal blood flow (RBF) and thus inducing and reversing hypertension were studied in uninephrectomized pregnant ewes; controls were 3 fetuses that were carried by uninephrectomized ewes in which RBF was not reduced and that did not become hypertensive. Within 24-72 h of maternal RBF reduction, fetal arterial PO2 had fallen (P < 0.001) and PCO2 had increased (P < 0.025); fetal arterial pressure also increased (P < 0.005). These effects persisted, despite restoration of maternal RBF and reversal of maternal hypertension. Within 24-72 h of reduction of maternal RBF, fetal urine flow had increased (P < 0.005), and it remained elevated over the first 3 h after RBF was restored; 24-72 h later it was lower (P < 0.025) and returned to control levels. The excretion of sodium, potassium, and chloride showed a similar increase when maternal RBF was reduced (P < 0.001), with return to control values 24-72 h after RBF had been restored. Fetal glomerular filtration rate did not change; thus the natriuresis and diuresis that occurred were due to reduced tubular solute and water reabsorption (P < 0.025). These changes in fetal renal function may be related, in part, to changes in fetal PO2 and PCO2, but they are most likely due to reduced maternal renal function due to the restriction in maternal RBF, inasmuch as they were reversed when RBF was restored.
Functional evidence for L-type Ca2+ channels controlling ANG II-induced adrenal catecholamine release in vivo
Authors: Martineau D. , Briand R. , Yamaguchi N.
Published: December 2017

The aim of the present study was to investigate the functional involvement of L- and/or N-type Ca2+ channels in adrenal catecholamine secretion in response to exogenous angiotensin II (ANG II) in anesthetized dogs. Plasma catecholamine concentrations in adrenal venous and aortic blood were determined by a high-performance liquid chromatography-electrochemical method. In the first series of experiments, repeated infusions of BAY K 8644 locally into the left adrenal gland at 15-min intervals resulted in significant and reproducible increases in adrenal catecholamine secretion. Nifedipine, similarly administered 5 min before BAY K 8644, diminished BAY K 8644-induced catecholamine secretion in a dose-dependent manner and completely blocked the catecholamine response at the highest dose tested. In the second series of experiments, local infusion of ANG II resulted in a significant increase in adrenal catecholamine secretion. The maximum catecholamine response to ANG II was attenuated by approximately 65% in the presence of nifedipine at the dose that abolished the BAY K 8644-induced catecholamine release. This inhibition by nifedipine remained unchanged in the presence of omega-conotoxin. The present study shows that dihydropyridine-sensitive L-type Ca2+ channels are operative in the adrenal medulla of the dog in vivo. The results indicate that the L-type Ca2+ channels are only partially implicated in the local regulation of ANG II-induced adrenal catecholamine secretion, suggesting the existence of another mechanism. However, omega-conotoxin-sensitive N-type Ca2+ channels are unlikely to be functionally involved in postsynaptic mechanisms mediating adrenal catecholamine secretion in response to exogenous ANG II under in vivo conditions.
Presence and activity of compounds with GnRH-like activity in the ovary of seabream Sparus aurata
Authors: Nabissi M. , Pati D. , Polzonetti-Magni A. M. , Habibi H. R.
Published: December 2017

The binding and activity of gonadotropin-releasing hormone (GnRH) were characterized in the mature gilthead seabream (Sparus aurata) ovary by use of an analogue of salmon GnRH([D-Arg6,Trp7,Leu8,Pro9-N(Et)]GnRH, sGnRH-A) as labeled ligand. The binding of 125I-sGnRH-A to the seabream ovarian membrane preparation was saturable, displaceable, reversible, and dependent on time, temperature and tissue concentration. Addition of unlabeled s-GnRH-A displaced the radio-ligand in a dose-related manner, indicating the presence of one class of high-affinity binding sites with an equilibrium dissociation constant of 45.5 +/- 6.2 nM. Addition of other GnRH peptides, including salmon GnRH ([Trp7,Leu8]GnRH) and chicken GnRH-II ([His5,Trp7,Tyr8]GnRH), also displaced 125I-sGnRH-A; all these peptides bound with lower affinities than sGnRH-A to the seabream ovarian binding site. In this study, we also demonstrated the presence of compounds with GnRH-like activity in the ovary of seabream. Seabream ovarian extract stimulated pituitary gonadotropin release from the goldfish pituitary and displaced 125I-sGnRH-A binding in the seabream ovary. Furthermore, addition of sGnRH-A to cultured seabream oocytes directly stimulated reinitiation of oocyte meiosis, as indicated by germinal vesicle breakdown. Overall, the present study characterizes GnRH-binding sites in the seabream ovary and supports the hypothesis that GnRH or compounds with GnRH-like activity play an autocrine/paracrine role in the regulation of ovarian function in the seabream ovary.
Effect of cholinergic agonists on bulbospinal C1 neurons in rats
Authors: Huangfu D. , Schreihofer M. , Guyenet P. G.
Published: December 2017

Cholinergic inputs to the rostral ventrolateral medulla (RVLM) may contribute to sympathetic tone generation. The present study analyzes the response of RVLM neurons to cholinergic agonists. In chloralose-anesthetized rats iontophoresis of carbachol excited RVLM sympathoexcitatory neurons (+69% from resting level of 11.9 +/- 2 spikes/s; n = 28). This effect was reduced 85% by iontophoresis of methylatropine and abolished by intravenous scopolamine. Iontophoresis of nicotine or hexamethonium was ineffective. In contrast, most RVLM respiratory units were inhibited by carbachol. Whole cell recordings of bulbospinal RVLM neurons were made in neonatal rat brain slices (54 cells, 24 C1 adrenergic neurons). In current-clamp recordings (without tetrodotoxin) carbachol produced depolarization, increased postsynaptic potential frequency, and decreased input resistance. In voltage-clamp recording (-50 to -60 mV; 1 microM tetrodotoxin) carbachol produced inward current [50% effective concentration (EC50): 10 +/- 1 microM; 12.6 +/- 2 pA at 30 microM; n = 16] that persisted in low Ca2+/high Mg2+ (n = 6). Muscarine (30 microM) caused smaller inward currents (2.6 +/- 0.6 pA; n = 16). The carbachol-induced current was reduced 46% by 5 microM methylatropine (n = 15) and 84% by 200 microM hexamethonium (n = 9). The current was linear as a function of the holding potential (extrapolated reversal potential: -22 +/- 2 mV). In conclusion, carbachol exerts both pre- and postsynaptic effects on C1 and other putative sympathoexcitatory RVLM neurons. In vitro the postsynaptic effect of carbachol has a mixed nicotinic and muscarinic pharmacology. In vivo, iontophoretically applied carbachol produces muscarinic excitation of barosensitive RVLM neurons.
Role of central ANG II receptors in stress-induced cardiovascular and hyperthermic responses in rats
Authors: Saiki Y. , Watanabe T. , Tan N. , Matsuzaki M. , Nakamura S.
Published: December 2017

The present study was carried out using a biotelemetry system to investigate whether central angiotensin II (ANG II) is involved in stress-induced cardiovascular and body temperature responses in rats. Intracerebroventricular injections of the nonselective ANG II-receptor antagonist saralasin and of the ANG II AT1-receptor antagonist losartan attenuated both the heart rate and pressor responses to immobilization stress in a dose-dependent manner. The elevation of plasma norepinephrine and epinephrine induced by immobilization stress was also suppressed by central ANG II-receptor blockade, suggesting a general attenuation of stress-induced sympathetic nervous and adrenomedullary activity by central ANG II-receptor blockade. The hyperthermia induced by immobilization stress was attenuated by central ANG II AT1-receptor blockade in a dose-dependent manner. The effects of central saralasin on the blood pressure response induced by immobilization stress were greater in Wistar-Kyoto rats than in spontaneously hypertensive rats. The present results suggest that central ANG II AT1-receptors are involved in expression of the tachycardia and hyperthermia, as well as the pressor response, induced by immobilization stress.
CCK is involved in both peripheral and central mechanisms controlling food intake in chickens
Authors: Rodriguez-Sinovas A. , Fernandez E. , Manteca X. , Fernandez A. G. , Gonalons E.
Published: December 2017

The aim of this work was to study the involvement of cholecystokinin (CCK) in the control of food intake in chickens. The following aspects were studied: 1) the effects of intravenous and intracerebroventricular sulfated octapeptide of CCK (CCK-8s) on voluntary food intake; 2) the effects of two CCK-receptor antagonists. L-365,260 and L-364,718, on food intake; and 3) the ability of such drugs to block the effects of CCK-8s on food intake in the chicken. Intravenous and intracerebroventricular CCK-8s caused a decrease in food intake. Intraperitoneal L-365,260, a CCK-receptor antagonist with low affinity for the two CCK receptors described in the chicken, increases food intake. Intracerebroventricular L-364,718, a drug that has high affinity for the chicken central CCK-receptor type, increased food intake. The effect of intravenous CCK-8s on food intake was not blocked by L-364,718 or L-365,260, whereas that of intracerebroventricular CCK-8s was blocked by intracerebroventricular L-364,718. It is concluded that central endogenous CCK plays a role in the control of food intake, which is dependent on central CCK-receptor type; nevertheless, peripheral CCK also decreases food intake acting on the peripheral CCK-receptor type. The fact that intracerebroventricular L-364,718 is able to increase food intake is related to its high affinity for the central CCK-receptor type of this species. Finally, three different speculations that might explain the fact that intraperitoneal L-365,260 increases food intake are discussed.
Contractile properties of rat, rhesus monkey, and human type I muscle fibers
Authors: Widrick J. J. , Romatowski J. G. , Karhanek M. , Fitts R. H.
Published: December 2017

It is well known that skeletal muscle intrinsic maximal shortening velocity is inversely related to species body mass. However, there is uncertainty regarding the relationship between the contractile properties of muscle fibers obtained from commonly studied laboratory animals and those obtained from humans. In this study we determined the contractile properties of single chemically skinned fibers prepared from rat, rhesus monkey, and human soleus and gastrocnemius muscle samples under identical experimental conditions. All fibers used for analysis expressed type I myosin heavy chain as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Allometric coefficients for type I fibers from each muscle indicated that there was little change in peak tension (force/fiber cross-sectional area) across species. In contrast, both soleus and gastrocnemius type I fiber maximal unloaded shortening velocity (Vo), the y-intercept of the force-velocity relationship (Vmax), peak power per unit fiber length, and peak power normalized for fiber length and cross-sectional area were all inversely related to species body mass. The present allometric coefficients for soleus fiber Vo (-0.18) and Vmax (-0.11) are in good agreement with published values for soleus fibers obtained from common laboratory and domesticated mammals. Taken together, these observations suggest that the Vo of slow fibers from quadrupeds and humans scale similarly and can be described by the same quantitative relationships. These findings have implications in the design and interpretation of experiments, especially those that use small laboratory mammals as a model of human muscle function.
Regulation of intracellular pH in avian renal proximal tubules
Authors: Kim Y. K. , Brokl O. H. , Dantzler W. H.
Published: December 2017

In proximal tubules isolated from chicken transitional nephrons, intracellular pH (pHi), measured with the pH-sensitive fluorescent dye 2'.7'-bis(2-carboxyethyl)-5,6-carboxyfluorescein (BCECF), was approximately 7.3-7.4 under control conditions [N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered medium with pH 7.4 at 39 degrees C] and was reduced to approximately 6.8 in response to NH4Cl pulse. The rate of recovery of pHi (dpHi/dt) from this acid level to the resting level and the resting pHi were 1) significantly reduced by the removal of Na+ from the bath, 2) significantly increased by the removal of Cl from the bath, and 3) unchanged by the removal of both Na+ and Cl from the bath. The addition of either amiloride or 4,4'-diisothiocyanostilbene-2,2'-disulfonate to the bath reduced dpHi/dt to about the same extent as the removal of Na+. These data suggest that both Na(+)-coupled and Cl-coupled acid-base fluxes at the basolateral membrane are involved in determining the resting pHi and the rate of recovery of pHi after acidification. The most likely possibilities appear to be a basolateral Na+/Hi exchanger, a basolateral Na(+)-coupled Cl/HCO3 exchanger, a basolateral Na(+)-HCO3(-)CO(3)2 cotransporter, and a basolateral Na(+)-independent Cl-/HCO3 exchanger.
A role for adenosine in metabolic depression in the marine invertebrate Sipunculus nudus
Authors: Reipschlager A. , Nilsson G. E. , Portner H. O.
Published: December 2017

Involvement of neurotransmitters in metabolic depression under hypoxia and hypercapnia was examined in Sipunculus nudus. Concentration changes of several putative neurotransmitters in nervous tissue during anoxic or hypercapnic exposure or during combined anoxia and hypercapnia were determined. Among amino acids (gamma-aminobutyric acid, glutamate, glycine, taurine, serine, and aspartate) and monoamines (serotonin, dopamine, and norepinephrine), some changes were significant, but none were consistent with metabolic depression under all experimental conditions applied. Only the neuromodulator adenosine displayed concentration changes in accordance with metabolic depression under all experimental conditions. Levels increased during anoxia, during hypercapnia, and to an even greater extent during anoxic hypercapnia. Adenosine infusions into coelomic fluid via an indwelling catheter induced a significant depression of the normocapnic rate of O2 consumption from 0.36 +/- 0.04 to a minimum of 0.24 +/- 0.02 (SE) mumol.g-1.h-1 after 90 min (n = 6). Application of the adenosine antagonist theophylline caused a transient rise in O2 consumption 30 min after infusion during hypercapnia but not during normocapnia. Effects of adenosine and theophylline were observed in intact individuals but not in isolated body wall musculature. The results provide evidence for a role of adenosine in inducing metabolic depression in S. nudus, probably through the established effects of decreasing neuronal excitability and neurotransmitter release. In consideration of our previous finding that metabolic depression in isolated body wall musculature was elicited by extracellular acidosis, it is concluded that central and cellular mechanisms combine to contribute to the overall reduction in metabolic rate in S. nudus.
Sex differences in the cardiovascular and renal actions of vasopressin in conscious rats
Authors: Wang Y. X. , Crofton J. T. , Share L.
Published: December 2017

The present study was carried out to investigate whether prostaglandins (PG) are involved in the mechanism that contributes to the sex difference in the antidiuretic and pressor actions of vasopressin. The experiments were performed in conscious male and nonestrous female rats. In hydrated rats, the graded infusion of vasopressin (10-1,000 pg.min 1.kg body wt-1) resulted in a dose-dependent antidiuresis: decreases in urine flow and free water clearance and an increase in urine osmolality. These responses were significantly greater in male than in nonestrous female rats. Pretreatment with a cyclooxygenase inhibitor, indomethacin (10 mg/kg body wt iv), significantly enhanced the antidiuretic response to vasopressin in both sexes. However, the magnitude of this enhancement was greater in female than in male rats. Thus indomethacin abolished the sex difference in the antidiuretic response to vasopressin. In a separate experiment in rats without water hydration and urine collection, infusion of pressor doses of vasopressin (1,000-6,000 pg.min-1.kg body wt-1) resulted in a greater increase in blood pressure in male than in nonestrous female rats. Treatment with indomethacin enhanced this response equivalently in both sexes and thus did not affect the sex difference in the pressor action of vasopressin. These data indicate that renal PG may mediate, at least in part, the sex difference in the antidiuretic action of vasopressin, whereas vascular PG seem not to play an important role in the sex difference in the pressor action of vasopressin.
Temperature-dependent shift of pHi in fish white muscle: contributions of passive and active processes
Authors: Van Dijk P. L. , Hardewig I. , Portner H. O.
Published: December 2017

This study was designed to determine the mechanisms causing temperature-induced pH shifts in the white muscle of the marine teleost Zoarces viviparus. The white musculature undergoes an intracellular acidification with increasing body temperature at a slope of the pH-temperature relationship equal to -0.016 +/- 0.003 U/degree C. This is in good accordance with the overall relationship between the change in pK and the change in temperature of the intracellular proteins, which was determined to be -0.013 +/- 0.001 U/degree C. Thus the dissociation state of muscle proteins is kept fairly constant in white muscle of Zoarces viviparus. The passive component of the observed pH shift, which is due to the physicochemical response of the intracellular buffers to temperature change, accounts for only 35% of the pH transition. Ventilatory adjustment of intracellular PCO2 does not contribute to the temperature-induced shift of intracellular pH (pHi) in Zoarces viviparus. Therefore, the remaining 65% of pH adjustment must be ascribed to ion exchange mechanisms. The nonbicarbonate buffer value amounted to 34.4 +/- 2.3 meq.pH-1 kg cell water-1 at 12 degrees C and decreased slightly but not significantly with temperature. On the basis of our data we calculated that a removal of 0.52 mmol base equivalents.kg cell water-1.degree C-1 was necessary to shift pHi to its new steady state.
Aging alters the serotonergic modulation of light-induced phase advances in golden hamsters
Authors: Penev P. D. , Turek F. W. , Wallen E. P. , Zee P. C.
Published: December 2017

Recent findings have raised the possibility that some of the age-related changes in the circadian system and the response of the circadian pacemaker to environmental stimuli may involve central serotonergic mechanisms. The present study compared the effects ofpretreatment with the serotonin agonist 8-hydroxy-2(di-n-propylamino)tetralin (5 mg/kg ip) on the magnitude of light-induced phase advances in young (2-4 mo) and old (18-20 mo) golden hamsters. The ability of this serotonin agonist to attenuate the photic phase resetting of circadian locomotor rhythmicity in young animals was decreased by 46% in old hamsters (P < 0.05). These results suggest that deficits in the mechanisms for serotonergic control of circadian function may interfere with the optimal adaptation of the senescent organism to its temporal environment.
Adrenergic, respiratory, and cardiovascular effects of core cooling in humans
Authors: Frank S. M. , Higgins M. S. , Fleisher L. A. , Sitzmann J. V. , Raff H. , Breslow M. J.
Published: December 2017

The adrenergic, respiratory, and cardiovascular responses to isolated core cooling were assessed in awake human subjects. Mild core hypothermia was induced by intravenous infusion of 30 or 40 ml/kg of cold saline (4 degrees C) on 2 separate days. A warm intravenous infusion (30 ml/kg, 37 degrees C) was given on a third day as a control treatment. Mean norepinephrine concentration increased 400% and total body oxygen consumption increased 30% when core temperature decreased 0.7 degrees C. Mean norepinephrine concentration increased 700% and total body oxygen consumption increased 112% when core temperature decreased 1.3 degrees C. Core cooling was associated with peripheral vasoconstriction and increased mean arterial blood pressure, whereas heart rate was unchanged. Plasma epinephrine and cortisol concentrations were unchanged during core cooling. There were no changes in any measured parameter with the warm infusion. These findings suggest that mild hypothermia induced by isolated core cooling is associated with an adrenergic response characterized by peripheral sympathetic nervous system activation without a significant adrenocortical or adrenomedullary response. The respiratory and cardiovascular responses to core cooling are characterized by a shivering-induced increase in metabolic rate, norepinephrine-mediated peripheral vasoconstriction, and increased arterial blood pressure.
Differential expression of angiotensin II receptors during early renal morphogenesis
Authors: Norwood V. F. , Craig M. R. , Harris J. M. , Gomez R. A.
Published: December 2017

Angiotensin II (ANG II) and its receptors, AT1 and AT2, may modulate kidney development. To define the temporal and spatial distribution of AT1 and AT2 receptors and their mRNAs during nephrogenesis, fetal, newborn, and adult rat kidneys were studied using reverse transcription-polymerase chain reaction and radioligand binding autoradiography. AT1 expression was minimal at embryonic day 14 (E14), highly expressed at E20, and persisted into adulthood. Conversely, AT2 expression was easily detected from E14 through postnatal day 7 but was undetectable by postnatal day 28. At E14, 76% of the receptors were AT2, 24% were AT1, and both were found in the undifferentiated mesenchyme. By E17, AT1 comprised 40% of the receptors and localized to mature nephron segments, whereas AT2 remained within both condensed mesenchyme and differentiating epithelia. The dissociation constants for AT1 and AT2 were 0.45 +/- 0.09 nM and 0.73 +/- 0.15 nM, respectively, at E17, similar to adult values. By E20, AT1 and AT2 colocalized to the outer medullary stripe, deep nephrons, medullary rays, and blood vessels, while AT2 continued to predominate in the actively differentiating cortex. The presence of both subtypes of receptors capable of binding ANG II during early nephrogenesis and the time-dependent and structure-specific regulation of receptor localization confirm a regulated developmental program for receptor expression and suggest important roles for AT1 and AT2 in renal morphogenesis.
Operant control of ambient temperature during sleep deprivation
Authors: Shaw P. J. , Bergmann B. M. , Rechtschaffen A.
Published: December 2017

Rats subjected to total sleep deprivation (TSD) by the disk-over-water method were provided with a continuously available operant by which they could increase ambient temperature (T(amb)). TSD rats progressively increased operant responses for heat to 700% of baseline levels. During the last quarter of sleep deprivation, they maintained mean T(amb) at 9 degrees C above baseline and held T(amb) over 40 degrees C for 35% of the day. In contrast, yoked control rats (TSC) did not change mean T(amb). Although both TSD and TSC rats showed a progressive decline in intraperitoneal temperature (T(ip)), TSD rats maintained an elevated T(amb) even during periods when T(ip) and brain temperatures (T(br)) were above baseline levels. Thus these results confirm and extend earlier findings that rats subjected to TSD show an increase in temperature set point (T(set)). The earlier studies, which utilized short daily trials in a thermal gradient, demonstrated an increase in T(set) early in the deprivation period. The present study, which obtained more extensive data on thermal preference at a range of body temperatures demonstrated an increasing T(amb) for almost all T(ip) and T(br) values, suggesting a progressive increase in T(set) over the course of sleep deprivation. Surprisingly, survival time was shorter than in previous TSD studies. Reduced survival could not be attributed to differences in T(br), T(ip), energy expenditure, or sleep loss from previous studies.
Purification, structural characterization, and cardiovascular activity of cod bradykinins
Authors: Platzack B. , Conlon J. M.
Published: December 2017

Incubation of plasma from the Atlantic cod Gadus morhua with trypsin generated two peptides identified as [Trp5,Leu8]bradykinin (cod BK) and [Arg0,Trp5,Leu8]bradykinin (cod [Arg0]BK). Bolus intraarterial injections of synthetic cod [Arg0]BK (0.1-10 nmol/kg) into conscious cod produced an immediate increase in ventral aortic pressure that was of relatively short duration (<5 min) and an increase in heart rate. Cod [Arg0]BK was approximately 10 times more potent than cod BK, and the maximal pressor response produced by the peptide was significantly (P < 0.05) greater. Bolus intra-arterial injections of either mammalian BK or cod des-Arg9,[Arg0]BK, in doses up to 100 nmol/kg, had no effect on pressure or heart rate. The data indicate that the ligand binding properties of the BK receptors in cod are different from those of the mammalian B1- and B2-receptor subtypes. The pressor response to 1 nmol/kg cod [Arg0]BK was reduced (by 51 +/- 6%; P < 0.05) in prasozin-treated fish, whereas in enalapril-treated fish, the response to the peptide was enhanced (by 42 +/- 12%; P < 0.05). The data indicate an involvement of catecholamines but not an activation of the renin-angiotensin system in mediating the vasopressor action of BK in the cod.
Inhibition of tumor necrosis factor prevents warming-induced sleep responses in rabbits
Authors: Takahashi S. , Krueger J. M.
Published: December 2017

Tumor necrosis factor (TNF) is a key regulatory component of sleep. In the present study, we determined the effects of intracerebroventricular injection of a TNF inhibitor, a soluble TNF receptor fragment (TNF-RF), on sleep responses of rabbits during and after exposure to mild increases in ambient temperature (T(amb)). Each rabbit (n = 8) was recorded under three conditions: 1) normal T(amb) (21 degrees C) with pyrogen-free saline (PFS), 50 microl i.c.v.; 2) 27 degrees C T(amb) with PFS, intracerebroventricularly; and 3) 27 degrees C T(amb) with the TNF-RF, 50 microg i.c.v. When T(amb) was increased to 27 degrees C from 21 degrees C, it was kept at that temperature for 6 h after injection. The higher T(amb) alone significantly increased non-rapid eye movement sleep, decreased rapid eye movement sleep, and increased brain temperature (T(br)) across the 23-h recording period. Electroencephalogram slow-wave activity was also significantly enhanced during the 6-h warming period. In contrast, all of the sleep responses associated with the higher T(amb) were absent if rabbits were pretreated with the TNF-RF. The elevated T(br) during the higher T(amb) was not affected by the TNF-RF. The present results suggest that brain TNF is involved in the mild increases in T(amb)-induced sleep responses.
Role of endotoxin in the response to experimentally induced bacteremia in chronically prepared rats
Authors: Carlson D. E. , Babus J. K. , Nguyuza N. , Melhem-Stancofski H. , Eastridge B. J.
Published: December 2017

Chronically prepared rats were injected intravenously with live Escherichia coli in doses from approximately 10(5) to approximately 10(9) colony-forming units (CFU). Significant dose-related increase in plasma adrenocorticotropin and corticosterone occurred after approximately 10(7) CFU. Fever occurred after approximately 10(7) CFU but not after approximately 10(9) CFU. These responses changed significantly but were not blocked completely when > 94% of the viable E. coli was removed from the inoculates. The remaining endotoxin activity in the inoculates resembled lipopolysaccharide (LPS) extracted from the same strain of E. coli on electrophoretic gels. Plasma endotoxin increased for > or = 240 min to 5.1 +/- 0.9 endotoxin units (EU)/ml after approximately 10(7) CFU and to 440 +/- 59 EU/ml after approximately 10(9) CFU. Endotoxin at approximately 10(9) CFU caused death within 24 h that was not predicted by the total activity of endotoxin that was injected. In contrast, extracted LPS with its strain and total activity matched to approximately 10(7) CFU mimicked the responses to this nonfatal dose. The total endotoxin activity of the injected bacteria appears to account for the effects of nonfatal doses of E. coli but not for the effects of fatal doses.