bluuebunny/crossref_metadata_2025 huggingface dataset:
Role of renal interstitial hydrostatic pressure in natriuretic response to ANP
Authors: Garcia-Estan J. , Roman R. J.
Published: December 2017

The present study evaluated the role of changes in renal interstitial hydrostatic pressure (RIHP) in the natriuretic response to atriopeptin III (AP III). In control animals, infusion of AP III (100 ng.kg-1.min-1 iv) increased fractional excretion of sodium, potassium, lithium, and water while glomerular filtration rate and renal blood flow were unaltered. The natriuretic response to AP III was associated with a significant elevation in RIHP from 5.6 +/- 0.8 to 8.1 +/- 1.0 mmHg. In rats pretreated with amiloride (1 mg/kg) to block sodium transport in the collecting duct, basal sodium excretion was elevated, but infusion of AP III still increased RIHP and the fractional excretion of sodium, water, and lithium by the same amount as was observed in the control animals. Removal of the renal capsule completely blocked the rise in interstitial pressure in the renal cortex in amiloride-treated rats, but it did not eliminate the elevation in sodium, water, and lithium excretion produced by AP III. To determine whether changes in renal medullary interstitial pressure could play a role in the residual natriuretic response to AP III in these animals, cortical and medullary interstitial pressure were simultaneously measured in rats with a decapsulated kidney. In this group, AP III increased renal medullary interstitial pressure, while cortical interstitial pressure was unaltered. These results are consistent with the view that changes in renal medullary hemodynamics and RIHP contribute to the natriuretic effect of atrial natriuretic peptide by elevating distal delivery of sodium from deep nephrons.
Acid-base-electrolyte balance responses to catecholamine antagonists in Ambystoma tigrinum
Authors: Stiffler D. F. , Kopecky M. E. , Thompson M. L. , Boutilier R. G.
Published: December 2017

Neotenic larval Ambystoma tigrinum were subjected to hypercapnia (3% CO2, 22 Torr) for 24 h under different conditions: alpha-adrenergic blockade using phentolamine, beta-adrenergic blockade using propranolol, and sham treatments. The sham animals were able to carry out a partial extracellular pH compensation that consisted of an increase in extracellular [HCO3-]. Animals treated with catecholamine antagonists did not compensate to the same extent. Analysis of plasma samples by high-performance liquid chromatography with electrochemical detection revealed a significant increase in circulating norepinephrine, but not epinephrine, during the high-CO2 exposure. Measurements of cutaneous ion transport showed that beta-antagonists block the increased Na+ influx associated with hypercapnia, whereas alpha-antagonists inhibited the decrease in cutaneous Cl- influx that is also associated with respiratory acidosis. Additionally, both alpha- and beta-blockers inhibited the increase in transcutaneous potential difference that accompanied the respiratory acidosis. The results are consistent with a role for circulating catecholamines in compensatory ion transport responses to respiratory acidosis in this species.
Effect of cholecystokinin on taste responsiveness in rats
Authors: Giza B. K. , Scott T. R. , Antonucci R. F.
Published: December 2017

Alterations in taste responsiveness have been suggested to mediate the suppression of feeding that accompanies exogenous administration of cholecystokinin (CCK). We tested this possibility in electrophysiological and behavioral experiments. First we monitored taste-evoked activity in the nucleus tractus solitarii of anesthetized rats during intravenous injection of 2 or 6 micrograms/kg of CCK or vehicle. We found no significant effects on taste activity during the 30-min period after CCK administration. Then we employed a conditioned taste-aversion paradigm to measure the rat's perceived intensity of a series of glucose concentrations under the same three experimental conditions. At 2 micrograms/kg, CCK had no effect; at 6 micrograms/kg there was a significant increase in the perceived intensity of 2 of the 15 test solutions, which we attribute to elevated vagal tone. The potential contribution of gastric distension was eliminated in the electrophysiological study and was minimized by brief exposures to stimuli in the behavioral experiment. Thus CCK administration, in the absence of significant gastric distension, does not appear to alter taste responsiveness.
17 beta-Estradiol augments endothelium-dependent contractions to arachidonic acid in rabbit aorta
Authors: Miller V. M. , Vanhoutte P. M.
Published: December 2017

Experiments were designed to determine the effects of chronic estrogen treatment on endothelium-dependent responses to arachidonic acid in the aorta of the rabbit. Ovariectomized rabbits were treated with either placebo or 17 beta-estradiol for 14 days. The aortas were removed, and rings cut from each blood vessel were suspended for measurement of isometric force. In rings contracted with a submaximal concentration of norepinephrine, endothelium-dependent contractions to arachidonic acid were augmented by estrogen treatment. Prostaglandin F2 alpha, E2, the thromboxane analogue U 46619, and prostacyclin contracted aortic smooth muscle. Only the contractions to prostacyclin were augmented by estrogen treatment. Estrogen treatment enhanced the contractions to norepinephrine in aortas with, but not in those without, endothelium; these contractions were not affected by inhibition of uptake of the neurotransmitter. Indomethacin inhibited contractions to norepinephrine in rings with endothelium from estrogen-treated rabbits. These results indicate that chronic treatment with estrogens can affect arterial reactivity to norepinephrine through an endothelium-dependent mechanism that may involve the metabolism of arachidonic acid by cyclooxygenase. The altered sensitivity of the smooth muscle to prostacyclin may contribute in part to the augmented contractions to arachidonic acid with estrogen treatment.
Effects of temperature and concomitant change in pH on muscle
Authors: Stevens E. D. , Godt R. E.
Published: December 2017

Contractile performance decreases with a decrease in temperature and increases with an increase in pH. In general, a decrease in ambient temperature is associated with an increase of the pH of the intracellular and extracellular fluids of ectotherms. Thus the concomitant increase in pH will to some extent counteract the effect of the decrease in temperature. We review the magnitude of this effect and show that it is modest for force (24%) but is small or negligible for speed or for variables involving time. Experiments with skinned fibers yield similar results to those with intact fibers. We argue that one important effect of the concomitant increase in pH is that it causes an increase in calcium sensitivity and that there may be a considerable metabolic saving associated with releasing less calcium at lower temperatures.
Sleep apneas and cardiac arrhythmias in freely moving rats
Authors: Sato T. , Saito H. , Seto K. , Takatsuji H.
Published: December 2017

We studied the mechanisms of occurrences of apneas and bradyarrhythmias during sleep in five Wistar-Kyoto rats. We recorded electroencephalograms, electrocardiograms, chest wall movement, and diaphragmatic electromyograms (EMGdi) for three continuous days in each freely moving rat and demonstrated that: 1) 99% of the apneas and 99% of the bradyarrhythmias occurred during paradoxical sleep (PS), 2) 98% of the apneas were due to spontaneous cessations of respiratory drive, 3) the percentages among apneas accompanied with bradyarrhythmias were only about 30% and independent of the apneic durations, 4) every autoregressive power spectrum contained two significant components in the ranges of 50-80 and 110-140 Hz, which would be analogous to high-frequency oscillations postulated to originate in the synaptic input to the phrenic motoneurons from respiratory centers, and 5) spectral patterns of EMGdi signals varied with sleep states. These results suggest that "PS-related" neural activity modulating central respiratory output is important in inducing apneas and promoting bradyarrhythmias.
ADH, renal, and circulatory responses to adrenergic stimulation in anterior third ventricle
Authors: Simon-Oppermann C. , Gunther O.
Published: December 2017

The anterodorsal part of the third ventricle of conscious ducks was perfused intracerebroventricularly (icv) for 10 min with norepinephrine (NE) or with its agonists phenylephrine (alpha 1, Phe), isoproterenol (beta, Iso), and clonidine (alpha 2, Clo) in artificial CSF (aCSF). Their effects on the plasma level of antidiuretic hormone (AVT, arginine vasotocin in birds), urine excretion, heart rate (HR), and mean arterial pressure (MAP) were investigated in steady-state water diuresis. The correct position of the icv cannula was confirmed by enhanced AVT release and antidiuresis in response to icv perfusion of aCSF made hypertonic (400 mosmol/kgH2O) by adding NaCl. Icv perfusion with hypertonic aCSF and 750 ng/min NE had comparable effects on AVT release and urine excretion, but hypertonic aCSF caused small increases in MAP and HR, whereas NE depressed both MAP and HR. Antidiuresis and circulatory depression caused by NE icv perfusion was dose dependent. Among the adrenergic agonists perfused at similar doses (188 ng/min), only Iso stimulated AVT release. Iso and Phe had small depressive effects on MAP and HR (less than 10%). Clo depressed circulation by greater than 20% for longer than 60 min, and AVT release became significantly reduced 30 min after the start of icv perfusion. The consistent results in ducks contrast with the equivocal data hitherto reported for central stimulations with NE or its agonists in mammals and may be due to the concentric perfusion system used in our study for localized stimulations in the vicinity of the paraventricular nucleus.
Progesterone-cortisol interaction in control of renin activity but not aldosterone
Authors: Keller-Wood M. , Silbiger J. , Wood C. E.
Published: December 2017

In addition to its effect of inhibiting adrenocorticotropic hormone (ACTH) secretion, cortisol (hydrocortisone) inhibits the renin-angiotensin system in both fetal and adult sheep. We have found that progesterone attenuates the inhibition of ACTH by cortisol. These studies test whether progesterone interacts with cortisol in control of the renin-angiotensin-aldosterone system. Conscious adult ewes were infused with vehicle, cortisol (4 micrograms.kg-1.min-1), progesterone (0.5 microgram.kg-1.min-1), or cortisol with progesterone for 60 min. Beginning 120 min after the start of the infusion, renin secretion was stimulated by infusing sodium nitroprusside (10 micrograms.kg-1.min-1 iv). Cortisol infusion decreased plasma K+ concentration and reduced the plasma renin activity (PRA) and aldosterone responses to nitroprusside. Progesterone alone had no effect on PRA, aldosterone, or K+. Progesterone reduced the inhibition of PRA, but not aldosterone or K+, by cortisol. The data also indicate that the suppression of renin, as well as the suppression of ACTH, involves receptors or intracellular mechanisms with which progesterone interacts, whereas the inhibition of aldosterone involves a mechanism that progesterone does not affect.
Ca2+ transport in myocardial sarcolemma from rainbow trout
Authors: Tibbits G. F. , Kashihara H. , Thomas M. J. , Keen J. E. , Farrell A. P.
Published: December 2017

Sacrolemmal vesicles were isolated from trout ventricles with a yield of 0.51 mg protein/g wet wt of a fraction enriched approximately 15-fold over the crude homogenate as estimated by K(+)-stimulated p-nitrophenylphosphatase (K(+)-pNPPase) activity. Although the K(+)-pNPPase specific activity compared favorably with that of the rat heart, there were some striking differences in the sodium dodecyl sulfate-polyacrylamide gel electrophoresis and specific phospholipid content (mumol/mg protein) of the sacrolemmal fractions between the two species. Two major sarcolemmal Ca2(+)-transport proteins were investigated, the Na(+)-Ca2+ exchanger and the dihydropyridine (DHP) receptor, a component of the voltage-dependent L-type Ca2+ channel. From the initial rates of Na(+)-dependent Ca2+ uptake, it was determined that the exchanger has an apparent Km for Ca2+ of 14 +/- 1 microM and a maximum velocity of 7.7 +/- 1.1 nmol.mg protein-1.s-1 at 21 degrees C. Experiments using the DHP ligand [3H] (+) PN 200-110 to characterize the equilibrium binding to the DHP receptor in the sarcolemmal fraction yielded a Kd of 0.08 nM and maximum binding sites of 3.06 +/- 0.49 pmol/mg protein. Given the smaller dimensions of the trout myocyte and the resultant higher sarcolemmal surface to cytosolic volume compared with the mammalian myocyte, these in vitro findings are consistent with the notion that Ca2+ transport across sarcolemma is a quantitatively important contributor of Ca2+ delivery to and removal from the contractile element.
Hypothalamic paraventricular nucleus lesions do not prevent anorectic effect of exercise in male rats
Authors: Rivest S. , Richard D.
Published: December 2017

The effects of a hypothalamic paraventricular nucleus (PVN) lesion on energy balance were investigated in exercise-trained rats. Male Wistar rats weighing initially 250 g were divided into four groups. Two groups of rats underwent a bilateral PVN lesion, whereas the two remaining groups were sham operated. The PVN lesions were done electrolytically. One group from each surgical treatment was exercised, while the other group was kept in sedentary conditions. Rats were exercised on a rodent motor-driven treadmill at moderate intensity, 1 h/day for 21 consecutive days. Food intake and body weight were measured each day during the study. At the end of the treatment period, rats were killed, and carcasses were analyzed for their energy content. Serum corticosterone was measured by a competitive protein-binding assay. Energy gain and energy intake were lower in exercised rats than in sedentary controls, regardless of whether they were sham or PVN lesioned. Concurrently, there was no difference in the energy gain between PVN-lesioned and sham-operated rats, despite the fact that PVN-lesioned rats ended the experiment with a larger body weight than the sham-lesioned animals. Serum corticosterone levels were lower in PVN-lesioned rats than in sham-lesioned rats. In conclusion, the present results indicate that the PVN, the hypothalamic nucleus predominantly controlling the pituitary-adrenal axis activity, is not a prominent structure in the regulation of energy balance in exercised male Wistar rats.
Permeability changes at blood-retinal barrier in diabetes and effect of aldose reductase inhibition
Authors: Lightman S. , Pinter G. , Yuen L. , Bradbury M.
Published: December 2017

Sensitive quantitative in vivo techniques were used to assess the permeability at the blood-retinal barrier (BRB) to [14C]sucrose in the anesthetized streptozocin-diabetic rat at various time points (3 wk, 6 mo, 13 mo) after induction of diabetes. The effects of concomitant administration of an aldose reductase inhibitor (ARI) on sorbitol levels in the retina and on BRB permeability were also measured. No increase in BRB permeability was found in rats diabetic for 3 wk or 6 mo, but after 13 mo of hyperglycemia there was an increase in permeability of 240%. No effect on permeability was seen in diabetic animals given the ARI despite the retinal sorbitol levels being decreased in the treated compared with the untreated diabetic group fed a normal diet. This study suggests that the accumulation of sorbitol within the cells of the BRB is not responsible for the breakdown of BRB permeability seen after 7-13 mo of hyperglycemia and that the enzyme aldose reductase is not involved in its pathogenesis.
Effect of dietary limiting amino acid in prepyriform cortex on food intake
Authors: Beverly J. L. , Gietzen D. W. , Rogers Q. R.
Published: December 2017

The mechanisms underlying the reduced intake of an amino acid-imbalanced diet (imbalanced diet) appears to involve a decrease in the content of the dietary limiting amino acid (DLAA) in the prepyriform cortex (PPC). Intake of imbalanced diet was increased from 45-50 to 70-75% of baseline after bilateral injection of the DLAA directly into the PPC, following an inverted U-shaped dose-response curve. Injections had no effect on intake of basal diets. Injection of the DLAA into the PPC reversed the aversion to imbalanced diet in choice studies, as rats selected an imbalanced diet over protein-free diet after such injections. Intake of imbalanced diet did not increase after a nonlimiting amino acid was injected into the PPC or after injections of the DLAA into other brain areas. Results were similar when either threonine or isoleucine was the DLAA. These results confirm that the decrease in the concentration of the DLAA in the PPC is involved in the reduction in intake of imbalanced diets.
Atrial natriuretic peptide infusion causes vasoconstriction after autonomic blockade in conscious dogs
Authors: Woods R. L. , Anderson W. P.
Published: December 2017

Many studies have shown that atrial natriuretic peptide (ANP) reduces mean arterial pressure (MAP) in conscious animals by lowering cardiac output (CO) with no change or even increased total peripheral resistance (TPR). Because ANP is thought to be a vasodilator, the lack of fall in TPR in conscious animals is generally considered to be due to autonomic reflex increases in vascular resistance. In the present study in conscious, trained, chronically instrumented dogs (n = 7), we measured hemodynamic and renal excretory responses to 30-min infusions of alpha-human ANP (alpha hANP; 25, 50, and 100 ng.kg-1.min-1) in the presence and absence of autonomic nervous system blockade using the ganglion blocking agent pentolinium. In the absence of blockade, MAP and CO fell, whereas TPR rose with alpha hANP infusions, but these changes did not reach significance. There were significant increases in renal vascular resistance (RVR; 16-25%) and mesenteric vascular resistance (MVR; 14-40%). During autonomic nervous system blockade, alpha hANP caused dose-related reductions in MAP (7-12%), due to falls in CO (13-34%). Remarkably, the absence of autonomic reflex responses exposed substantial dose-related increases in TPR (5-33%). Autonomic blockade did not alter the ANP-induced increases in MVR but did abolish the rises in RVR. In summary, ANP caused vasoconstriction in mesenteric vasculature and substantial vasoconstriction in other nonrenal areas, independent of autonomic reflexes.
Responses of harbor seal and pig heart to progressive and acute hypoxia
Authors: White F. C. , Elsner R. , Willford D. , Hill E. , Merhoff E.
Published: December 2017

Myocardial oxidative and glycolytic reserves were evaluated in four harbor seals, Phoca vitulina richardsi, and six domestic pigs, Sus scrofa (hematocrits: 58 +/- 5 and 34 +/- 1%., respectively). Progressive hypoxia was induced by lowering arterial hemoglobin-oxygen saturation in 10% decrements, each maintained for 10-min periods, until the onset of heart failure. Myocardial oxygen consumption rate (VO2), lactate release/uptake rate (L), and triple product, an index of myocardial energetic demand, were determined at each saturation level. Onset of L began in pigs at Sao2 = 57 +/- 5% and in seals at Sao2 = 35 +/- 4%. Cumulative oxygen consumption (VO2) during hypoxia, determined from the onset of cardiac lactate release, was 435 ml O2/100 g in seals and 172 ml O2/100 g in pigs. Cumulative lactate release during the same period was 14 mM/100 g in seals and 4.6 mM/100 g in pigs. The pigs' left ventricular contractile response (dP/dtmax) was greater than that of seals throughout the time of lactate release. Total myocardial energetic sources were higher in seals than in pigs, and seals were better able to tolerate myocardial hypoxia than were pigs. In a separate experiment, two seals and six pigs were made acutely hypoxic until cessation of cardiac output (seals, 17.5 min; pigs, 7.4 min) and were then reoxygenated. Both seals recovered promptly to control levels of cardiac mechanical function, whereas none of the pigs recovered. Additionally, five pigs were beta-blocked with 0.10 mg/kg of propranolol and were subjected to acute hypoxia. Tolerance to cardiac hypoxia in beta-blocked pigs was significantly increased compared with that of control animals.(ABSTRACT TRUNCATED AT 250 WORDS)
Vasopressin and oxytocin in rat brain in response to prostaglandin fever
Authors: Landgraf R. , Malkinson T. J. , Veale W. L. , Lederis K. , Pittman Q. J.
Published: December 2017

Urethan-anesthetized rats were used to identify effective stimuli for the release of the peptides arginine vasopressin (AVP) and oxytocin into the ventral septal area (VSA) of the brain. Febrile responses to intracerebroventricular injection of prostaglandin E1 (PGE1) were observed in rats whose body temperatures were maintained at 35, 37, or 39 degrees C. Microinjection of the AVP antagonist d(CH2)5Tyr(Me)AVP into the VSA enhanced fever only when PGE1 administration was associated with a significant rise in body temperature. Passive elevation (“artificial fever”) or reduction of body temperature in the absence of a PGE1 stimulus was not affected by the antagonist. Push-pull perfusion of the VSA and the dorsal hippocampus, followed by radioimmunoassay of perfusates for AVP and oxytocin, revealed enhanced release into the VSA of AVP only when PGE1 administration was followed by a rise in body temperature. Oxytocin was released whenever body temperature was raised. Peptide concentrations in simultaneous perfusates of dorsal hippocampus did not change in response to PGE1 administration or to passive elevation of body temperature. We conclude that AVP is released into the VSA, but not the dorsal hippocampus, of the rat during a fever induced by PGE1. Oxytocin is released into the VSA, but not the hippocampus, when temperature is elevated.
Simulation of mechanoenergetics of asynchronously contracting ventricle
Authors: Suga H. , Goto Y. , Yaku H. , Futaki S. , Ohgoshi Y. , Kawaguchi O.
Published: December 2017

We simulated mechanoenergetics of ventricular asynchronous contraction using a model comprising two compartmentalized asynchronous time-varying elastic elements, E1 and E2. Their elastances [e1(t) and e2(t)] waxed and waned cyclically with a variable time lag (tau). The pressure-volume area (PVA1 or PVA2) circumscribed by the maximum (emax) and minimum e1(t) or e2(t) lines and the contracting pressure-volume trajectory of E1 or E2 quantifies the mechanical energy generated by a contraction of E1 or E2. Similarly, the PVA circumscribed by the resultant Emax (ventricular contractility index) line, the end-diastolic pressure-volume (P-V) line, and the systolic P-V trajectory quantifies the mechanical energy of the entire ventricle. PVA of the ventricle is equal to the sum of PVA1 and PVA2. We found that Emax decreased with increases in tau despite constant emax, and hence ventricular PVA decreased with increases in tau. This simulation helps us to better understand the mechanism of decreased oxygen consumption with increasing ventricular asynchrony reported in the literature.
Mechanisms of pressor response produced by stimulation of nucleus ambiguus
Authors: Machado B. H. , Brody M. J.
Published: December 2017

We showed previously that activation of nucleus ambiguus (NA) induced bradycardia and increased arterial pressure. In this study, we compared responses produced by electrical and chemical (glutamate) stimulation of NA and adjacent rostral ventrolateral medulla (RVLM). Equivalent pressor responses were elicited from both areas. However: 1) The response from RVLM was elicited at a lower frequency. 2) Regional vascular resistance changes were different, i.e., electrical stimulation of NA increased vascular resistance in hindquarters much more than the renal and mesenteric beds. In contrast, electrical and chemical stimulation of RVLM produced a more prominent effect on the renal vascular bed. 3) Bradycardia was elicited from NA at lower current intensity. 4) Glutamate produced bradycardia only when injected into NA. Studies in rats with sinoaortic deafferentation showed that bradycardic response to activation of NA was only partly reflex in origin. We conclude that 1) NA and RVLM control sympathetic outflow to regional vascular beds differentially and 2) the NA region involves parasympathetic control of heart rate and sympathetic control of arterial pressure.
Quantitative genetics of maximal oxygen consumption in a garter snake
Authors: Garland T. , Bennett A. F.
Published: December 2017

Broad-sense heritabilities and genetic correlations of maximal oxygen consumption (VO2max), blood hemoglobin levels, and ventricle mass were estimated in a natural population of snakes. Traits were measured for six or fewer presumed full-sibling offspring from each of 45 wild-caught gravid garter snakes (Thamnophis sirtalis). VO2max was highly reproducible between replicate trial days (r = 0.88). In an attempt to reduce maternal effects, correlations of each character with body mass, snout-vent length, age at testing, litter size, dam mass, and dam snout-vent length were removed by computing residuals from multiple-regression equations. These residuals were used in subsequent genetic analyses. Approximate coefficients of variation of residuals were 16% for VO2max, 19% for hemoglobin level, and 13% for ventricle mass. Broad-sense heritabilities were highly significant for all characters [P less than 0.0001; VO2max heritability (h2) = 0.88; hemoglobin level h2 = 0.63; ventricle mass h2 = 0.41], suggesting that they could respond genetically to selection. Phenotypic correlations (rP) among residual characters were significant only between VO2max and ventricle mass (rP = +0.27). VO2max and ventricle mass exhibited a significant (broad-sense) genetic correlation of +0.64; this might facilitate the correlated evolution of these two traits in response to natural or artificial selection. Ventricle mass and hemoglobin level showed a significant environmental correlation of +0.43. Treadmill endurance crawling time (Evolution 42: 335-350, 1988) showed a weak but significantly positive rP with VO2max (rP = +0.17).
Diminished epinephrine response to hypoglycemia despite enlarged adrenal medulla in trained rats
Authors: Stallknecht B. , Kjaer M. , Mikines K. J. , Maroun L. , Ploug T. , Ohkuwa T. , Vinten J. , Galbo H.
Published: December 2017

Studies in humans have indicated that trained athletes compared with sedentary subjects have an increased capacity to secrete epinephrine. To investigate whether this is due to an adaptation induced by physical training or a selection phenomenon, rats were swim trained (T) 10 wk for 6 h/day or served as controls being either sedentary freely eating (C), food restricted (FR), sham swim trained (ST), or cold stressed (CS). Adrenal glands were weighted and cross sectioned for light microscopic determination of size of the adrenal medulla. Endurance-trained compared with control rats had heavier adrenal glands (P less than 0.05), higher catecholamine content in the glands (P less than 0.05), and higher adrenal medulla volumes (P less than 0.05) [males: 2.74 +/- 0.16 (T) vs. 2.05 +/- 0.16 (C), 1.90 +/- 0.10 (ST), and 2.21 +/- 0.08 mm3 (CS)] [females: 2.55 +/- 0.11 (T) vs. 1.92 +/- 0.06 mm3 (C)]. Cold stress or sham swim training did not increase adrenal weight or volume of adrenal medulla (P greater than 0.05). To stimulate adrenal medulla secretion, rats had an insulin-induced hypoglycemia. Insulin dose needed to suppress plasma glucose below 4.0 mM was four times greater in sedentary compared with trained rats. During hypoglycemia the epinephrine response was much smaller in trained than in untrained rats (P less than 0.05). In conclusion, in rats strenuous endurance training causes an enlargement of the adrenal medulla. However, possibly reflecting an adaptation within the central nervous system to reduced blood glucose levels induced by repeated exercise bouts, the epinephrine response to insulin-induced hypoglycemia is markedly diminished after training.
Obese and lean Zucker rats differ in preferences for sham-fed corn oil or sucrose
Authors: Greenberg D. , Weatherford S. C.
Published: December 2017

Obese Zucker rats show greater preference for fatty foods in dietary selection studies than do lean rats. We wished to evaluate the preference for dietary fats in Zucker rats in the absence of postingestive cues. Zucker rats (6 lean and 6 obese) were fitted with gastric cannulas for sham feeding. All sham-feeding tests lasted for 30 min. On training days, rats were sham fed 100% corn oil or, on alternate days, rats were sham fed various concentrations of sucrose in volumes yoked to intakes of corn oil. On preference test days, rats were offered 100% corn oil and one sucrose concentration simultaneously for sham feeding. During preference tests, obese rats preferred 100% corn oil to 10% sucrose, whereas lean rats preferred 10% sucrose to 100% corn oil. Obese rats equally preferred 17.5% sucrose and 100% corn oil, whereas lean Zucker rats equally preferred 2.5% sucrose and 100% corn oil. When sucrose concentration was increased to 20% both obese and lean Zucker rats preferred sucrose to 100% corn oil. These results combined with our previously reported results showing that intraduodenally administered fats do not differ in satiating potency for obese and lean Zucker rats (6) strongly suggest that the preference of obese rats for fatty foods is largely mediated by orosensory mechanisms.
Effect of weight cycling on susceptibility to dietary obesity
Authors: Graham B. , Chang S. , Lin D. , Yakubu F. , Hill J. O.
Published: December 2017

Weight cycling, defined as repeated episodes of weight loss followed by weight regain, has been suggested to make rats more energy efficient and produce a state of energy balance favoring accumulation of excess body fat. In addition, weight cycling may favor accumulation of fat in central vs. peripheral adipose depots. In the present study, we gave two groups of female Wistar rats ad libitum access to an obesity-producing high-fat diet (60% of calories from fat). Both groups had previously eaten a low-fat stock diet, but one group had been subjected to three bouts of weight cycling. Rats that were previously weight cycled gained less body weight and body fat when given the high-fat diet than did controls. The lower rate of weight gain was due to a lesser increase in food intake, since daily energy expenditure was significantly lower in previously cycled rats than in controls. In summary, weight cycling does not appear to predispose rats to becoming obese on a high-calorie diet and apparently produces some effect on food intake that reduces, at least in the short run, weight gain on the high-calorie diet.
Cardiovascular and sensory responses to forearm ischemia and dynamic hand exercise
Authors: Maixner W. , Gracely R. H. , Zuniga J. R. , Humphrey C. B. , Bloodworth G. R.
Published: December 2017

The relationship between cardiovascular responses and pain produced by the submaximal-effort tourniquet procedure was evaluated in healthy humans. Graded increases in ischemic pain were associated with graded elevations in arterial blood pressure, forearm vascular resistance, and venous tone. Many of the vascular responses to muscle ischemia were typical of the cardiovascular components of the defense reaction and correlated with both the sensory and affective aspects of ischemic pain. The cardiovascular responses to arm ischemia were distinguishable from those produced by rhythmic hand exercise used to produce ischemia. Dynamic hand exercise produced a transient increase in arterial blood pressure, heart rate, and measures of hand discomfort. These responses were enhanced when dynamic hand exercise was conducted under ischemic conditions. The tightly coupled and coordinated cardiovascular responses elicited by ischemic pain represent integrated adaptive responses to painful stimulation.
Effects of portal infusion of hypertonic solution on jejunal electrolyte transport in anesthetized dogs
Authors: Morita H. , Ohyama H. , Hagiike M. , Horiba T. , Miyake K. , Yamanouchi H. , Matsushita K. , Hosomi H.
Published: December 2017

Jejunal electrolyte absorption was measured in the jejunal loops of anesthetized dogs during infusions of hypertonic solutions via the portal vein. The net Na absorption was not influenced by the 9% NaCl infusion into the inferior vena cava, although it was significantly attenuated by the portal 9% NaCl infusion. This effect may not be due to the osmotic stimulus, since the portal 50% glucose or 6.5% LiCl infusion had no significant influence on the net Na absorption. To determine the mechanism of the decrease in the net Na absorption during the portal hypertonic NaCl infusion, the net Na absorption was measured after the section of anterior and posterior hepatic nerves (SAPH) or intravenous atropine injection. Both SAPH and the intravenous atropine injection completely blocked the effect of the portal 9% NaCl infusion on the net Na absorption. These results indicate that 1) net Na absorption in dog jejunum is depressed by the hypertonic NaCl infusion via the portal vein; 2) the effect is NaCl specific and may not be due to the osmotic stimulus; and 3) the afferent limbs of this effect are the anterior and posterior hepatic nerves, and the efferent limb of this effect is the vagus nerve. Thus the hepatojejunal reflex may play an important role in the regulation of body fluid homeostasis.
A renaissance of sulfobromophthalein infusion method for animal studies of hepatobiliary function?
Authors: Mikulecký M. , Quale J.
Published: December 2017

Pages R456–R457: M. Mikuleckyacute; J. Quale. “A renaissance of sulfobromophthalein infusion method for animal studies of hepatobiliary function?” In the Reply to the Letter to the Editor the name of Laura Mandel, who coauthored the Reply, was omitted. The authors of the Reply were John Quale and Laura Mandel.
Kinetic analysis of zinc metabolism in humans after simultaneous administration of 65Zn and 70Zn
Authors: Wastney M. E. , Gokmen I. G. , Aamodt R. L. , Rumble W. F. , Gordon G. E. , Henkin R. I.
Published: December 2017

Zinc kinetics were studied and compared after oral simultaneous administration of two tracers, radioactive (65Zn) and stable (70Zn) isotope, to four normal human volunteers. Both tracers and zinc concentration were measured in plasma, red blood cells (RBC), urine, and feces for up to 78 days. Radioactive zinc was also measured by external counting over whole body, liver, and thigh. Data from each individual were analyzed using a compartmental model for zinc metabolism. Values calculated for absorption, fractional zinc excretion in urine, exchange with RBC, and secretion into gut using 70Zn data did not differ from values calculated using 65Zn data. Results show that human zinc metabolism can be investigated using stable isotopes as tracers to determine parameters of whole body zinc metabolism, including zinc absorption, excretion, and secretion.
Glutamine metabolism in a holostean (Amia calva) and teleost fish (Salvelinus namaycush)
Authors: Chamberlin M. E. , Glemet H. C. , Ballantyne J. S.
Published: December 2017

Amino acid metabolism was examined in mitochondria from the lateral red muscle of a teleost (lake char, Salvelinus namaycush) and a nonteleost fish (bowfin, Amia calva). Isolated mitochondria oxidize a wide variety of substrates and have high respiratory control ratios. In both species, glutamine is oxidized more rapidly than any other amino acid. The rate of glutamine oxidation by bowfin mitochondria exceeds that of lake char mitochondria, and the bowfin displays correspondingly higher levels of mitochondrial phosphate-dependent glutaminase. It is suggested that amino acids in general, and glutamine in particular, are important oxidative substrates for nonteleost red muscle. The teleost red muscle, however, may rely on both glutamine and fatty acids as oxidative substrates. It appears that glutamate derived from glutamine is oxidized primarily via glutamate dehydrogenase, whereas exogenous glutamate is oxidized primarily via aspartate aminotransferase. Complete oxidation of glutamine may be accomplished in the absence of other substrates by conversion of glutamine-derived malate to pyruvate via malic enzyme. To assess the relative abilities of various tissues to synthesize and oxidize glutamine, the activities of glutamine synthetase and glutaminase were measured. The results of these studies indicate that the organization of glutamine metabolism of fish differs markedly from that in mammals.
Differential alterations in plasma IL-6 and TNF levels after trauma and hemorrhage
Authors: Ayala A. , Wang P. , Ba Z. F. , Perrin M. M. , Ertel W. , Chaudry I. H.
Published: December 2017

Tumor necrosis factor (TNF) and interleukin 6 (IL-6) are purported to be important mediators of inflammatory responses. It is not known whether the plasma levels of these cytokines are altered after trauma and hemorrhage. Our objectives were to determine whether there is any elevation of plasma TNF or IL-6 after trauma and hemorrhage and to what extent these changes are due to tissue trauma vs. simple hemorrhage. Trauma was induced in Sprague-Dawley rats under light ether anesthesia by performing a 5-cm midline laparotomy. On closure, animals were catheterized, awakened, hemorrhaged to a mean blood pressure of 40 mmHg, and maintained at that pressure until 40% of maximum shed blood volume was returned in the form of Ringer lactate (RL). Animals were then resuscitated with RL equivalent to four times shed blood volume. Blood samples (0.5 ml) were taken before inducing hemorrhage, at maximal bleed out (45 min), and at 4 and 6 h posthemorrhage to obtain plasma. IL-6 and TNF levels were measured using cytokine-dependent cellular assays. TNF levels were significantly elevated at 45 min into hemorrhage and remained so up to 4 h after hemorrhage. IL-6 levels were also elevated 45 min into hemorrhage and remained so up to 6 h posthemorrhage. IL-6, unlike TNF, was already significantly increased after midline laparotomy and before initiation of hemorrhage compared with unmanipulated animals. Thus induction of IL-6 by trauma may be partially independent of those mechanisms in hemorrhage that are involved in the release of TNF.
Atrial pressure, distension, and pacing frequency in ANP secretion in isolated perfused rabbit atria
Authors: Cho K. W. , Seul K. H. , Kim S. H. , Seul K. M. , Koh G. Y.
Published: December 2017

It has been suggested in this laboratory that the principal stimulus for the secretion of atrial natriuretic peptide (ANP) is the reduction of atrial distension and that the secretion of ANP is dependent on both atrial reduction volume and reduction frequency. To investigate the relationship among the changes in atrial pressure, distension, pacing frequency, and ANP secretion, we performed a series of experiments in the isolated perfused rabbit atria. Increase in atrial pressure without changes in transmural pressure and thus without volume changes did not raise immunoreactive ANP (irANP) secretion. Atrial distension without changes in intracavitary atrial pressure increased irANP secretion with the reduction. Electrical stimulation with atrial distension resulted in an increase in irANP secretion in proportion to pacing frequency. Incremental response of irANP secretion to electrical stimulation was accentuated by increasing atrial distension. Neither atrial pacing without distension nor distension without pacing raised irANP secretion. These results suggest that the direct and principal stimulus for irANP secretion in response to atrial pacing and distension is the length shortening of atrial myocytes and that the incremental response of irANP secretion to increasing pacing frequency is the result of an increase in frequency of the length shortening of atrial myocytes.
Effects of atrial natriuretic peptide on water and NaCl absorption across the intestine
Authors: Matsushita K. , Nishida Y. , Hosomi H. , Tanaka S.
Published: December 2017

Previous studies have demonstrated that atrial natriuretic peptide (ANP) causes natriuresis and diuresis. However, it is not established whether ANP also alters fluid and electrolyte balance via actions on intestinal absorption of water and sodium chloride. Therefore, the purpose of the present study was to investigate the effects of ANP on water and NaCl absorption across the intestine. First, we determined that ANP was taken up from the intestinal circulation in conscious dogs. During the intravenous infusion of ANP (0.3 microgram.kg-1.min-1), 27.4% of the ANP delivered to the intestinal vascular bed were removed from the circulation at that vascular bed, whereas only 1% of the ANP delivered to the hepatic circulation was removed at the hepatic vascular bed. Second, we determined the effects of the ANP infusion on splanchnic circulation in conscious dogs. ANP decreased hepatic arterial blood flow by 14%, portal venous blood flow by 16%, total hepatic blood flow by 15%, and cardiac output by 14%. Finally, we studied the effects of ANP on intestinal absorption of water and NaCl. ANP suppressed net absorption of water by 61%, Na+ by 43%, and Cl- by 42% across the jejunum but not the ileum. These results suggest that ANP modulates water and NaCl homeostasis across the jejunum but not across the ileum.
Elevated central venous pressure: a consequence of exercise training-induced hypervolemia?
Authors: Convertino V. A. , Mack G. W. , Nadel E. R.
Published: December 2017

Resting blood volumes and arterial and central venous pressures (CVP) were measured in 14 men before and after exercise training to determine whether training-induced hypervolemia is accompanied by a change in total vascular capacitance. In addition, resting levels of plasma arginine vasopressin (AVP), atrial natriuretic peptide (ANP), aldosterone (Ald), and norepinephrine (NE) were measured. The same measurements were conducted in seven subjects who did not undergo exercise and acted as controls. Exercise training consisted of 10 wk of controlled cycle exercise for 30 min/day, 4 days/wk at 75-80% of maximal O2 uptake (VO2max). A training effect was verified by a 20% increase in VO2max, a resting bradycardia, and a 9% increase in blood volume. Mean arterial blood pressure was unaltered by exercise training, but resting CVP increased by 16% (P less than 0.05). The percent change in blood volume from before to after training was linearly related to the percent change in CVP (r = 0.903, P less than 0.05). As a consequence of elevations in both blood volume and CVP, the volume-to-pressure ratio was unchanged after exercise training. Plasma AVP, ANP, Ald, and NE were unaltered. Our results indicate that elevated CVP is a consequence of training-induced hypervolemia without alteration in total effective venous capacitance.
Neuropeptide Y suppresses sympathetic activity to interscapular brown adipose tissue in rats
Authors: Egawa M. , Yoshimatsu H. , Bray G. A.
Published: December 2017

To investigate the effects of neuropeptide Y (NPY) on sympathetic nerve activity to interscapular brown adipose tissue (IBAT), we injected NPY into the third cerebroventricle (icv), medial preoptic area (MPOA), anterior hypothalamic area (AHA), paraventricular hypothalamic nucleus (PVN), ventromedial hypothalamic nucleus (VMN), and lateral hypothalamic area (LHA) of anesthetized rats. Multiunit discharges from sympathetic nerves to IBAT were recorded electrophysiologically. The icv injection of NPY suppressed sympathetic nerve activity in a dose-dependent manner, followed by a gradual recovery. The microinjection of NPY (25 pmol) unilaterally into the PVN also significantly suppressed the sympathetic nerve activity to IBAT. In contrast, microinjection of NPY into the MPOA significantly increased the sympathetic nerve activity. The injection of saline into either the PVN or MPOA had no significant effect on sympathetic nerve activity. The microinjection of NPY (25 pmol) into the AHA, VMN, or LHA did not change sympathetic nerve activity to IBAT. We conclude that central administration of NPY affects the sympathetic nerve activity to IBAT and that the suppressive effect of NPY, which may act in part through the PVN, is dominant to the stimulatory effect. The result is consistent with the hypothesis that NPY is a neurochemical modulator of the sympathetic nervous system which controls energy expenditure in IBAT.
Coronary vasoconstriction during stimulation in hypothalamic defense region
Authors: Arthur J. M. , Bonham A. C. , Gutterman D. D. , Gebhart G. F. , Marcus M. L. , Brody M. J.
Published: December 2017

Previous studies have identified a site in lateral hypothalamus (LH) in which electrical stimulation elicits coronary vasoconstriction. We injected the retrogradely transported tracer Fast Blue to determine which brain regions project to LH. Projections to or through LH were found from the paraventricular nucleus (PVN) of the hypothalamus, bed nucleus of the stria terminalis (BNST), and dorsal raphe nucleus (DRN). In chloralose-anesthetized cats, electrical stimulation in DRN and BNST failed to increase coronary vascular resistance (CVR). However, stimulation lateral to PVN in the anterior hypothalamic area (AHA), a region not labeled by the tracer, caused a transient decrease in coronary blood flow similar to that elicited from LH. The increase in CVR was accompanied by hemodynamic changes that are characteristic of the defense reaction including a cholinergically mediated decrease in hindquarter vascular resistance. This response is likely due to activation of fibers of passage and not cell bodies, since cell bodies in the region were not retrogradely labeled and coronary vasoconstriction was not seen following microinjection of several excitatory amino acids into AHA. These data suggest that coronary vasoconstriction may be a component of the defense reaction elicited by electrical activation of AHA.
Fetal renal response to atrial natriuretic factor decreases with maturation
Authors: Castro R. , Ervin M. G. , Leake R. D. , Ross M. G. , Sherman D. J. , Fisher D. A.
Published: December 2017

The presence of atrial natriuretic factor (ANF) in fetal tissues and plasma early in gestation suggests that ANF may have a physiological role in cardiocirculatory homeostasis in utero. However, reported responsiveness of the fetal kidney to ANF varies markedly. To characterize the ontogeny of fetal renal responsiveness to ANF, chronically catheterized ovine fetuses at 114 +/- 1 days (n = 6) and 131 +/- 1 days (n = 6) received successive (30 min each) intravenous infusions of ANF at rates of 5, 25, and 100 ng.min-1.kg-1. Mean (+/- SE) fetal plasma ANF levels increased from 328 +/- 54 to 1,866 +/- 482 and 521 +/- 135 to 1,579 +/- 295 pg/ml in the younger and more mature fetuses, respectively. Mean urine volume (0.17 +/- 0.03 to 0.37 +/- 0.09 ml.min-1.kg-1) and GFR (0.9 +/- 0.2 to 1.8 +/- 0.4 ml.min-1.kg-1) increased in the early gestation fetuses but did not change in the older fetuses. Mean urine sodium excretion and osmolar clearance increased by 352 and 155% in the early gestation fetal lambs and 118 and 50% in the older animals. The fetal plasma ANF clearance rates (PCANF) were lower in the early vs. the late gestation fetuses (68 +/- 15 vs. 116 +/- 28 ml.min-1.kg-1, respectively). These results demonstrate a decrease in fetal renal responsiveness to ANF with advancing fetal age. Multiple factors appear to contribute, including changes in PCANF and maturational changes in glomerular filtration rate, renal tubular function and ANF receptor metabolism.