bluuebunny/crossref_metadata_2025 huggingface dataset:
Skeletal development in newborn and weanling northern elephant seals
Authors: Patterson-Buckendahl P. , Adams S. H. , Morales R. , Jee W. S. , Cann C. E. , Ortiz C. L.
Published: December 2017

The neonatal period in the northern elephant seal (Mirounga angustirostris) differs markedly from that of most mammals. An intense 1-mo nursing period is followed by 2-3 mo during which seal pups consume neither food nor water. Because skeletal development in other species is rapid during this period, we determined the capability of elephant seals to continue skeletal growth under fasting conditions. We analyzed indirect markers of bone turnover [serum osteocalcin and alkaline phosphatase activity and urinary calcium and hydroxyproline (Hyp) excretion] in samples obtained sequentially from live pups throughout the fast. Serum osteocalcin was low at the beginning of the fast, peaked between 17 and 42 days, and then decreased to initial levels after 10 wk. Alkaline phosphatase activity increased linearly through 9 wk of fasting. Urinary calcium was relatively constant through 9 wk but decreased after 10 wk, whereas free and total Hyp decreased linearly. Clearance of 3H-labeled Hyp showed that virtually all (> 99%) free Hyp was oxidized and that only bound Hyp, for which there is no degradative mechanism, was excreted. Kinetics of 45Ca clearance, a direct measurement of mineral turnover, was virtually identical to that for young humans. Histomorphometry of ulnae obtained from pups which died of natural causes (usually trauma inflicted by adult males) indicated active surfaces (osteoid plus eroded) between 30 and 60% of total surface of highly porous bone containing < 60% bone area/tissue area. Thus all indicators of skeletal activity confirmed that young elephant seals continue skeletal development, notwithstanding the prolonged period during which they take in no food or water.
Acute blockage of the ubiquitin-mediated proteolytic pathway during invertebrate quiescence
Authors: Anchordoguy T. J. , Hand S. C.
Published: December 2017

Many organisms withstand adverse environmental conditions by entering a reversible state of quiescence that may last for months or years. In this report we provide evidence that the reduction in adenylate energy status and the associated intracellular acidosis occurring during anoxia-induced quiescence combine to inhibit, directly or indirectly, the initial step in the ubiquitin-mediated proteolytic pathway in embryos of the brine shrimp Artemia franciscana. The levels of ubiquitin-conjugated proteins drop to 37% of control (aerobic) values during the first hour of anoxia and reach 7% in 24 h. ATP falls to 5% of control values under anoxia, and AMP rises reciprocally. This energy limitation is accompanied by a simultaneous depression of intracellular pH (pHi). By comparison, when embryos are subjected to artificial acidosis under aerobic conditions (pHi drops sharply, but ATP does not change for hours), ubiquitin-conjugated proteins decline to 58% after 1 h. Thus, while the proximate mechanism for the suppression of ubiquitination has not been proven, alterations in the adenylate pool and the decrease in pHi both appear to contribute to the suppression of ubiquitination. Western blot analysis indicates that the decline in ubiquitin-conjugated protein is rapidly reversed on return of embryos to control conditions. We conclude that this arrest of ubiquitination likely serves to suppress ubiquitin-mediated degradation of protein, thereby preserving macromolecular integrity and potentially explaining the remarkable extension of protein half-life observed under anoxia in these embryos.
Perinuclear zone and diagonal band lesions enhance angiotensin responses of rat supraoptic neurons
Authors: Cunningham J. T. , Nissen R. , Renaud L. P.
Published: December 2017

Sinoaortic denervation in the rat is associated with an increased sensitivity of vasopressin neurons in the supraoptic nucleus (SON) to peripheral angiotensin II (ANG II). Lesion studies have indicated that the diagonal band of Broca (DBB) and the perinuclear zone of the SON in the lateral hypothalamus (PNZ) are essential components in the central pathway for the baroreceptor inhibition of vasopressin SON neurons. The present study examined the effect of ibotenate lesions in either the DBB or the lateral hypothalamus, which includes the PNZ, on the responses of SON neurons to peripherally administered ANG II (500 pmol/kg ia). Extracellular recordings obtained from vasopressin SON neurons in pentobarbital-anesthetized rats indicate that DBB and PNZ lesions not only interrupted the baroreceptor-mediated inhibition of SON neurons but also significantly increased the excitatory effects of ANG II on putative vasopressin SON neurons. These results suggest that ibotenate lesions of the DBB and the lateral hypothalamus that include the PNZ affect the ANG II-induced activation of putative vasopressin SON neurons in a manner consistent with results obtained from baroreceptor-denervated rats.
Chronic nucleus tractus solitarius lesions do not prevent hypovolemia-induced vasopressin secretion in rats
Authors: Schreihofer A. M. , Stricker E. M. , Sved A. F.
Published: December 2017

The present study examined the hypothesis that hypovolemia stimulates vasopressin (VP) secretion by removing tonic inhibitory baroreceptor input. Serial hemorrhage (4 samples of 2 ml/300 g body wt taken every 10 min) increased plasma VP levels in conscious rats devoid of cardiac and arterial baroreceptor reflex responses due to chronic bilateral lesions of nucleus tractus solitarius (NTS). The VP response to hemorrhage was similar to that seen in control rats and chronic sinoaortic-denervated (SAD) rats. After subcutaneous injection of 30% polyethylene glycol, NTS-lesioned rats, SAD rats, and control rats had elevated VP levels that correlated with the induced depletion of plasma volume. Additionally, in alpha-chloralose-anesthetized control rats, chronic SAD rats, and chronic NTS-lesioned rats, bilateral vagotomy had minimal effects on basal VP levels, and vagotomy in chronic NTS-lesioned rats did not prevent hemorrhage-evoked increases in VP secretion. These results do not support the idea that hemorrhage-induced VP secretion occurs through reduction in tonic inhibitory baroreceptor input. Instead, neither cardiac nor arterial baroreceptor input appears to be necessary for hypovolemia-induced VP secretion in rats.
TxA2 receptor activation elicits organ-specific increases in microvascular permeability in the rat
Authors: Bertolino F. , Valentin J. P. , Maffre M. , Bessac A. M. , John G. W.
Published: December 2017

We investigated whether the stable thromboxane A2 (TxA2) analogue U-46619 had any direct effect on extracellular fluid partition. In anesthetized open-chest rats, U-46619 (1.25 and 20 micrograms/kg iv) dose dependently increased mean pulmonary arterial pressure and hematocrit, whereas mean systemic arterial pressure was raised only at the low dose of agonist. The increase in hematocrit (13.2 +/- 2.9% at 20 micrograms/kg; P < 0.05) still occurred in bilaterally nephrectomized rats and in binephrectomized plus splenectomized rats (11.6 +/- 2.7 and 12.2 +/- 4.6%, respectively; both P = NS vs. U-46619 in control rats), corresponding to a calculated decrease in plasma volume of 22.1 +/- 4.5, 19.6 +/- 4.0, and 19.2 +/- 5.8%, respectively. Plasma protein concentration increased less than hematocrit, and the coefficient of reflection was significantly lower in these groups, suggesting protein extravasation. Additional experiments showed that U-46619 (1.25 and 10 micrograms/kg iv) dose dependently increased the vascular leak of albumin mainly in lung, kidneys, and spleen but not in brain, liver, mesentery, and cardiac and skeletal muscles. Pretreatment with the TxA2 receptor antagonist SQ-29,548 (2.5 mg/kg iv bolus plus 2.5 mg.kg-1.h-1 as maintenance) abolished all effects of U-46619, including the increase in mean pulmonary arterial pressure, hematocrit, plasma protein concentration, and albumin extravasation and the decrease in mean systemic arterial pressure, plasma volume, and coefficient of reflection.(ABSTRACT TRUNCATED AT 250 WORDS)
Osmoregulatory modulation of thermal sweating in humans: reflex effects of drinking
Authors: Takamata A. , Mack G. W. , Gillen C. M. , Jozsi A. C. , Nadel E. R.
Published: December 2017

To gain better insight into the interaction between thermoregulation and osmoregulation, we examined the thermal sweating response to drinking in cell-dehydrated humans. Cell dehydration (CDH) was induced by infusion of a 3% NaCl solution, at 1.2 ml/kg, for 2 h; infusion of a 0.9% NaCl solution in a separate experiment served as a control (euhydrated condition, EH). After infusion, subjects were heated by immersion of the lower legs in 42 degrees C water at an ambient temperature of 28 degrees C for 90 min. Subjects drank 4.3 ml/kg of H2O (approximately 38 degrees C) at 60 min of heating. The 3% NaCl infusion increased plasma osmolality by 13.6 +/- 0.8 mosmol/kgH2O and plasma arginine vasopressin concentration ([AVP]) by 3.3 +/- 0.7 pg/ml. Neither variable was altered with 0.9% NaCl infusion. Before drinking, esophageal temperature (Tes) had increased by 0.91 +/- 0.08 degrees C in CDH and by 0.40 +/- 0.11 degrees C in EH. Local chest sweating rate (SRch) had increased by 0.67 +/- 0.08 and 0.63 +/- 0.07 mg.min-1.cm-2 in CDH and EH, respectively. Thus the change in SRch per unit rise in Tes was much lower in CDH than in EH. Drinking immediately increased SRch and reduced Tes in CDH, with a reduction in plasma [AVP] and thirst rating. Drinking did not change thermoregulatory and osmoregulatory responses in EH. These results suggest that the act of drinking itself eliminates, at least partially, an osmotic inhibitory input to the thermoregulatory center, as well as osmotic AVP secretion and thirst.
Role of epinephrine in TNF and IL-6 production from isolated perfused rat liver
Authors: Liao J. , Keiser J. A. , Scales W. E. , Kunkel S. L. , Kluger M. J.
Published: December 2017

A bidirectional communication exists between the nervous system and the immune system. Evidence has accumulated suggesting that cytokines-immune peptides influence sympathetic neuronal survival and that cytokines can promote the secretion of catecholamines. Using an isolated perfused rat liver (IPRL) preparation, we have shown that the liver is an important source of circulating cytokines in response to lipopolysaccharide (LPS) and that corticosterone dose dependently influenced LPS-induced production of tumor necrosis factor (TNF) and interleukin-6 (IL-6). In this study, we investigated the direct effect of epinephrine (another stress hormone) on the production of TNF and IL-6 in liver. We demonstrated that epinephrine (1 microM/ml) alone did not induce TNF bioactivity but significantly increased IL-6 bioactivity from IPRL effluent. When the IPRL was infused with LPS, epinephrine significantly decreased TNF bioactivity. Epinephrine in LPS-treated livers also significantly increased IL-6 bioactivity. Both responses were totally inhibited by the beta-blocker propranolol (10 microM/ml). Anisomycin, a protein synthesis inhibitor, infused into the IPRL completely blocked the rise in TNF and IL-6 concentrations in the effluent leaving the IPRL, supporting the hypothesis that the synthesis (or release) of these cytokines was dependent on protein synthesis. We then attempted to determine whether epinephrine exerts similar effects in vitro. Using isolated Kupffer cells and hepatocytes, we found that epinephrine alone had no effect on TNF and IL-6 production in Kupffer cells and hepatocytes but significantly decreased LPS-induced TNF bioactivity and increased LPS-induced IL-6 bioactivity in Kupffer cells. Our data support the hypothesis that epinephrine can promote IL-6 secretion from IPRL.(ABSTRACT TRUNCATED AT 250 WORDS)
Glucocorticoids and insulin: complex interaction on brown adipose tissue
Authors: Strack A. M. , Horsley C. J. , Sebastian R. J. , Akana S. F. , Dallman M. F.
Published: December 2017

Glucocorticoids and insulin effect long-term reciprocal changes in food intake and body weight. We tested the interactions of corticosterone and insulin on caloric efficiency, white adipose tissue (WAT) stores, and brown adipose tissue (BAT). Two experiments were performed: 1) adrenalectomized rats were treated with corticosterone with or without streptozotocin-induced diabetes and 2) adrenalectomized, corticosterone-treated, diabetic rats were treated with insulin. By 4-5 days later, > or = 50% of the variance in caloric efficiency, plasma triglycerides, and WAT stores was explained by regression of these variables on corticosterone (catabolic) and insulin (anabolic). When the ratio of the hormones was normal, but concentrations high, overall gain of energy stores decreased and energy was redistributed to fat. Both hormones were anabolic on BAT lipid storage; the hormones played a complex role in the regulation of uncoupling protein (UCP) in BAT. Although corticosterone inhibited and insulin stimulated UCP, these effects were only evident in diabetics and with normoglycemia, respectively. For BAT variables, < or = 50% of the variance was explained by regression on corticosterone and insulin, suggesting that the effects of these hormones are mediated through an intermediate such as sympathetic nervous system input to BAT.
Central effect of angiotensin III on caudal hypoglossal neurons in rats
Authors: Yang C. C. , Chan J. Y. , Chan S. H.
Published: December 2017

We communicated the central effect of angiotensin III (ANG III), a potent signal for extracellular dehydration, on single neurons in the caudal hypoglossal nucleus of Sprague-Dawley rats anesthetized with pentobarbital sodium. A significant number (121 of 168) of caudal hypoglossal neurons responded to intracerebroventricular application of ANG III (80 or 160 pmol), with either an increase (n = 83) or decrease (n = 38) in their spontaneous discharge. These effects of ANG III were significantly reversed by intracerebroventricular application of the nonpeptide angiotensin AT1 receptor antagonist losartan (40 nmol), but not by the AT2 antagonist, PD-123319. The hypoglossal neuronal responses to repeated administration of ANG III (80 pmol), delivered at an interval < or = 18 min, exhibited acute tachyphylaxis. Intracerebroventricular administration of the cholinergic dipsogen, carbachol (50 ng), or the osmotic stimulant, hypertonic saline (0.5 M), also elicited responses in ANG III-responsive hypoglossal neurons. These results suggest that neurons in the caudal hypoglossal nucleus may serve as the final common pathway for extracellular and, possibly, intracellular thirst in the rat. Furthermore, it is likely that the action of ANG III is mediated by the AT1 subtype of angiotensin receptors.
Suppression of men's responses to seasonal changes in day length by modern artificial lighting
Authors: Wehr T. A. , Giesen H. A. , Moul D. E. , Turner E. H. , Schwartz P. J.
Published: December 2017

We recently reported that humans have conserved mechanisms, like those that exist in other animals, which detect changes in day length and make corresponding adjustments in the duration of nocturnal periods of secretion of melatonin and of other functions. We detected these responses in individuals who were exposed to artificial "days" of different durations. The purpose of the present study was to determine whether men who are exposed to natural and artificial light in an urban environment at 39 degrees N are still able to detect and respond to seasonal changes in duration of the natural photoperiod. We measured profiles of circadian rhythms during 24-h periods of constant darkness (< 1 lx) and found no summer-winter differences in durations of nocturnal periods of active secretion of melatonin, rising levels of cortisol, high levels of thyrotropin, and low levels of rectal temperature. The results of this and our previous study suggest that modern men's use of artificial light suppresses responses to seasonal changes in the natural photoperiod that might otherwise occur at this latitude.
Acclimatization to high altitude increase muscle sympathetic activity both at rest and during exercise
Authors: Mazzeo R. S. , Brooks G. A. , Butterfield G. E. , Podolin D. A. , Wolfel E. E. , Reeves J. T.
Published: December 2017

This investigation examined the relationship between alterations in plasma norepinephrine associated with 21 days of high-altitude exposure and muscle sympathetic activity both at rest and during exercise. Healthy sea level residents, divided into a control group (n = 5) receiving a placebo or a drug group (n = 6) receiving 240 mg/day of propranolol, were studied while at sea level, upon arrival (acute), and after 21 days of residence (chronic) at 4,300 m. Arterial norepinephrine levels and net leg uptake and release of norepinephrine were determine both at rest and during 45 min of submaximal exercise via samples collected from femoral arterial and venous catheters. Arterial norepinephrine levels increased significantly after chronic altitude exposure both at rest (84%) and during exercise (174%) compared with sea level and acute values. A net uptake of norepinephrine was found in resting legs at sea level (0.28 +/- 0.05 nmol/min) and with acute exposure (0.07 +/- 0.06 nmol/min); however, a significant switch to net leg norepinephrine release was observed with chronic altitude exposure (0.51 +/- 0.11 nmol/min). With exercise, a net release of norepinephrine by the leg occurred across all conditions with chronic exposure, again eliciting the greatest values (5.3 +/- 0.6, 8.0 +/- 1.7, and 14.4 +/- 3.1 nmol/min for sea level, acute, and chronic exposure, respectively). It was concluded that muscle sympathetic activity is significantly elevated both at rest and during submaximal exercise as a result of chronic high-altitude exposure, and muscle is a major contributor to the increase in plasma norepinephrine levels associated with prolonged altitude exposure. The presence of dense beta-blockade did not alter this adaptation to altitude.
Antifreeze glycoproteins promote intracellular freezing of rat cardiomyocytes at high subzero temperatures
Authors: Mugnano J. A. , Wang T. , Layne J. R. , DeVries A. L. , Lee R. E.
Published: December 2017

Despite recent reports that antifreeze glycoproteins (AFGPs) protect mammalian cells during low-temperature preservation, T. Wang, Q. Zhu, X. Yang, J. R. Layne, and A. L. DeVries (Cryobiology 31: 185-192, 1994) reported that AFGPs failed to protect rat hearts during freezing. Rather, the presence of AFGPs exacerbated cardiac damage after freezing. This study examined the effects of freezing (-4 degrees C) in the presence of AFGPs at the cellular level with the use of cryomicroscopy. Large, blunt ice crystals formed in the solutions without AFGPs and excluded most cardiomyocytes from the plane of ice formation. After thawing, cells appeared similar in morphology to unfrozen cells. Ice in 0.5 mg/ml AFGP solution was more dendritic and prismatic than ice formed in the absence of AFGPs. On thawing, many cells exhibited spontaneous contraction, resulting in cell death. Spicular ice formed rapidly in the 10 mg/ml AFGP solution. These needlelike ice crystals appeared to penetrate the cardiomyocytes, resulting in intracellular freezing followed by cell lysis. These AFGP-induced changes in ice crystal structure may account for the injury observed in whole heart and cardiomyocyte experiments.
ACE inhibition prevents Na and water retention and MABP increase during reduction of renal perfusion pressure
Authors: Boemke W. , Seeliger E. , Rothermund L. , Corea M. , Pettker R. , Mollenhauer G. , Reinhardt H. W.
Published: December 2017

Two groups of six dogs were studied during 4 control days and 4 days of reduced renal perfusion pressure (rRPP) servo controlled at 20% below the individual dog's 24-h mean arterial blood pressure (MABP) during control days, i.e., below the threshold for renin release. On rRPP days, endogenous activation of plasma aldosterone and angiotensin II was inhibited by the angiotensin-converting enzyme inhibitor captopril. The dogs were kept on a high-Na and high-water intake. Unlike studies during rRPP alone, there was no Na and water retention during rRPP+captopril. Glomerular filtration rate dropped by approximately 9%, and MABP remained in the range of control days. Plasma renin activity rose to values 14 times greater than control, whereas plasma aldosterone decreased by approximately 60%. Atrial natriuretic peptide remained in the range of controls. In conclusion, angiotensin-converting enzyme inhibition can prevent the otherwise obligatory Na and water retention and systemic MABP increase during a 20% reduction in renal perfusion pressure. This is achieved most likely via the captopril-induced fall in angiotensin II and plasma aldosterone levels.
Effect of pregnancy on activation of central pathways following atrial distension
Authors: Deng Y. , Kaufman S.
Published: December 2017

Stimulation of the atrial volume receptors increases neural traffic to the ventrolateral medulla, which in turn sends output to, and receives input from, the lateral hypothalamic area. An integrated reflex and hormonal response is thus initiated. We wished to investigate first whether atrial distension results in activation of selected nuclei in the forebrain and, second, whether pregnancy modifies this response. Rats were implanted with indwelling intracardiac balloons positioned at the superior vena caval/right atrial junction. One week later, the balloons were inflated. The animals were then anesthetized, their brains fixed by perfusion, and the tissue prepared for visualization of c-fos activity. Atrial distension caused a significant increase in c-fos expression in the paraventricular nucleus, the medial preoptic area, and the lateral septum. This response was markedly attenuated in the pregnant animals. In conclusion, during pregnancy central pathways that are normally activated in responses to volume expansion, fail to respond to atrial distension. We propose that this allows blood volume to increase in the pregnant animal, without triggering homeostatic mechanisms.
Intracerebroventricular injection of prostaglandin E2 increases splenic sympathetic nerve activity in rats
Authors: Ando T. , Ichijo T. , Katafuchi T. , Hori T.
Published: December 2017

The effects of central administration of prostaglandin E2 (PGE2) and its selective agonists on splenic sympathetic nerve activity (SNA) were investigated in urethan- and alpha-chloralose-anesthetized rats. An intra-third-cerebroventricular (13V) injection of PGE2 (0.1-10 nmol/kg) increased splenic SNA in a dose-dependent manner. An I3V injection of an EP1 agonist, 17-phenyl-omega-trinor PGE2 (1-30 nmol/kg), also resulted in a dose-dependent increase in splenic SNA, with a time course similar to that of PGE2-induced responses. In contrast, EP2 agonists, butaprost (10-100 nmol/kg I3V) and 11-deoxy-PGE1 (10-100 nmol/kg I3V), had no effect on splenic SNA. An I3V injection of M & B-28767 (an EP3/EP1 agonist, EP3 >> EP1) increased splenic SNA only at high doses (10-100 nmol/kg). Pretreatment with an EP1 antagonist, SC-19220 (200 and 500 nmol/kg), completely blocked the responses of splenic SNA to PGE2 (0.1 nmol/kg) and M & B-28767 (10 nmol/kg), respectively. These findings indicate that brain PGE2 increases splenic SNA through its action on EP1 receptors.
Effect of oral protein loading on renal hemodynamics in human pregnancy
Authors: Barron W. M. , Lindheimer M. D.
Published: December 2017

Glomerular filtration rate (GFR) and ERPF increase approximately 50% in human pregnancy. To determine if pregnant women have additional “renal reserve,” inulin and p-aminohippurate clearances (Cin, CPAH) were measured in maximally hydrated women before and after a 300-g steak meal, once during late gestation, and again > or = 3 mo postpartum. Protein loading increased Cin [106 +/- 5 (SE) to 119 +/- 4 ml/min, P < 0.003], but not CPAH (587 +/- 35 to 624 +/- 32 ml/min, NS) in the nonpregnant state, but neither clearance was altered during gestation (Cin: 156 +/- 7 to 160 +/- 9.6 ml/min, NS; CPAH: 831 +/- 36 to 899 +/- 37 ml/min, NS). A natriuresis occurred only postpartum (+142 mu eq/min, P < 0.02), which could be explained by the increased GFR alone, since indexes of filtrate delivery and reabsorption (V/GFR, CH2O/GFR, CH2O/V) and fractional sodium excretion changed little. Dopamine excretion, uninfluenced by protein, did not correlate with increments in GFR. A carbohydrate meal (time controls) had no effect on the above described parameters. We make the following conclusions. If protein and pregnancy achieve hyperfiltration by similar mechanisms, these pathways appear “exhausted” in gestation. Also, oral protein loading does not measure maximal renal reserve, since basal GFR in late gestation was substantially greater than that measured after protein feeding in nonpregnant subjects.
Single-nephron adaptations to partial renal ablation in cats
Authors: Brown S. A. , Brown C. A.
Published: December 2017

To evaluate remnant nephron hyperfiltration, cats underwent sham surgery (group 1, n = 6) or three-fourths nephrectomy (group 2, n = 6). Four to six weeks later, micropuncture studies demonstrated increases (P < 0.01) of single-nephron glomerular filtration rate (SNGFR) in group 2 (28.1 +/- 2.8 vs. 56.0 +/- 5.9 nl/min). In group 2 the mean estimated glomerular capillary pressure of 74.0 +/- 1.7 mmHg exceeded (P < 0.01) the value for group 1 (62.6 +/- 1.4 mmHg). The mean effective filtration pressure (EFPm) for group 2 (28.7 +/- 3.1 mmHg) was greater (P < 0.05) than that in group 1 (20.8 +/- 1.9 mmHg). Similarly, the mean ultrafiltration coefficient (Kf) in group 2 of 2.03 +/- 0.24 nl.min-1.mmHg-1 exceeded (P < 0.05) the corresponding value for group 1 of 1.35 +/- 0.06 nl.min-1.mmHg-1. Morphological studies demonstrated glomerular enlargement and mesangial matrix expansion in group 2 (P < 0.05). Proteinuria, as assessed by the urine protein-to-creatinine ratio, was increased (P < 0.05) after partial renal ablation. These results demonstrate that increases in SNGFR in feline remnant nephrons occur in association with glomerular hypertension, glomerular hypertrophy, expansion of mesangial matrix, and proteinuria, and furthermore, that the observed increases in SNGFR are attributable to an augmentation of EFPm and Kf.
Antegrade and retrograde fluid transport through the vas deferens
Authors: Kihara K. , Sato K. , Ando M. , Azuma H. , Oshima H.
Published: December 2017

Intraluminal pressure of the seminal tract at seminal emission from the ejaculatory duct and the mode of transport of cauda epididymal contents were investigated to explore the mechanism of sperm transport. Direct electrical stimulation of any site of the cauda epididymis and vas deferens, which generated nerve-transmitted muscle contraction, caused elevation of the intraluminal pressure only at the cauda epididymis, whereas stimulation of the testis, caput, and corpus epididymis caused no response. The dye instilled in the cauda was emitted into the urethra during the stimulation. Shortly after discontinuation of the stimulation, retrograde movement of residual dye in the vas resulted in its ultimate reentry into the cauda epididymis. Significant decrease of the muscle tonus just after contraction was observed at the cauda. Distension of the wall of the vas generated elevation of the intraluminal pressure only at the site distended. The above results indicate the presence of rapid antegrade and retrograde movement of the sperm and the crucial role of the cauda epididymis on the sperm transport.
Age and regulation of fluid and electrolyte balance during repeated exercise sessions
Authors: Zappe D. H. , Bell G. W. , Swartzentruber H. , Wideman R. F. , Kenney W. L.
Published: December 2017

A common response after only 3-4 days of repeated exercise in younger individuals is an expansion of plasma volume (PV); however, it is not known if older individuals have a similar response. In this study, six older (O) (67 +/- 1 yr) and six younger (Y) men (24 +/- 2 yr) cycled for 4 successive days at 50% maximal oxygen consumption (Vo2max) for 90 min in a warm environment [30 degrees C temperature dry bulb (Tdb), 24 degrees C temperature wet bulb (Twb)]. On day 4, PV was increased (P < 0.05) in Y (10.0 +/- 1%) but not (P > 0.05) in O (1.7 +/- 2%). The increased PV was associated with a greater (P < 0.05) daily fluid intake during the exercise period in Y (45 +/- 3 ml. day-1.kg body wt-1) compared with O (32 +/- 2 ml.day-1.kg body wt-1) and an increase (P < 0.05) in the total circulating protein (TCP) content in Y (0.23 +/- 0.1 g/kg body wt) but not in O (0.10 +/- 0.1 g/kg body wt). Throughout the 4-day exercise period there were similar reductions in 24-h urine flow rate (UV) and urinary sodium excretion (UNaV) in Y and O. Additionally, acute renal clearance measures made during exercise on days 1 and 4 showed similar (P > 0.05) reductions in UNaV between Y (-55 +/- 10%) and O (-44 +/- 6%). However, during exercise in O there were no changes (P > 0.05) in UV (2 +/- 12%) and urine osmolality (UOsm) (-12 +/- 6%) from resting values compared with Y, where UV was decreased (P < 0.05) by 41 +/- 9% and UOsm was increased (P < 0.05) by 39 +/- 8%. Therefore, the inability of the older subjects to increase PV after repeated days of exercise is not related to an impaired renal fluid and Na+ conservation ability, despite a reduced urine concentrating ability during exercise, but to other factors (e.g., fluid intake and TCP) that appear necessary for the hypervolemic response.
Neurophysin expression is stimulated by dopamine D1 agonist in dispersed hypothalamic cultures
Authors: Mathiasen J. R. , Larson E. R. , Ariano M. A. , Sladek C. D.
Published: December 2017

We have exposed primary dispersed hypothalamic cultures from 14-day-old fetal Sprague-Dawley rats to substances known to either elevate adenosine 3',5'-cyclic monophosphate (cAMP) levels or increase vasopressin (VP) secretion. The levels of VP in the medium collected from the cultures were determined by radioimmunoassay, and the number of neurophysin (NP)-positive cells after immunohistochemistry was counted. cAMP-elevating agents, 3-isobutyl-1-methylxanthine (200 microM) and forskolin (25 microM), in combination (I-F) maintained NP synthesis and VP secretion in 19-day cultures. I-F replacement by K+ (28 mM), isoproterenol (10 microM), glutamate (10 microM), or bicuculline (10 microM) during the last week of culture resulted in maintenance of NP expression and transient stimulation of VP secretion, but these agents did not induce NP expression independently of I-F treatment. In contrast, exposure to the dopamine D1 agonist SKF-38393 (10 microM) significantly increased NP expression independently and after replacement of I-F. Dopamine D1A receptors were detected by immunofluorescence on NP-expressing cells, providing a morphological basis for this response. These results suggest a role for D1A receptors in the regulation of VP gene expression.
Pyruvate and hepatic pyruvate dehydrogenase levels in rat strains sensitive and resistant to dietary obesity
Authors: Nagase H. , Bray G. A. , York D. A.
Published: December 2017

This study compared the effects of exogenous pyruvate and lactate on the serum levels of pyruvate, lactate, glucose, alanine, and insulin, as well as the activity of hepatic pyruvate dehydrogenase (PDH) in strains of rat that were either sensitive [Osborne-Mendel (OM)] or resistant (S5B/Pl) to high-fat diet-induced obesity. Serum pyruvate and lactate were significantly higher and glucose lower in ad libitum-fed OM rats, but these differences disappeared after an 18-h fast. The increase in pyruvate and lactate after exogenous pyruvate administration was significantly greater in S5B/Pl rats than OM rats. There were no differences in serum alanine with strain or diet. The total PDH activity was similar across strains and diets but the proportion of PDH in its activated form (PDHa) was decreased in ad libitum-fed S5B/Pl rats. Pyruvate injection increased insulin and hepatic PDHa activity in OM rats fed both high- and low-fat diets, but these responses were greatly attenuated or absent in S5B/Pl rats. The data are consistent with the hypothesis that modulation of carbohydrate oxidation by PDH may be related to susceptibility to obesity when rats are fed a high-fat diet.
Inhibition of brown fat activity during hypothalamic stimulation in the rat
Authors: Woods A. J. , Stock M. J.
Published: December 2017

Previous work has shown that low-level electrical stimulation of the ventromedial hypothalamus (VMH) in anesthetized rats produces a sustained decrease (phase 1) in interscapular brown adipose tissue (IBAT) temperature followed by a rise (phase 2) after the stimulus has stopped [Woods, A. J., and M. J. Stock. Am. J. Physiol. 266 (Regulatory, Integrative Comp. Physiol. 35): R328-R337, 1994]. In this study, rat oxygen consumption was found to decrease (24%) and then increase (74%) during phase 1 and 2, respectively. The effect of norepinephrine, alpha-adrenoceptor antagonists, substance P, and neuropeptide Y, with and/or without VMH stimulation, suggested that vasoconstriction was unlikely to account for the phase 1 decreases in thermogenesis and temperature. However, measurement with radio-labeled microspheres showed that IBAT capillary blood flow was reduced by 70% during phase 1, and this, plus a 50% decrease in blood oxygen extraction, indicated that phase 1 could be due to vasodilatation of arteriovenous anastomoses. It was postulated that phase 1 resulted from release of neuropeptides, such as substance P, causing diversion of arterial blood away from IBAT capillaries, thereby increasing convective heat loss and inhibiting heat production during phase 1.
Metabolic and hormonal changes during the molt of captive gray seals (Halichoerus grypus)
Authors: Boily P.
Published: December 2017

Body mass, resting metabolic rates (RMRs), and serum thyroid hormones concentrations of six captive gray seals (Halichoerus grypus) were measured at regular intervals before, during, and after the annual molt. Changes in body mass suggested that the animals had increased energy expenditures during the last stage of the molt. These were associated with significantly elevated RMRs during the molt, the increase being more pronounced in juveniles ( < or = 53%) than in adults ( < or = 17%). The increase in RMR probably reflects the cost of generating a new pelt or to sustain a high skin temperature. Serum total and free thyroxine concentrations were elevated for all animals during the molt, but only juveniles had elevated serum triiodothyronine concentration. The increase in thyroid hormones occurred only during the last stage of the molt, suggesting that the role of thyroid hormones during the molt may be to sustain rapid hair growth in the last stage of molt or to maintain elevated heat production, rather than to initiate hair growth.
Stimulation of metabotropic glutamate receptors in the dorsomedial hypothalamus elevates heart rate in rats
Authors: DiMicco J. , Monroe A. J.
Published: December 2017

This study examined the potential role of metabotropic glutamate receptors (mGluRs) in the dorsomedial hypothalamus (DMH) by assessing the cardiovascular effects of microinjecting the agonist trans-1-aminocyclopentane-1, 3- dicarboxylate (tACPD) into this region in urethan-anesthetized rats. Dose-related tachycardia was observed after unilateral microinjection of 1S 3R-tACPD (10-200 pmol/50nl) but not after injection of 1R, 3S-tACPD, which has been reported to have little or no activity at mGluRs. Microinjection of dihydroxyphenylglycine, an agonist at mGluRs linked to phosphoinositide hydrolysis, resulted in increases in heart rate that correlated closely in magnitude to those seen after injection of the same dose of 1S, 3R-tACPD. Coinjection of the N-methyl-D-aspartate (NMDA) receptor antagonist DL-2- amino-5-phosphonopentanoic acid, given at doses shown to elicit selective blockade of NMDA ionotropic glutamate receptors, reduced the increase in heart rate evoked by 100 pmol 1S, 3R-tACPD alone. Thus the DMH contains functional mGluRs, and stimulation of these receptors activates the same sympathoexcitatory mechanism characterized previously to provoke dose-related tachycardia.
The importance of taste and palatability in carbohydrate-induced overeating in rats
Authors: Sclafani A. , Lucas F. , Ackroff K.
Published: December 2017

Rats offered a carbohydrate solution (sugar or polysaccharide) in addition to chow typically overeat and gain excessive weight. The present study sought to determine if the palatable taste of these solutions contributes to the overeating response. Adult female rats were fitted with chronic intragastric catheters and given ad libitum access to chow and a drinking fluid that was paired with intragastric infusions. For one group (P + S), the flavored solution was a highly preferred mixture of 2% Polycose and 0.2% saccharin paired with intragastric infusions of 30% Polycose. For a second group (SOA), the flavored solution (0.03% sucrose octaacetate) had unpreferred bitter taste and was paired with intragastric infusions of 32% Polycose. Thus both groups were effectively exposed to the postingestive effects of 32% Polycose but paired with a palatable (P + S) or unpalatable (SOA) flavor. A control group had water to drink paired with intragastric water infusions. During the 4-wk experimental period, the P + S group consumed 34% more total energy (chow + Polycose) and gained more weight than did the SOA and control groups. The P + S group also consumed substantially more flavored solution and more energy as Polycose compared with the SOA group. The SOA group did not gain reliably more weight than the control group, although their total energy intake was 13% higher than that of the controls. In a choice test conducted at the end of the experiment, the P + S group displayed a strong preference (98%) for the Polycose + saccharin solution over water. In contrast to the control group, which avoided the SOA solution relative to water, the SOA group preferred the SOA solution (71%) confirming prior reports of Polycose-conditioned SOA preferences. These results demonstrate that palatability has a major effect on the overeating and obesity produced by carbohydrate solutions. In the absence of a highly preferred taste, the postingestive actions of Polycose produce only a small hyperphagic effect and no excess weight gain.
Determinants of renal vasoconstriction after systemic inhibition of nitric oxide synthesis in rats
Authors: Brand-Schieber E. , Pucci M. , Nasjletti A.
Published: December 2017

The effects of NG-nitro-L-arginine (L-NNA, 10 mg/kg i.v.) on renal hemodynamics were examined in control rats, rats in which renal perfusion pressure was prevented from rising after L-NNA by constricting the abdominal aorta, and rats in which tubuloglomerular feedback was inhibited by furosemide pretreatment, ureteral ligation, or both interventions combined. In control rats, L-NNA increased (P < 0.05) renal vascular resistance (274 +/- 27%) along with systemic arterial (54 +/- 4%) and renal perfusion (54 +/- 5%) pressures and decreased (P < 0.05) renal blood flow (57 +/- 4%). In rats in which renal perfusion pressure was prevented from increasing along with systemic arterial pressure (54 +/- 4%), the L-NNA-induced elevation of renal vascular resistance (173 +/- 27%) was less intense (P < 0.05). In another study, where renal perfusion pressure was fixed at pre-L-NNA levels, L-NNA-induced increases in renal vascular resistance (130 +/- 20%) were attenuated (P < 0.05) further with furosemide pretreatment (52 +/- 12%), with ureteral ligation (75 +/- 10%), and with furosemide pretreatment and ureteral ligation combined (32 +/- 8%). These data suggest that vasoconstrictor mechanisms linked to tubuloglomerular feedback and perfusion pressure elevation contribute to renal vasoconstriction after systemic inhibition of nitric oxide synthesis with L-NNA.
Renal cortical and medullary blood flow responses during water restriction: role of vasopressin
Authors: Franchini K. G. , Cowley A. W.
Published: December 2017

Experiments were performed in unanesthetized rats to determine responses to 48 h water restriction of the renal regional microcirculation (cortex, outer medulla, and inner medulla) using implanted optical fibers and laser-Doppler flowmetry. The role of vasopressin (AVP) as a mediator of renal regional blood low changes and its contribution to urinary concentrating ability were assessed by continuous intramedullary interstitial infusion of specific V1 receptor antagonist d(CH2)5 [Tyr-(Me)2, Ala-NH2]AVP (2ng . kg-1 . min-1). Inner medullary blood flow decreased 34% at the end of 48 h of water restriction, whereas cortical and outer medullary flow did not change. This fall in inner medullary blood flow was substantially attenuated (18%) by the continuous interstitial infusion of the antagonist. Plasma AVP levels increased from control levels of 3.4 +/- 1.1 to 20.5 +/- 5.4 pg/ml (P < 0.05) by the end of the 48-h period of water restriction. Arterial pressure increased slightly but significantly during water restriction in the control rats. Infusion of antagonist impaired the maximal urinary concentrating ability, as demonstrated by the lower urine osmolality in this group than in the control group (1,893 +/- 49 vs. 2,419 +/- 225 mosmol/kg H2O; P < 0.05) measured during the second day of water restriction. Sodium and urea concentration decreased 20 and 22%, respectively, indicating that both contributed to the lower urine osmolality observed in the group of rats receiving the antagonist. We conclude that water restriction induces a selective decrease in inner medullary blood flow, which is mediated almost completely by endogenously released AVP. This vascular effect of AVP contributes to the maximum concentrating ability of the kidney.
Oral sensory stimulation improves glucose tolerance in humans: effects on insulin, C-peptide, and glucagon
Authors: Teff K. L. , Engelman K.
Published: December 2017

In animals, bypassing the oropharyngeal receptors by intragastric administration of glucose results in glucose intolerance. To determine whether the absence of oral sensory stimulation alters glucose tolerance in humans, we monitored plasma levels of glucose and hormones after intragastric administration of glucose, with and without subjects tasting food. Plasma glucose area under the curve (AUC) was significantly lower after oral sensory stimulation (3,433 +/- 783 vs. 5,643 +/- 1,397 mg.dl-1. 195 min-1; P < 0.03; n = 8). Insulin and C-peptide AUCs were higher during the first one-half of the sampling period (insulin, 5,771 +/- 910 vs. 4,295 +/- 712 microU. ml-1.75 min-1; P < 0.05; C-peptide, 86 +/- 10 vs. 66 +/- 9 ng.ml-1. 75 min-1; P < 0.03) and lower during the second one-half of the sampling period compared with the control condition (1,010 +/- 233 vs. 2,106 microU.ml-1. 120 min-1; P < 0.025; 31 +/- 8 vs. 56 +/- 18 ng.ml-1. 120 min-1; P < 0.05; insulin and C-peptide, respectively). Oral sensory stimulation markedly increased plasma glucagon compared with the control condition (1,258 +/- 621 vs. -2,181 +/- 522 pg.ml-1. 195 min-1; P < 0.002). These data provide evidence in humans that oral sensory stimulation influences glucose metabolism and suggest that the mechanisms elicited by this cephalic stimulation are necessary for normal glucose homeostasis.
Nonabsorbable fat (sucrose polyester) and the regulation of energy intake and body weight
Authors: De Graaf C. , Hulshof T. , Weststrate J. A. , Hautvast J. G.
Published: December 2017

A substantial number of people have difficulties in controlling their body weight and energy/fat intake. Fat substitutes may be helpful in solving these problems. We here report the first study on the longer-term effects of the nonabsorbable fat sucrose polyester (SPE) on energy intake in normal-weight subjects. We studied the longer-term (12 days) effects of the consumption of warm meals with normal dietary fat (5.0 MJ, 1,195 kcal) or meals in which 52 g of fat were replaced by the fat replacer SPE (3.1 MJ, 740 kcal) on spontaneous food intake (measured by dietary records), body weight, and gastrointestinal complaints in healthy volunteers in two studies. In the first study the 48 subjects were unaware of the treatment, whereas in the second study the 47 subjects were informed of what they received. In both studies men and women consumed less energy per day during the SPE (11.2 MJ) compared with the fat treatment (12.7 MJ) (P values < 0.0001) for the whole 12-day period. This was accompanied by equivalent changes in body weight. The percentage of energy from fat decreased from 43% during the fat treatment to 32% during the SPE treatment. During the SPE treatment, more gastrointestinal complaints and a higher frequency of defecation were reported. Information about the treatment did not affect. the outcomes. It is concluded that the use of a fat replacer such as SPE helps in reducing fat and energy intake in normal-weight people.
Indispensable amino acid deficiency and increased seizure susceptibility in rats
Authors: Gietzen D. W. , Dixon K. D. , Truong B. G. , Jones A. C. , Barrett J. A. , Washburn D. S.
Published: December 2017

Repeated subthreshold stimulation of limbic brain areas increases seizure susceptibility in experimental models of epilepsy. In addition, acute dietary indispensable amino acid (IAA) deficiency activates the anterior piriform cortex (APC), a seizure-prone limbic brain area in the rat. Based on these two findings, we hypothesized that activation of the APC by chronic exposure to IAA-deficient diets might increase seizure susceptibility. Several nonessential amino acid neurotransmitters are important in seizures, but deficiencies of nontransmitter IAAs have not been well studied in seizure models. In four trials, we made injections of pentylenetetrazole intraperitoneally or of bicuculline into the APC in histidine-, isoleucine-, or threonine-deficient rats and controls. Increased susceptibility to seizures in the deficient animals was observed as increased severity of the seizures, decreased threshold for the dose of the chemostimulant and time to seizure, or a combination thereof. Pair-fed controls showed that this effect was not due to an energy deficit. This novel but robust finding suggests that IAA deficiency may increase vulnerability to seizures by repeated activation of the APC.