bluuebunny/crossref_metadata_2025_split huggingface dataset:
Intravenous morphine causes hypertension, hyperglycaemia and increases sympatho-adrenal outflow in conscious rabbits
Authors: May Clive N. , Ham Ian W. , Heslop Kirsten E. , Stone Frances A. , Mathias Christopher J. 
Published: August 2015

1. In conscious rabbits, intravenous morphine (3 mg/kg) caused hypertension, bradycardia, hyperglycaemia and sedation. These changes were accompanied by large increases in plasma adrenaline and smaller increases in plasma noradrenaline.
2. These effects of morphine were prevented by intravenous naloxone, demonstrating their dependence on stimulation of opiate receptors.
3. Pretreatment with the antihistamines cimetidine and chlorpheniramine enhanced the morphine-induced rise in blood pressure, excluding a role for histamine release in the hypertensive action of morphine.
4. The centrally acting α2-adrenergic agonist clonidine prevented the morphine-induced hypertension and rise in plasma catecholamines, suggesting that these effects are exerted via central pathways. Clonidine alone reduced blood pressure and heart rate and produced hyperglycaemia.
5. α-Adrenergic blockade with phenoxybenzamine reduced the increase in blood pressure after morphine, although the increase in plasma catecholamines was augmented.
6. Pentobarbitone anaesthesia prevented the morphine-induced cardiovascular changes, the increase in plasma catecholamines and the hyperglycaemia.
7. These findings indicate, that in conscious rabbits, morphine induces hypertension by stimulation of opiate receptors leading to increased sympatho-adrenal activity. The hyperglycaemia appears to be in response to secretion of adrenaline. These effects probably result from a central action of morphine.
Alterations in high-density lipoprotein subfractions during postprandial lipidaemia induced by fat with and without ethanol
Authors: Franceschini G. , Moreno Y. , Apebe P. , Calabresi L. , Gatti E. , Noé D. , De Fabiani E. , Zoppi F. , Sirtori C. R. 
Published: August 2015

1. Serum lipid and apolipoprotein levels, distribution and composition of high-density lipoprotein (HDL) sub-fractions and lecithin:cholesterol acryltransferase activity were analysed in nine normolipidaemic subjects, in whom a hypertriglyceridaemic state was induced by the acute administration of ethanol (40 g) plus fat (70 g) or of fat only.
2. Triglyceride (TG) levels increased by 180% 4–6 h after fat plus ethanol intake, the hypertriglyceridaemic response being inversely correlated with the basal HDL2 mass (r = −0.82). Serum apolipoprotein (apo) B levels rose by 8%, HDL–cholesterol decreased by 10% and HDL–TG increased by 57% at 6–8 h.
3. When ethanol was omitted, serum cholesterol and TG rose by 6% and 70%, respectively; both apo AI and apo B levels went up by 8%, whereas HDL-cholesterol rose progressively (15%) at 12 h.
4. The flotation rates of both HDL2 and HDL, increased, reaching a maximum 6–8 h after ethanol plus fat intake. These changes were due to an increase in TG and phospholipid contents, whereas cholesteryl esters and proteins decreased.
5. The alterations in HDL are attributable to the increase in TG-rich lipoproteins, to the stimulated cholesterol esterification (+ 15%) and to an enhanced transfer of newly formed cholesteryl esters to apo-B-containing lipoproteins in exchange for TG.
6. Changes in HDL properties were evident only when ethanol was given concomitantly with fat.
7. These findings suggest that in the postprandial phase lipoprotein changes may occur, which facilitate an improved removal of cholesterol from tissues.
Effect of high salt intake on sodium, potassium-dependent adenosine triphosphatase activity in the erythrocytes of normotensive men
Authors: Quintanilla Antonio P. , Weffer Maria I. , Koh Haengil , Rahman Mohammed , Molteni Agostino , Del Greco Francesco 
Published: August 2015

1. We measured ouabain-insensitive adenosine triphosphatase (ATPase), sodium, potassium-dependent adenosine triphosphatase (Na+,K+-ATPase) and intracellular Na+ and K+ in the erythrocytes of 19 healthy volunteers, before and after supplementation of their normal diet with 6.0–8.9 g of salt (102–137 mmol of NaCl) per day, for 5 days.
2. The subjects had a small but significant gain in weight. Mean plasma renin activity decreased from 1.57 to 0.73 pmol of angiotensin I h−1 ml−1 and plasma aldosterone from 0.46 to 0.24 nmol/l.
3. Total ATPase activity fell from 197.9 nmol of inorganic phosphate h−1 mg−1 during the control period to 173.5 during the high-salt period (P &lt; 0.0125). Na+,K+-ATPase activity fell from 162.2 to 141.4 nmol of inorganic phosphate h−1 mg−1 (P &lt; 0.05). Intracellular Na + and intracellular K+ did not change.
4. These results are consistent with the hypothesis that salt-induced volume expansion causes the release of a factor inhibitory to the Na+ pump.
Sodium influx in human leucocytes: A novel technique for assessment of sodium–proton antiport activity
Authors: Ng L. L. , Harker M. 
Published: August 2015

1. A triple-isotope method for measuring initial 22Na uptake rates in unactivated human leucocytes in the presence of serum, using 3H2O, [14C]sucrose and 22Na, is described.
2. This 22Na influx is inhibited by amiloride, with half-maximal inhibition at a concentration of 10−5 mol/l.
3. About 70% of the 22Na influx in normal human leucocytes is inhibited by 1 mmol/l amiloride, with an external Na+ concentration of 10 mmol/l.
4. External Na+ antagonizes this inhibition by amiloride. The Km for external Na+ is 9 mmol/l.
5. Intracellular acidification from either external Na+ depletion or ammonium chloride incubation leads to an activation of amiloride-sensitive Na+ influx.
6. The amiloride-sensitive Na+–H+ antiport provides the major influx pathway for Na+ in unactivated human leucocytes in the presence of serum.
Differences in glomerular binding and response to angiotensin II between normotensive and spontaneously hypertensive rats
Authors: Messenger E. A. , Stonier C. , Aber G. M. 
Published: August 2015

1. Angiotensin II (ANG II) binding and the physiological response to exogenous ANG II have been studied in isolated glomerular preparations from normotensive (NTR) and spontaneously hypertensive (SHR) rats.
2. The binding of 125I-labelled ANG II by glomeruli from SHR was significantly greater than that by glomeruli from NTR, whereas the binding affinity constant (Ka) showed that the SHR ANG II glomerular receptor had a lower affinity for the hormone than the NTR glomerular receptor.
3. Glomeruli from SHR were significantly less responsive to exogenous ANG II than those from NTR.
4. Sodium loading resulted in a significant increase in ANG II binding by glomeruli from NTR, whereas a decrease in binding occurred in glomeruli from SHR.
5. Although a high sodium intake caused a reduction in the response of glomeruli from both NTR and SHR to exogenous ANG II, these changes were not statistically significant. In NTR this was associated with a decrease in the concentration of agonist required to cause half-maximal response (EC50), whereas an increase in EC50 was shown by glomeruli from SHR.
Adenine phosphoribosyltransferase deficiency: A simple diagnostic test
Authors: Maddocks J. L. , Al-Safi S. A. 
Published: August 2015

1. A simple method for diagnosing adenine phosphoribosyltransferase (APRT) deficiency using urine is described.
2. T.l.c. of 1 μl of urine from a child with APRT deficiency was performed and adenine was easily detected by its brilliant blue phosphorescence at liquid nitrogen temperature.
3. Four physicochemical characteristics of adenine were recorded: RF value, and the colour, decay time and pH sensitivity of phosphorescence.
4. Adenine was not detected in the urine of 116 subjects used as controls. These included healthy individuals and patients with inherited metabolic disorders, diseases of purine metabolism and of the kidney and urinary tract. Some of them were taking a variety of drugs including purine derivatives.
5. The test correctly diagnosed three cases of APRT deficiency out of 10 urine samples tested blind.
Muscle adenosine 5′-triphosphate and creatine phosphate concentrations in relation to nutritional status and sepsis in man
Authors: Tresadern J. C. , Threlfall C. J. , Wilford K. , Irving M. H. 
Published: August 2015

1. Intramuscular concentrations of adenosine 5′-triphosphate (ATP) and creatine phosphate were measured in the vastus lateralis muscle of 28 non-septic malnourished patients and 31 septic malnourished patients. Similar measurements were made on the rectus abdominis muscle of about one-third of these patients. All results were compared with those obtained from 15 normally nourished non-septic control subjects.
2. Objective measurements of nutritional status (both anthropometric and biochemical) and sepsis were recorded in all subjects.
3. The vastus lateralis muscle of the non-septic and septic malnourished patients had intramuscular concentrations of ATP and total adenine nucleotides (TAN) that were up to 30% lower than control values, depending on the reference base used.
4. In the rectus abdominis muscle, ATP and TAN concentrations were up to 60% lower than control values, and creatine phosphate up to 47% lower, again depending on the reference base used.
5. In both muscles, the changes were more marked in those patients who were septic as well as malnourished.
Unimpaired excretion of an acute salt load in conscious hypoproteinaemic dogs
Authors: Joles J. A. , Koomans H. A. , Boer P. , Dorhout Mees E. J. 
Published: August 2015

1. The role of hypoproteinaemia in the sodium retention seen in conditions such as the nephrotic syndrome is incompletely known.
2. To define the influence of severe hypoproteinaemia on kidney function, we studied the effect of an intravenous infusion of an isotonic saline load (133 mmol of sodium), as 1 litre of Ringer lactate solution, on sodium excretion and renal haemodynamics in conscious dogs before and after reduction of plasma protein from 68 ± 3 to 36 ±2 g/l by repeated plasmapheresis and a low protein diet.
3. During hypoproteinaemia, 2 days after a period of plasmapheresis, glomerular filtration rate and effective renal plasma flow were lower than in the control study. After the sodium load, both rose to values nearly identical with the pre-infusion levels found in normoproteinaemia, the filtration fraction remaining unchanged. This contrasted with the rise in filtration fraction after expansion in normoproteinaemia, where filtration fraction increased from 32 to 39% due to a rise in glomerular filtration rate.
4. After expansion, natriuresis rose to similar levels in normoproteinaemia (0.18 ±0.06 mmol/min) and hypoproteinaemia (0.20 ± 0.06 mmol/min), and increments in fractional excretion of sodium, potassium and chloride were also similar. However, baseline excretion was higher in the hypoproteinaemic dogs due to their overhydrated condition in this period immediately after plasmapheresis.
5. The fractional excretion of lithium, an alleged marker of proximal tubular sodium reabsorption, rose to comparable levels.
6. Hence, both the increase in filtration and decrease in reabsorption of sodium after an isotonic saline load are not affected by severe reduction in plasma protein concentration. Apparently, the pathways to augment natriuresis after acute expansion function normally in hypoproteinaemia.
Metabolic and cardiovascular effects of infusions of low doses of isoprenaline in man
Authors: Mansell P. I. , Fellows I. W. , Birmingham A. T. , Macdonald I. A. 
Published: August 2015

1. The cardiovascular and metabolic responses to low doses of isoprenaline (15 and 5 ng min−1 kg−1 body weight infused over 30 min) were determined in six healthy males. The study was performed to investigate whether there were sustained effects after the termination of the isoprenaline infusions, as has been observed previously after the infusion of adrenaline.
2. The isoprenaline infusions produced dose-dependent increases in heart rate, systolic blood pressure and metabolic rate, but similar increases in calf blood flow and decreases in diastolic blood pressure for the two infusion rates. Finger tremor was increased in amplitude by the 15 ng min−1 kg−1 infusion only. The changes in each of these physiological variables largely resolved within a few minutes of discontinuing the isoprenaline infusions.
3. There were no changes in arterialized venous plasma adrenaline or noradrenaline levels during the isoprenaline infusions. Mean peak plasma isoprenaline levels were 0.16 ±0.02 nmol/l during the 5 ng min−1 kg−1 infusion and 0.71 ±0.05 nmol/l during the 15 ng min−1 kg−1 infusion.
4. Plasma insulin levels increased with isoprenaline but blood glucose concentrations were unchanged, consistent with a direct effect of isoprenaline on β2-adrenoceptors mediating insulin release from pancreatic β-cells. Blood glycerol concentration also increased with isoprenaline but blood lactate concentration was unaltered.
5. The present study demonstrates pronounced cardiovascular and metabolic effects of low dose isoprenaline infusions. Differences in the rate of resolution of the changes induced by isoprenaline and by adrenaline seen in previous studies may result from a significant difference in their metabolism.
Effects of opioid antagonism on the haemodynamic and hormonal responses to exercise
Authors: Staessen Jan , Fiocchi Roberto , Bouillon Roger , Fagard Robert , Hespel Peter , Lijnen Paul , Moerman Emmanuel , Amery Antoon 
Published: August 2015

1. Physical effort involves, along with an increase in the plasma concentration of β-endorphin, profound adaptations of the circulation and the endocrine system. The effects of opioid antagonism on the responses of blood pressure, heart rate and several hormones to exercise were therefore studied in 10 normal men. They exercised in the supine position up to 33% and 66% of their maximal exercise capacity and received in a randomized double-blind cross-over protocol, either saline or naloxone (10 mg intravenously, followed by a continuous infusion of 10 mg/h).
2. Intra-arterial pressure and heart rate were continuously monitored, but were not affected by naloxone.
3. At rest, opioid antagonism produced a rise in plasma renin activity and in plasma adrenocorticotropin, Cortisol and aldosterone, but only the stimulation of the two adrenocortical hormones differed significantly from the control experiments; at rest naloxone also prevented the fall in plasma adrenaline, which occurred with saline infusion. Furthermore, the exercise-induced rises in plasma angiotensin II, aldosterone, Cortisol, noradrenaline and adrenaline were higher on naloxone than on saline, while a similar tendency was also present for the increases with exercise in plasma renin activity and plasma adrenocorticotropin. Neither at rest nor during exercise did opioid antagonism alter plasma lactate and glucose and serum insulin and growth hormone.
4. In conclusion, (1) endogenous opioids are not involved in the responses of blood pressure and heart rate to supine exercise; (2) at rest and during exercise, the endogenous opioids inhibit the secretion of adrenocorticotropin, aldosterone, Cortisol, noradrenaline and adrenaline; (3) they also inhibit the plasma renin-angiotensin II system indirectly via the catecholamines.
Angiotensin II augments sympathetically induced venoconstriction in man
Authors: Benjamin N. , Collier J. G. , Webb D. J. 
Published: August 2015

1. The constriction produced by a single deep breath was measured simultaneously in two adjacent hand veins in normal volunteers. One vein was infused with angiotensin II (ANG II) while the other acted as a control.
2. At a dose lower than that required to produce direct venous constriction (1 pmol/min), ANG II significantly augmented the constriction caused by a deep breath in eight subjects (P &lt; 0.01). The same dose had no effect on the venoconstriction caused by infused noradrenaline (NA) in a further six subjects.
3. It is concluded that ANG II at low doses may cause venoconstriction indirectly by augmenting sympathetically induced venous tone via a presynaptic mechanism. This observation may help to explain the apparent venodilating property of angiotensin-converting enzyme inhibitors in clinical situations where the renin–angiotensin system is stimulated.
Free and total carnitine and acylcarnitine content of plasma, urine, liver and muscle of alcoholics
Authors: De Sousa C. , Leung N. W. Y. , Chalmers R. A. , Peters T. J. 
Published: August 2015

1. Plasma and urine free and total carnitine and acylcarnitine levels were assayed in 12 control subjects and 20 chronic alcoholics with fatty liver. Although the alcoholics had a wider range of values than the controls, there was no significant difference between the two groups.
2. Hepatic free and total carnitine and long- and short-chain acylcarnitines were assayed by a radioenzymatic method in samples from seven control subjects and seven alcoholics. No significant differences in any of the indices were noted between the patient and control groups and it was concluded that carnitine deficiency did not contribute to alcoholic fatty liver in patients without cirrhosis.
3. Skeletal muscle free and total carnitine and long-and short-chain acylcarnitines were assayed in eight alcoholics and seven control subjects. The alcoholics had significantly higher total and free carnitine levels. It is suggested that this reflects a selective enrichment of the biopsy sample with type I carnitine-rich fibres due to the type II fibre atrophy found in approximately half the patients.
Vasopressin-mediated contractions in mesenteric arteries from spontaneously hypertensive rats: Differences in response compared with Wistar–Kyoto animals
Authors: Bund S. J. , Heagerty A. M. , Aalkjaer C. , Swales J. D. 
Published: August 2015

1. The sensitivity of mesenteric resistance arterioles to [arginine]vasopressin (AVP) was investigated in spontaneously hypertensive rats (SHR) and control Wistar–Kyoto rats (WKY). No difference in pAVP (–log dose of AVP producing 50% of the maximum response) was observed [SHR 0.21 ±0.03 m-units/ml (n = 10) vs WKY 0.15 ±0.06 m-units/ml (n = 9)], although SHR vessels exhibited greater absolute tension development.
2. Both strains of rat displayed tachyphylaxis to repeated stimulation with AVP, and oscillatory tension changes were observed in all vessels from SHR and rarely in WKY vessels at activating concentrations of AVP.
3. AVP did not elicit a contractile response after noradrenaline-induced calcium depletion.
4. After vessels were depleted of calcium by using a combination of calcium-free media and noradrenaline stimulation, restoration of calcium in the presence of AVP elicited a greater contractile response in SHR vessels.
5. The results therefore provide evidence for an increased calcium response to AVP in SHR resistance vessels, although this was only demonstrable by calcium recovery experiments.
Atrial natriuretic factor increases after a protein meal in man
Authors: Rodríguez-Iturbe Bernardo , Herrera José , Gutkowska Jolanta , Parra Gustavo , Coello Jesús 
Published: August 2015

1. The renal function changes induced by dietary protein are thought to result from the activity of hormonal factors that remain as yet undefined. Since a meat meal and high dose atrial natriuretic factor (ANF) infusions have similar effects on glomerular filtration rate, natriuresis and kaliuresis, we decided to investigate the possibility that a protein meal could stimulate ANF activity.
2. We studied 10 normal volunteers who had a fixed protein and sodium intake for 7 days before the experiments. The subjects received a meat meal (1–1.5 g of protein/kg) and, on a separate occasion, a carbohydrate meal that had a similar caloric, sodium and potassium content. Diuresis was stimulated with water ingestion, and urine collections were obtained before the meals (baseline) and after the meals for a period of 3 h. Blood samples were obtained 30 min and 5 min before the meals and every hour for 3 h in the period after the meal.
3. The protein meal, but not the carbohydrate meal, was associated with parallel increments in plasma immunoreactive ANF (i-ANF), natriuresis, kaliuresis and glomerular filtration rate (estimated from creatinine clearances) which reached peak values 2–3 h after the meal. The mean increment of plasma i-ANF after the protein meal represented a twofold increase over baseline levels.
4. We conclude that ANF may participate in the physiological response to an oral protein load.
Reciprocal renal effects of dopamine and 5-hydroxytryptamine formed within the rat kidney
Authors: Itskovitz Harold D. , Chen Yih-Huey , Stier Charles T. 
Published: August 2015

1. Clearance of inulin and p-aminohippurate and excretion of water and sodium were measured for eight to 11 clearance periods of 20 min duration in anaesthetized, 3% volume-expanded rats, before and after intravenous infusions of the amino acids l-dopa (l-3,4-dihydroxyphenylalanine) and 5-hydroxytryptophan. During the final two clearance periods, the peripheral decarboxylase inhibitor, carbidopa (S-α-hydrazino-3,4-dihydroxy-α-methylbenzenepropanoic acid monohydrate), was infused additionally.
2. Renal formation of dopamine (3,4-dihydroxyphenethylamine) and 5-hydroxytryptamine was demonstrated during infusions of l-dopa and 5-hydroxytryptophan, respectively; carbidopa blocked the renal formation of these biogenic amines.
3. During infusion of dopa, a diuresis and a natriuresis were observed; during the infusion of 5-hydroxytryptophan, slight reductions in clearances of inulin and p-aminohippurate, but significant reductions in sodium and water excretion, were measured.
4. The addition of carbidopa diminished diuretic and natriuretic responses to dopa as renal dopamine excretion decreased; the infusion of carbidopa also ameliorated the antinatriuretic and antidiuretic effects of 5-hydroxytryptophan, as 5-hydroxytryptamine excretion decreased.
5. Although dopa and 5-hydroxytryptophan are substrates for the same enzyme, aromatic l-amino-acid decarboxylase, simultaneous infusions of both amino acids at comparable rates gave no evidence of competitive inhibition of amine synthesis. However, the infusion of dopa, after 5-hydroxytryptophan, decreased its antinatriuretic and antidiuretic effects.
6. These data raise the possibility that dopamine and 5-hydroxytryptamine are formed as reciprocal intrarenal hormones by the identical enzyme, aromatic l-amino-acid decarboxylase, which is located within cells of the renal tubule.
Rebound of aldosterone but not of corticosterone after suppression of adrenal function by triamcinolone acetonide in rats
Authors: Meier Gabriele 
Published: August 2015

1. The effects of microcrystalline ‘depot’ triamcinolone acetonide on renal excretion and blood levels of aldosterone, 18-hydroxycorticosterone and corticosterone were studied in rats over a 13 day period. The renal excretion of all of these steroids was found to be suppressed on day 1 after triamcinolone acetonide administration. Corticosterone excretion remained suppressed for 6 days, whereas aldosterone and 18-hydroxycorticosterone excretion normalized within 3 days.
2. While corticosterone excretion was returning to control values, the excretion of aldosterone rose to values above the pretreatment levels (the rebound phenomenon). 18-Hydroxycorticosterone excretion paralleled that of aldosterone, but the rebound was of less statistical significance.
3. The findings in urine were confirmed by plasma steroid determinations. A suppression of plasma aldosterone, 18-hydroxycorticosterone and corticosterone was observed in the first 24 h after triamcinolone acetonide injection. On day 4 only corticosterone showed lowered levels. An aldosterone rebound could be seen at 18.00 hours, the circadian maximum in rats.
4. These findings suggest that in addition to the effects on glucocorticoids, mineralocorticoids have to be taken into account in the restoration of the adrenal function after corticoid therapy. The aldosterone rebound observed during this sensitive period may be important in preventing disturbances of electrolyte and water homoeostasis.