bluuebunny/crossref_metadata_2025_split huggingface dataset:
Intracellular Na+ and Ca2+ Activities in Essential Hypertension
Authors: Zidek W. , Vetter H. , Dorst K.-G. , Zumkley H. , Losse H. 
Published: August 2015

1. The intracellular Na+ and Ca2+ activity and Na+ concentration were measured in erythrocytes of normotensive subjects, with and without a familial disposition to hypertension, in essential hypertensive patients with and without a family history of hypertension, and in patients with secondary hypertension.
2. In normotensive subjects without a genetic trait of hypertension intracellular Na+ activity and concentration were 7.00 ± 1.38 mmol/l and 5.67 ± 0.95 mmol/l respectively. The intracellular Ca2+ activity was 4.82 ± 4.49 μmol/l. In normotensive subjects with a familial hypertensive disposition intracellular Na+ activity and concentration were 9.74 ± 1.43 mmol/l (P &lt; 0.01) and 6.63 ± 0.88 mmol/l (P &lt; 0.05). Intracellular Ca2+ was 9.59 ± 9.71 μmol/l (P &lt; 0.05).
3. Essential hypertensive patients without a familial genetic trait had an elevated intracellular Na+ activity (8.35 ± 2.08 mmol/l, P &lt; 0.05). Intracellular Na+ concentration was 6.64 ± 0.79 mmol/l (P &lt; 0.05). The intracellular Ca2+ activity was markedly elevated to 25.33 ± 19.03 μmol/l (P &lt; 0.01). The essential hypertensive patients with a familial disposition had an elevated intracellular Na+ activity (17.19 ± 4.37 mmol/l, P &lt; 0.001) and Ca2+ activity (32.8 ± 32.51 μmol/l, P &lt; 0.01). The intracellular Na+ concentration was 6.25 ± 1.23 mmol/l.
4. The results indicate that in essential hypertension intracellular Na+ activity is increased, particularly in patients with a familial disposition for hypertension. Intracellular Ca2+ is increased in essential hypertension whether or not there was a family disposition to hypertension.
Measurements of Myofibrillar Protein Breakdown in Newborn Human Infants
Authors: Burgoyne J. L. , Ballard F. J. , Tomas F. M. , Dobozy A. , MacLennan A. H. , Fitzgerald A. , Dahlenburg G. W. 
Published: August 2015

1. Myofibrillar protein breakdown was calculated from the urinary excretion ratio of Nτ-methylhistidine (3-methylhistidine) to creatinine in newborn premature and full-term infants. Representative values were obtained from single voidings provided that the infant's metabolic status was stable.
2. Nτ-Methylhistidine in infant urine was measured by a rapid Auto Analyser method and shown to give similar values to those obtained by ion-exchange separation techniques.
3. The molar excretion ratio of Nτ-methylhistidine to creatinine averaged 0·0159 in urine samples obtained within 12 h after birth. A similar ratio was found in amniotic fluid collected at birth. It is argued that this ratio does not reflect a low rate of myofibrillar protein breakdown in the foetus, but rather a more effective transplacental passage of Nτ-methylhistidine than of creatinine.
4. The urinary ratio increased during the first 2 days after birth to a plateau at 0·0372. This represents a myofibrillar protein degradation rate of 3·40% day−1 in full-term infants.
5. The molar excretion ratio during the period 40–120 h after birth increased in premature infants and reflects a fractional degradation rate of 5·34% day−1 in those infants weighing less than 1 kg at birth.
6. Lower excretion ratios were found in some infants of diabetic mothers and in athyroid infants.
7. The urinary excretion ratio of Nτ-methylhistidine to creatinine is presented as a useful method for evaluating the breakdown rate of myofibrillar protein in neonates and can be applied to a number of abnormal nutritional or hormonal states.
The Effects of Localized Hypoventilation on Ventilation/Perfusion Ratios and Gas Exchange in the Dog Lung
Authors: Suggett A. J. , Barer Gwenda R. , Mohammed F. H. , Gill G. W. 
Published: August 2015

1. Hypoventilation of one lobe of lung was studied in open-chest anaesthetized dogs. Lobar blood flow, pulmonary-artery pressure and gas exchange were measured, the latter from breath-by-breath analysis with a mass spectrometer.
2. Hypoventilation of the lobe by reducing the respiratory pump stroke led, at each step, to a reduction in blood flow to that lobe. The flow () reduction was variable, but always less than the ventilation () reduction, so that the ratio to the lobe was reduced. O2 tension and pH fell and CO2 tension rose in effluent blood. Thus regulation achieved by flow reduction varied between individuals and was of low gain.
3. Anatomical or series dead space (VD series) was reduced in proportion to ventilation. When VD series was less than the apparatus dead space, some gas exchange still took place.
4. Oxygen uptake () and CO2 output () were reduced during hypoventilation. fell more than , so that the respiratory exchange ratio (R) was reduced.
5. Whether the deterioration in gas tensions in effluent blood during hypoventilation of the lobe was due to shunt of blood past unventilated alveoli, or to mismatching, was not resolved.
6. The plateau phase of the CO2-output curves at low tidal volumes was usually regular; thus either hypoventilation was uniform, or some ventilation units were totally closed.
The Effects on Respiration in the Cat of the Sudden Excitation of Cerebral Vascular Nociceptors by Carbon Dioxide
Authors: Hanson M. A. , Nye P. C. G. , Torrance R. W. 
Published: August 2015

1. Injection of CO2-saturated saline in a distal direction into either a vertebral artery or an internal maxillary artery in pentobarbitone-anaesthetized cats produced abrupt changes in respiration. Vertebral-artery injections produced a transient inhibition of respiration, followed by a stimulation of it. Internal-maxillary-artery injections produced only the inhibition.
2. Injections during inspiration usually shortened that inspiration, reduced its volume and prolonged the following expiration. In the first 30% of an expiration they prolonged that expiration, but given in the next 50% they shortened it. In the last 20% of expiration internal-maxillary-artery injections again slightly prolonged the expiration.
3. Phenyl diguanide injected into either a vertebral or an internal maxillary artery also produced abrupt effects on respiration.
4. The effects of CO2-saturated saline were abolished by intravenous acetazolamide, suggesting that nociceptors may be affected by a change in local pH.
5. The effects may arise from the excitation of vascular nociceptors, and our observations may suggest a way of studying in animals the receptors responsible for headache.
The Antidiuretic Effect of Chronic Hydrochlorothiazide Treatment in Rats with Diabetes Insipidus: Water and Electrolyte Balance
Authors: Walter S. J. , Skinner J. , Laycock J. F. , Shirley D. G. 
Published: August 2015

1. The antidiuretic effect of hydrochlorothiazide in diabetes insipidus was investigated in rats with the hereditary hypothalamic form of the disease (Brattleboro rats).
2. Administration of hydrochlorothiazide in the food resulted in a marked fall in urine volume and a corresponding rise in osmolality. These effects persisted throughout the period of treatment (6–7 days).
3. Body weight and extracellular volume were significantly reduced in the thiazide-treated rats.
4. Hydrochlorothiazide caused an increase in urinary sodium excretion only on the first day of treatment. The resulting small negative sodium balance (in comparison with untreated rats) remained statistically significant for 2 days only. Thiazide-treated rats gradually developed a potassium deficit which was statistically significant from the fourth day of treatment.
5. Total exchangeable sodium, measured after 7 days of thiazide treatment, was not significantly different from that of untreated rats. However, plasma sodium was reduced in thiazide-treated animals, whereas erythrocyte sodium concentration was elevated.
6. It is concluded that the antidiuresis resulting from chronic hydrochlorothiazide administration is associated with a reduction in extracellular volume, but not with a significant overall sodium deficit. Hydrochlorothiazide appears to cause a redistribution of the body's sodium such that the amount of sodium in the extracellular fluid compartment is reduced.
Calcium-Induced Contraction and Effect of Calcium Antagonist on Arterial Smooth Muscle of Spontaneously Hypertensive Rats
Authors: Kawaguchi Yoshinori , Aoki Kyuzo , Yamamoto Masahiko , Hotta Ken 
Published: August 2015

1. Calcium reactivity of arterial smooth muscle and the effect of diltiazem (calcium antagonist) were investigated in helical strips of mesenteric arteries from 6-week-old male spontaneously hypertensive rats (SHR) and age-and sex-matched normotensive Wistar-Kyoto (WKY) rats. Blood pressure was 130 ± 5 mmHg for SHR and 110 ± 5 mmHg for WKY rats (means ± sd).
2. At high Ca2+ concentration (3 × 10−4 to 3 × 10−3 mol/l) the calcium-induced tension of mesenteric arterial strips per cross-sectional area was significantly greater in SHR than in WKY rats in noradrenaline (10−5 mol/l)-containing solution or in high K+ (121 mmol/l) solution (P &lt; 0.001). At low Ca2+ concentration (10−5 mol of noradrenaline/l and 3 × 10−5 mol/l in high K+), the tension was smaller in SHR strips than in WKY rat strips (P &lt; 0.05).
3. The Ca2+ sensitivity of SHR strips was significantly lower than that of WKY strips in noradrenaline-containing solution or in high K+ solution.
4. Diltiazem, a calcium antagonist, shifted the dose-response curve of Ca2+-induced tension to the right equally in SHR and WKY rat strips. The inhibition of the maximum tension by the drug was greater in SHR strips than in WKY rat strips in noradrenaline-containing solution, but there was no difference in high K+ solution.
5. The results suggest that the contractile abnormality might be a possible cause of hypertension in SHR.
Biological Activity of Angiotensin II-(4-8)-Pentapeptide in Man
Authors: Kono T. , Oseko F. , Ikeda F. , Imura H. , Khosla M. C. , Bumpus F. M. 
Published: August 2015

1. When the angiotensin II-(4-8)-pentapeptide was infused intravenously at rates of 0.31-5.55 nmol min−1 kg−1 for 10–120 min into five normal men or two patients with Bartter's syndrome, no significant change was observed in blood pressure, plasma renin activity and plasma aldosterone, and the lowest dose did not inhibit the captopril-induced increase in plasma renin activity in the normal men.
2. An intravenous infusion of the pentapeptide at 9–0 nmol min−1 kg−1 for 15 min significantly raised blood pressure in the five normal men but not in patients with Bartter's syndrome. Blood pressure returned to the pre-treatment level 60 min after the cessation of the infusion in the normal men.
3. At the same dose level none of the seven subjects examined showed any significant change in plasma renin activity and plasma aldosterone.
4. Angiotensin II-(5-8)-tetrapeptide was infused intravenously into one of the normal men at a rate of 41.5 nmol min−1 kg−1 for 15 min, but it caused no significant change in blood pressure, plasma renin activity and plasma aldosterone.
5. These results suggest that the pentapeptide and probably the tetrapeptide do not possess renin-suppressing and steroidogenic actions in man but that the former peptide does elicit a modest pressor action with a prolonged duration.
Inactivation of Bradykinin and Angiotensin I Conversion in Conscious Rats with Two-Kidney, One-Clip Hypertension
Authors: Trindade Inge E. K. , Krieger Eduardo M. 
Published: August 2015

1. The extents of pulmonary degradation of bradykinin (BK) and angiotensin I (ANG I) to angiotensin II (ANG II) conversion were measured simultaneously to determine whether converting enzyme activity, in vivo, is altered in two-kidney, one-clip hypertensive rats (15, 60 and 180 days after renal artery clipping).
2. Inactivation of BK (estimated by comparing equipressor doses injected intravenously and intra-aortically) was markedly increased in these hypertensive rats: 98.5% (15 days), 98.4% (60 days) and 99.5% (180 days) vs 95.6% in control rats. All groups of hypertensive rats exhibited hyper-reactivity to intra-aortic BK, requiring doses 14–38 times smaller than the control rats to produce the same depressor response.
3. The percentage of ANG I conversion (calculated from equipressor doses of ANG I and ANG II injected intravenously) was elevated after 15 days (46.0% vs 28.1% in control rats), unchanged after 60 days (27.7%) and slightly elevated after 180 days (36.0%). Hyporeactivity to ANG II was observed 15 and 180 days after renal artery clipping (doses six times were needed to produce a standard increase in mean arterial pressure). No alterations were found in the rats at 60 days after artery clipping.
4. The increased degradation of BK cannot be explained solely by elevation of converting enzyme activity since no parallel increase in ANG I conversion was observed, indicating that other bradykininases in the lung may be involved.
Radiotracer Methodology for the Simultaneous Estimation of Total, and Renal, Sympathetic Nervous System Activity in Humans
Authors: Esler Murray , Blombery Peter , Leonard Paul , Jennings Garry , Korner Paul 
Published: August 2015

1. A radiotracer method, based on the measurement of noradrenaline spillover to plasma, has been developed to estimate simultaneously total, and organ-specific, sympathetic nervous system tone in humans.
2. Total, and renal, noradrenaline spillover to plasma was measured in four patients with essential hypertension. Renal noradrenaline spillover was 0.42 ± 0.25 nmol/min (mean ± sd), constituting approximately 16% of total noradrenaline spillover (2.58 ± 0.20 nmol/min).
3. There is a need to study regional sympathetic nervous tone, of organs particularly involved in blood pressure regulation, in patients with essential hypertension. Local increases in sympathetic tone might not be detected by biochemical tests of overall sympathetic nervous system activity.
The Renal Nerves in Dogs: Noradrenergic and Dopaminergic?
Authors: Ball S. G. , Gunn I. G. , Macarthur K. J. D. , Douglas I. H. S. , Inglis G. C. 
Published: August 2015

1. Plasma levels of dopa, dopamine, noradrenaline and adrenaline were measured in blood sampled from the renal vein and from the aorta at the origin of the renal artery in six anaesthetized greyhound dogs.
2. Plasma levels of dopa and adrenaline were lower in the renal vein than in the artery, indicating net extraction by the kidney, whereas both noradrenaline and dopamine were secreted into the circulation.
3. Similar measurements of noradrenaline and dopamine in arterial and venous blood were made in a separate group of seven dogs before and during stimulation of the renal nerves and after renal denervation.
4. Stimulation of the renal nerves caused secretion of noradrenaline and of dopamine into the renal vein. After denervation there was no evidence of secretion of noradrenaline into the circulation, whereas dopamine secretion continued, but at a reduced rate, suggesting an extraneuronal source of dopamine.
5. An imbalance of activity between noradrenergic sodium-retaining nerves and an opposing dopamine-secreting natriuretic system could raise blood pressure.
Serotonergic Mechanisms in the Nucleus Tractus Solitarius May Regulate Blood Pressure and Behaviour in the Rat
Authors: Laguzzi R. , Talman W. T. , Reis D. J. 
Published: August 2015

1. Highly localized microinjections of serotonin into the nucleus tractus solitarius in rats produced dose-dependent hypotension and bradycardia and electroencephalogram (EEG) changes consistent with an alerting response.
2. Microinjection of the serotinin antagonist metergoline blocked the cardiovascular and EEG effects of serotonin but did not affect the same responses elicited by the microinjection of l-glutamate.
3. Microinjections of l-glutamate produced similar effects; acetylcholine, which lowered arterial pressure and heart rate, did not affect the EEG.
4. Bilateral injections of metergoline into the nucleus tractus solitarius occasionally produced a rise in arterial pressure but did not affect the baroreceptor reflex.
5. Serotonin may integrate cardiovascular and behavioural responses mediated by the nucleus tractus solitarius.
6. Neuronal populations within the nucleus tractus solitarius may be neurochemically and functionally differentiated.
Increased Noradrenaline Content of Hypothalamic Nuclei in Association with Worsening of Hypertension after High Sodium Intake in the Young Spontaneously Hypertensive Rat
Authors: Winternitz S. R. , Wyss J. M. , Meadows J. R. , Oparil S. 
Published: August 2015

1. High sodium intake results in an exacerbation of hypertension accompanied by evidence of increased peripheral sympathetic activity in the young spontaneously hypertensive rat (SHR) of the Okamoto strain.
2. To examine the hypothesis that high sodium intake increases peripheral sympathetic activity via an influence on central noradrenergic pathways involved in cardiovascular regulation, the effect of dietary sodium intake on noradrenaline stores of individual hypothalamic nuclei was examined in young SHR.
3. After 2 weeks of high sodium intake, the noradrenaline content of the anterior and dorsomedial hypothalamic nuclei of SHR was increased when compared with SHR receiving normal sodium intake. Increases in the noradrenaline content of anterior hypothalamic nucleus persisted at 4 weeks. No changes were seen in other regions examined.
4. These observations lend support to the hypothesis that sodium and the sympathetic nervous system have synergistic effects in the pathogenesis of hypertension in the SHR.
‘Structural Autoregulation’ of the Preglomerular/Postglomerular Resistance Ratio and Hence of Glomerular Filtration Rate in the Clipped (Low Pressure) Kidney in Two-Kidney, One-Clip Renal Hypertension
Authors: Göthberg Gunnar , Folkow Björn 
Published: August 2015

1. The chronically clipped left kidneys of two-kidney, one-clip renal hypertensive rats (duration &gt;4 weeks) showed a 45% decrease in organ weight compared with left kidneys from age-matched normotensive Wistar rats (0.59 ± 0.09 vs 1.12 ± 0.05 g).
2. These ‘low-pressure’ kidneys exhibited at maximal vasodilatation a 40% decrease in total renal vascular resistance per unit kidney weight, a reduction in the preglomerular/postglomerular resistance ratio (filtration curve displaced markedly to the left of the control), though combined with some decrease in maximal glomerular filtration capacity.
3. Thus the vascular bed of chronically clipped low-pressure kidneys displays a ‘downward’ structural autoregulation, which by lowering of the total renal vascular resistance and the preglomerular/postglomerular resistance ratio serves to maintain blood flow and to increase filtration pressure thereby raising the filtration fraction.
Antihypertensive Effect of Calcium Antagonists in Rats Differs from That of Vasodilators
Authors: Kazda S. , Garthoff B. , Thomas G. 
Published: August 2015

1. Calcium antagonists of the dihydropyridine type such as nifedipine and nitrendipine are potent antihypertensive drugs in various forms of hypertension in rats. Long term treatment with calcium antagonists lowers high blood pressure and reduces cardiac hypertrophy in spontaneously hypertensive rats and additionally prevents mortality in renal (two-kidney, one-clip) and salt-induced (Dahl salt-sensitive) hypertensive rats.
2. Vasodilators of the hydralazine type only lower blood pressure in spontaneous hypertensive rats but do not influence cardiac hypertrophy. Minoxidil lowers blood pressure in spontaneous and slightly in renal hypertensive rats but does not reduce heart hypertrophy in renal hypertension and may even aggravate hypertrophy in spontaneous and salt-induced hypertension.
3. The antihypertensive effect of calcium antagonists is not only due to peripheral vasodilatation. Calcium antagonists may also improve renal function by lowering renovascular resistance. Reduced volume load may contribute to the reversal of heart hypertrophy seen after calcium antagonists compared with vasodilators.
Pressor Effect of Coffee and Cigarette Smoking in Hypertensive Patients
Authors: Freestone S. , Ramsay L. E. 
Published: August 2015

1. Patients with mild hypertension who habitually smoked cigarettes and consumed caffeine were examined after abstaining from caffeine and cigarettes overnight. Their mean blood pressure (147/89 mmHg) was substantially lower than values recorded in the clinic (164/102 mmHg) and remained so when they continued to abstain (149/94 mmHg at 2 h).
2. Smoking two cigarettes (3.4 mg of nicotine) elevated blood pressure by 10/8 mmHg but for only 15 min.
3. Drinking coffee (200 mg of caffeine) elevated blood pressure by up to 10/7 mmHg between 1 and 2 h.
4. Combined coffee and cigarette smoking caused a sustained rise in blood pressure from 5 to 120 min to levels similar to those measured in the clinic (162/102 mmHg at 2 h). The interaction of coffee and cigarettes on blood pressure, but not on pulse rate, was significant.
5. Caffeine ingestion with or without smoking may be important in the genesis of mild hypertension.
The Effect of Potassium and Bicarbonate Ions on the Rise in Blood Pressure Caused by Sodium Chloride
Authors: Morgan T. O. 
Published: August 2015

1. A group of eight patients with mild hypertension, sensitive to sodium intake, were studied.
2. Sodium chloride (70 mmol daily) caused their blood pressure to rise by 19/14 mmHg.
3. Sodium bicarbonate (70 mmol daily) caused their blood pressure to rise by 12/5 mmHg.
4. Sodium chloride given together with potassium chloride (70 mmol of each daily) caused their blood pressure to rise by 9.6 mmHg.
5. These results suggest that sodium bicarbonate causes a smaller rise in blood pressure than sodium chloride does and that potassium chloride reduces the blood pressure raising effect of sodium chloride.
6. A low sodium, high potassium and an alkaline diet may therefore be a more effective dietary method to reduce blood pressure than a diet low in sodium alone.
Kidney Size and Body Size in the Context of Salt and Blood Pressure
Authors: Simpson F. O. , Doesburg R. , Dempster A. G. , Kihara M. , Yamori Y. , Koshinaga J. 
Published: August 2015

1. Kidney weight was analysed for Japanese and New Zealanders of European origin who had died sudden deaths.
2. Kidney weight was relatively greater in Japanese than in New Zealanders.
3. Kidney weight was closely related to body surface area and weight and less closely to height and body mass index.
4. As kidney function is related to kidney size and thus in turn to body size it is advisable to take account of body size in analyses of sodium intake and excretion in relation to blood pressure.
Haemodynamic Effects of Ketanserin, a Selective 5-Hydroxytryptamine (Serotonin) Receptor Antagonist, in Essential Hypertension
Authors: Wenting G. J. , Veld A. J. Man In 'T , Woittiez A. J. , Boomsma F. , Schalekamp M. A. D. H. 
Published: August 2015

1. The new peripherally acting selective 5-hydroxytryptamine receptor blocking agent ketanserin was given (10 mg intravenously) to 17 patients with essential hypertension.
2. Systemic mean systolic arterial pressure fell from 192 ± 6 to 146 ± sem 10 mmHg and mean diastolic arterial pressure fell from 90 ± 4 to 68 ± 5 mmHg. Right atrial pressure, pulmonary arterial pressure and pulmonary capillary ‘wedge’ pressure, measured in 12 patients, were also significantly lowered. Heart rate, cardiac output and plasma noradrenaline rose after ketanserin, probably due to baroreflex-mediated sympathetic stimulation, but the changes were small compared with the fall in systemic arterial pressure.
3. Phenylephrine (50, 100 and 200 μg intravenously) was given to five patients before ketanserin and during continuous infusion of ketanserin (2 mg/h after a loading dose of 10 mg) and dose-response curves for mean systemic arterial pressure were constructed. The pressor response to phenylephrine was not shifted by ketanserin. Thus ketanserin, in a dose capable of lowering systemic arterial pressure, does not act as an α-adrenoceptor antagonist.
4. 5-Hydroxytryptamine receptor blockade appears to cause dilatation of resistance vessels and possibly also of capacitance vessels. The data suggest a hitherto unknown role for 5-hydroxytryptamine in the maintenance of high blood pressure.