bluuebunny/crossref_metadata_2025 huggingface dataset:
Cardiovascular Reflexes and Autonomic Neuropathy
Authors: Ewing D. J.
Published: August 2015

Clinical features of autonomic neuropathy include postural hypotension, sweating abnormalities, disturbance of body temperature regulation, gastric fullness and nausea, intermittent nocturnal diarrhoea, constipation, bladder problems and impotence. In diabetic patients, gustatory sweating and hypoglycaemic unawareness also sometimes occur (Johnson & Spalding, 1974). The onset of symptoms is usually insidious and permanent, but may occasionally be acute and reversible (Young, Asbury, Corbett & Adams, 1975). Autonomic dysfunction can arise from three main causes: first, those where the damage to the autonomic nervous system is isolated, as in primary postural hypotension (Bannister, Sever & Gross, 1977) and familial dysautonomia (Brunt & McKusick, 1970); secondly, those caused by toxic or pharmacological agents which interfere with autonomic reflexes; thirdly, those associated with systemic disease, of which diabetes mellitus is the most common. Other diseases which may cause autonomic dysfunction include amyloidosis, porphyria, tetanus, polyneuritis, tabes dorsalis, parkinsonism, chronic renal failure and alcoholism, and occasionally autonomic neuropathy has been associated with carcinoma of the bronchus or the pancreas (Johnson & Spalding, 1974).

Although it is possible to localize lesions within the autonomic nervous system to afferent or efferent sympathetic or parasympathetic pathways (Johnson & Spalding, 1974; Moskowitz, 1977), many of the available tests are complex and invasive and often lack adequate control measurements (Young et al., 1975). Because of the patchy nature of autonomic neuropathy, current interest has centred around the search for bedside tests that are ‘global’, reproducible and non-invasive. This review summarizes the present state of knowledge of simple tests of cardiovascular reflex function in the clinical evaluation of autonomic neuropathy, particularly in diabetic subjects.
Effect of Prolactin on Glomerular Filtration Rate
Authors: Riley A. L. , Hagen T. C. , Stefaniak J. E.
Published: August 2015

1. The effect of infusion of ovine prolactin was studied in anaesthetized dogs pretreated with bromocryptine to reduce the release of endogenous prolactin.

2. Prolactin, injected intravenously and also directly into one kidney, resulted in a 12–18% increase in glomerular filtration rate (GFR) by both kidneys.

3. This increased GFR was not associated with any demonstrable changes in whole-kidney blood flow, distribution of intrarenal blood flow, fractional excretion of sodium or osmolar or free-water clearance.

4. We conclude that ovine prolactin produced an increase in GFR not dependent on an increase in whole-kidney plasma flow.
The Compliance of the Resistance Vessels in Skeletal Muscle of Hypertensive Patients
Authors: Hartling O. J. , Svendsen T. L. , Nielsen P. E. , Trap-Jensen J.
Published: August 2015

1. The compliance of the resistance vessels in the anterior tibial muscle was compared in normotensive and hypertensive subjects by measuring the increase in muscle blood flow produced by an increase in vascular transmural pressure.

2. The transmural pressure was increased by exposing the leg to a pressure of 50 mmHg below atmospheric pressure. Muscle blood flow was measured by means of the local 133xenon wash-out technique, and the measurement was performed during reactive hyperaemia to avoid reflex vasoconstriction when the transmural pressure was augmented.

3. At ambient pressure, muscle blood flows were equal in the two groups. However, when the subatmospheric pressure was applied the blood flow increased twice as much in the normotensive as in the hypertensive subjects. This suggested a smaller compliance of the resistance vessels in hypertensive subjects and supported the concept that there are structural changes of the resistance vessels in arterial hypertension.

4. In a small group of hypertensive patients who were well treated for two years, and had a normal blood pressure, the compliance was reduced to the same extent as in the untreated hypertensive patients, indicating that structural vascular changes are not readily reversible despite appropriate antihypertensive treatment.
Changes in Hepatic Enzymes and Organelles in Alcoholic Liver Disease
Authors: Seymour Carol A. , Peters T. J.
Published: August 2015

1. Liver biopsy specimens obtained from patients with alcoholic liver disease of varying severity were assayed for lysosomal and microsomal enzyme activities, the results being compared with values previously obtained in control subjects.

2. Analytical subcellular fractionation by sucrose-density-gradient centrifugation was performed on extracts of the biopsies and the properties of the lysosomes, plasma membrane, biliary canaliculi and endoplasmic reticulum membranes were determined. Increased activities of plasma membrane marker enzymes, particularly γ-glutamyl transpeptidase believed to be localized to the biliary canalicular membrane, were demonstrated. These findings were most marked in alcoholic cirrhosis. The centrifugation studies revealed no abnormalities in the properties of these membranes.

3. Although the total activities of the endoplasmic reticulum marker enzyme neutral α-glucosidase were unaltered in alcoholic liver disease, centrifugation studies showed a decrease in the density distribution of the membrane-bound enzyme in cirrhosis indicating an increase in the proportion of smooth endoplasmic reticulum membranes.

4. Apart from a small decrease in activity of certain acid hydrolases in fatty liver and in cirrhosis the activities of the lysosomal enzymes were unaffected by alcoholic liver disease.

5. Measurements of lysosomal integrity and density-gradient-centrifugation studies revealed no significant abnormalities in the various patient groups apart from increased stability and reduced equilibrium density of certain lysosomes in fatty liver. It is concluded that lysosomal disruption is not implicated in the pathogenesis of alcoholic liver disease.
The Effect of Vibration on Blood Flow in Skeletal Muscle in the Rabbit
Authors: Hudlická O. , Wright A.
Published: August 2015

1. The blood flow in rabbit gastrocnemius, as measured by photoelectric drop-counter, increased when the muscle was vibrated at frequencies of 22–62 Hz.

2. Blood flow increased rapidly within 1–2 s of the start of vibration, and lasted for the whole time vibration was applied.

3. The increase in blood flow was negatively correlated with the initial blood flow, being greater with lower flows.

4. The magnitude of increase was similar in both innervated and acutely denervated muscles.

5. The arterial blood pressure did not change apart from a very brief fall at the beginning of vibration. Venous pressure rose and, consequently, the perfusion pressure was lower. The increase in blood flow thus indicates a considerable dilatation in the resistance vessels of skeletal muscle.
Small-Intestinal Changes Induced by an Elemental Diet (Vivonex) in Normal Rats
Authors: Nelson L. M. , Carmichael H. A. , Russell R. I. , Lee F. D.
Published: August 2015

1. Rats were fed with the elemental diet Vivonex for 1 or 3 months and their jejunal histology was compared with that of an equal number of rats fed on a normal diet.

2. After 1 month of Vivonex feeding a significant reduction in the ratio of crypt height: villus height (CH: VH) was found in the Vivonex-fed rats (n = 4) compared with the control rats (n = 4) (P < 0.05).

3. After 3 months the CH:VH ratio was also reduced in the Vivonex-fed rats (n = 18) compared with control rats (n = 18) (P < 0.002). Villus height was significantly increased (P < 0.002) and crypt height decreased (P < 0.05).

4. Jejunal protein content, alkaline phosphatase and disaccharidase activity were also determined in 12 control and 12 Vivonex-fed rats from the 3 months study.

5. Alkaline phosphatase activity was increased from a control value of 201 ± 8 to 243 ± 15 munits/cm in the Vivonex-fed rats (n = 12) (P < 0.05) but no significant changes in lactase, sucrase or maltase activities were found.

6. The observed decrease in the CH:VH ratio suggested an improved survival of the mature enterocyte population during elemental diet feeding.
Circulating Catecholamines and Systolic Time Intervals in Labile and Sustained Hypertension
Authors: Cousineau D. , de Champlain J. , Lapointe L.
Published: August 2015

1. Average supine circulating total catecholamine concentrations were found to be higher than the normal range in about 50% of patients with labile hypertension and in about 30% of patients with sustained essential hypertension.

2. These higher resting concentrations were mainly due to an increase in adrenaline in labile hypertension and to an increase in noradrenaline in sustained hypertension.

3. Patients with elevated catecholamine concentrations were also characterized by a higher heart rate, by an increased myocardial contractility and by greater hypotensive response after treatment with β-adrenoreceptor blocking agents.

4. These studies suggest the existence of subgroups of hypertensive patients with increased sympathetic tone.
Plasma Noradrenaline Concentrations and Haemodynamics in the Early Stage of Essential Hypertension
Authors: Miura Y. , Kobayashi K. , Sakuma H. , Tomioka H. , Adachi M. , Yoshinaga K.
Published: August 2015

1. Plasma noradrenaline concentrations and haemodynamic status were simultaneously studied in young patients with uncomplicated essential hypertension and in age-matched normal controls.

2. Resting plasma noradrenaline in the controls tended to increase slightly, but progressively, with age. The hypertensive subjects had significantly higher plasma noradrenaline concentrations than those in the controls, but these values did not show any age-related variation. The response of plasma noradrenaline to the standing position tended to increase with age in the controls, whereas plasma noradrenaline in the hypertensive subjects showed a wide range of responses without any fixed relationship with age.

3. The cardiac index was significantly greater in the labile hypertensive subjects than in the controls, whereas total peripheral resistance was significantly greater in the sustained hypertensive subjects than in the labile patients and in the controls. Mean arterial pressure in these patients was closely related with the values of total peripheral resistance rather than with the cardiac index.

4. Of the patients with raised plasma noradrenaline 80% showed significantly increased values of either total peripheral resistance or cardiac index. Plasma noradrenaline was correlated significantly to total peripheral resistance, and marginally to mean arterial pressure.

5. These findings support the view that sympathetic nervous overactivity is an important factor underlying the haemodynamic findings in these patients.
Free and Conjugated Catecholamines in Human Hypertension
Authors: Kuchel O. , Buu N. T. , Unger TH. , Genest J.
Published: August 2015

1. Noradrenaline and adrenaline in the adrenal vein of essential hypertensive patients are almost exclusively (99%) unconjugated or free. However only 17% of dopamine is free, the rest is conjugated. The further the site of sampling from the adrenal vein the closer come the free catecholamines to their normal peripheral venous proportion (noradrenaline + adrenaline 20%, dopamine less than 1% of total catecholamines). Deviations from these patterns help to detect the site and type of secretion of phaeochromocytoma.

2. Essential hypertensive patients have, compared with control subjects, higher conjugated plasma dopamine, less urinary free and conjugated dopamine with blunted urinary free dopamine and sodium responsiveness to frusemide. Conjugated noradrenaline + adrenaline, mean arterial pressure and age are positively interrelated.

3. Patients with primary aldosteronism have elevated plasma and urinary total dopamine. After removal of the adenoma urinary dopamine excretion decreases to normal.

4. Elevated conjugated dopamine appears to reflect a compensatory activation of the dopaminergic vasodilator pathway in hypertension, the total urinary dopamine excretion an intrinsic deficiency or compensatory increase of a dopamine-modulated natriuretic mechanism.
Relation of Plasma Noradrenaline to Blood Pressure, Age, Sex and Sodium Balance in Patients with Stable Essential Hypertension and in Normotensive Subjects
Authors: Brecht H. M. , Schoeppe W.
Published: August 2015

1. Plasma noradrenaline was measured in 125 patients with stable essential hypertension (WHO I—II) and in 107 normotensive control subjects lying and standing.

2. In normotensive subjects and in patients with essential hypertension no sex-related differences of plasma noradrenaline were found between age-matched groups.

3. Plasma noradrenaline was not related to sodium balance indexed by urinary sodium/creatinine ratio.

4. In patients with essential hypertension plasma noradrenaline increases with age.

5. Mean plasma noradrenaline concentrations are significantly higher in patients with essential hypertension compared with age-matched normotensive subjects both lying and standing.

6. In patients with essential hypertension diastolic blood pressure and heart rate correlated significantly with supine plasma noradrenaline concentrations.
Enhanced Hypothalamic Noradrenaline Biosynthesis in Goldblatt I Renovascular Hypertension
Authors: Dequattro Vincent , Eide Ivar , Myers Mark R. , Eide Kari , Kolloch Rainer , Whigham Howard
Published: August 2015

1. Hypertension was induced in rats by renal artery clip with the contralateral kidney removed (Goldblatt I) or left intact (Goldblatt II).

2. Plasma noradrenaline was increased 62% in the Goldblatt I animals after 3 weeks.

3. Hypothalamic tyrosine hydroxylase and dopamine β-hydroxylase activities, and the concentration of noradrenaline were increased in the Goldblatt I animals after 3 weeks.

4. Enhanced hypothalamic noradrenaline synthesis may be a pathogenic factor in Goldblatt I renovascular hypertension.
A Renal Carcinoma Secreting Inactive Renin
Authors: Leckie Brenda , Brown J. J. , Fraser R. , Kyle K. , Lever A. F. , Morton J. J. , Robertson J. I. S.
Published: August 2015

1. A patient presented with mild hypertension, a raised plasma total renin concentration but a normal plasma angiotensin II concentration. The discrepancy was due to a high concentration of inactive renin in the plasma.

2. A renal carcinoma was detected and removed. The tumour contained a higher proportion of inactive renin than was found in uninvolved areas of the kidney. After unilateral nephrectomy, the plasma concentration of inactive renin fell to normal.

3. Six months later, plasma inactive renin concentration again increased and a metastasis was detected in a rib. Excision of the rib together with radiotherapy resulted in a fall in plasma inactive renin to normal.

4. The inactive renin in plasma and tumour extracts was activated to the same extent by acid treatment and by trypsin.
The Effects of Calcium and Calcium-Ionophores (X 537 a and a 23187) on Renin Release in the Isolated Perfused Rat Kidney
Authors: Schwertschlag U. , Hackenthal E. , Hackenthal R. , Rohs G. H.
Published: August 2015

1. Calcium depletion from the medium of the isolated perfused kidney reduced renin release and renal perfusate flow.

2. Reintroduction of calcium increased renin release and perfusate flow.

3. The ionophore X 537 A (0·1–4 μmol/l) increased renin release both in the presence and absence of calcium in the medium.

4. The ionophore A 23187 (1–10 nmol/l) increased as well as decreased renin release. There was a positive correlation between direction of this effect and renal perfusate flow.

5. The results are compatible with the view that the effects of calcium and ionophores on renin release are the sum of direct and indirect effects of these agents, the predominant indirect effect being the modification of vascular tone.
Soluble Pep Statins: A New Approach to Blockade in Vivo of the Renin–Angiotensin System
Authors: Evin G. , Gardes J. , Kreft C. , Castro B. , Corvol P. , Menard J.
Published: August 2015

1. Synthesis of several pepstatin A derivatives was performed with the aim of increasing water solubility without altering the capacity to inhibit the renin—angiotensinogen reaction.

2. Pepstatinyl-arginine-O-methyl ester was studied in vitro and in vivo and compared with pepstatin A and with the arginine salt of pepstatin A.

3. This compound inhibited in vitro the reaction between purified hog renin and the synthetic renin N-acetyl-tetradecapeptide or the natural rat renin substrate. The inhibitory constant was of the same order of magnitude as that of pepstatin A.

4. In renal hypertensive rats, the bolus injection of pepstatinyl-arginine-O-methyl-ester or of the arginine salt of pepstatin decreased blood pressure to the same extent as a bolus injection of Sar1, Ala8-angiotensin II.
Tonin–Angiotensin II System in Hypertension
Authors: Boucher R. , Garcia R. , Gutkowska J. , Demassieux S. , Genest J.
Published: August 2015

1. A single intravenous administration of rabbit tonin antiserum into one-kidney one-clip hypertensive rats restored blood pressure to normal in seven out of ten animals. There was little change in blood pressure in two-kidney one-clip hypertensive, uninephrectomized or sham-operated rats.

2. Infusion of tonin in control rats did not modify arterial blood pressure. However, in indomethacin salt-treated rats a marked increase in arterial blood pressure was observed under tonin infusion.

3. Plasma tonin activity was significantly increased in human essential and renovascular hypertension.

4. These findings strongly suggest that tonin is important in the maintenance of high blood pressure. However, other factors (possibly prostaglandins and sodium) have to be modified in order to activate the tonin—angiotensin II system.
An Altered Relation between Arterial Pressure and Plasma Angiotensin II Concentration Resulting from Prolonged Infusion of Angiotensin II
Authors: Bean B. L. , Brown J. J. , Casals-Stenzel J. , Fraser R. , Lever A. F. , Morton J. J. , Petch B. , Riegger A. J. G. , Robertson J. I. S. , Tree M.
Published: August 2015

1. Infusion of angiotensin II into dogs at constant dose over 2 weeks caused a progressive rise in arterial pressure.

2. When the infusion was stopped the pressure dropped slowly from hypertensive levels over 48 h.

3. Dose—response studies at weekly intervals showed progressive elevation, without steepening, of the plasma angiotensin II—blood pressure curve.

4. Thus, during prolonged administration of angiotensin II, a given plasma concentration of the peptide can sustain a higher arterial pressure than it can during acute infusions.
Neuronal and Vascular Reactivity in Isolated Perfused Kidneys during the Development of Spontaneous Hypertension
Authors: Collis Michael G. , Vanhoutte Paul M.
Published: August 2015

1. Vascular reactivity was studied in Tyrode solution perfused kidneys from young (7 weeks) and mature (4–6 months) spontaneously hypertensive rats (SH rats).

2. The response to nerve stimulation was greater in the kidneys from young SH rats than in those from young control rats, both in control solution and after inhibition of the disposition of noradrenaline; both groups exhibited the same sensitivity to noradrenaline, angiotensin II and barium chloride.

3. The response to nerve stimulation was normal in kidneys from mature SH rats, but responses to noradrenaline, angiotensin II and barium chloride were greater than the control.

4. Cocaine potentiated the response to nerve stimulation more in the kidneys from mature SH rats than in those from the control rats.

5. The results suggest that renal sympathetic nerves release more noradrenaline than normal in the young SH rats, which could be an important factor in causing hypertension.

6. In the established phase of spontaneous hypertension the vascular reactivity to exogenous agonists is increased, probably as a consequence of high blood pressure; the more efficient neuronal uptake causes normalization of the response to sympathetic nerve stimulation.
Role of Vasopressin in Blood Pressure Control of Spontaneously Hypertensive Rats
Authors: Möhring Jan , Kintz Jacqueline , Schoun Josiane
Published: August 2015

1. The role of arginine—vasopressin (AVP) and of angiotensin in blood pressure control of spontaneously hypertensive rats (SH rats, stroke-prone strain) was studied.

2. In SH rats, which drank water or 1% NaCl, plasma AVP concentrations were elevated during the benign course of hypertension and increased further when the animals entered the malignant phase. Blood pressure correlated significantly with plasma AVP concentrations in SH rats on water, but not in SH rats on saline.

3. The injection of a specific AVP antiserum lowered blood pressure significantly in SH rats on water and in SH rats on saline.

4. When the correlation between blood pressure and plasma AVP of SH rats on water was compared with the respective correlation obtained during infusion of AVP into normotensive rats, a marked shift to the left became apparent, the factor of displacement amounting to more than 1000.

5. Saralasin did not affect blood pressure of SH rats on water, except for two rats with malignant hypertension. However, in SH rats on saline, saralasin lowered blood pressure significantly.

6. It is concluded that in SH rats AVP plays an important vasopressor role in blood pressure control and that sensitization to the vasopressor effect of AVP occurs in these animals. The renin—angiotensin system is significantly involved in blood pressure control of SH rats only when they are subjected to high salt intake.
Effects of Labetalol on Systemic and Pulmonary Haemodynamics at Rest and during Exercise in Hypertensive Patients
Authors: Fagard R. , Amery A. , Reybrouck T. , Lijnen P. , Billiet L.
Published: August 2015

1. Labetalol was administered to 18 hypertensive patients for an average duration of 2·44 weeks, with an average final daily dose of 1·65 g.

2. Labetalol decreased resting heart rate by 16% and maximal exercise heart rate by 21%; the phenylephrine-induced rise of systolic brachial artery pressure was reduced by 36%.

3. During labetalol brachial artery pressure was lowered by 29/15 mmHg in the recumbent position, by 41/23 mmHg at rest sitting, and by 53/23 mmHg at maximal exercise; total peripheral resistance was not significantly affected at rest recumbent, but was reduced at sitting and at exercise; cardiac output decreased in all conditions.

4. Labetalol reduced mean pulmonary artery and capillary wedge pressures only in the sitting position. Pulmonary vascular resistance remained unchanged.

5. The drug produced significant decreases of plasma renin activity and of plasma aldosterone concentration.
Labetalol in Hypertensive Patients with Angina Pectoris: Beneficial Effect of Combined α- and β-Adrenoreceptor Blockade
Authors: Lubbe W. F. , White D. A.
Published: August 2015

1. Eight hypertensive patients with angina pectoris had placebo added to their existing medications for 8 weeks, then incremental doses of active labetalol with simultaneous stepwise reduction in other medicines until blood pressure was satisfactorily controlled; after that only labetalol and thiazide (8 weeks) and finally labetalol-placebo together with previous β-adrenoreceptor antagonists and thiazide for 4 weeks were administered.

2. During the labetalol plus thiazide period resting blood pressures and measurements obtained during isotonic exercise, isometric exercise and the cold pressor test were significantly lower than during the initial placebo addition period. Angina scores were significantly reduced during this period.

3. During the final treatment with placebo, β-adrenoreceptor antagonist and thiazide, blood pressures remained reduced, but angina was significantly worse.

4. Labetalol which antagonizes both α- and β-adrenoreceptors produced better relief of angina pectoris than β-adrenoreceptor antagonists during improvement in blood pressure in hypertensive patients.
Effect of Selective and Non-Selective β-Adrenoreceptor Blockade on Calf Blood Flow in Hypertensive Patients
Authors: Clement D. L.
Published: August 2015

1. Dose—response curves of isoprenaline were constructed in nine hypertensive patients before and after either propranolol or metoprolol.

2. The decrease of diastolic blood pressure and increase of heart rate with isoprenaline were significantly more inhibited by propranolol than by metoprolol.

3. The increase in calf blood flow with isoprenaline was significantly more depressed after propranolol than after metoprolol.

4. The results suggest that the response of the vessels in the limbs to sympathetic stimulation is much less affected after metoprolol than after propranolol.
Benzothiadazine Diuretics and Death from Myocardial Infarction in Hypertension
Authors: Jones J. V. , Dunn F. G. , Fife R. , Lorimer A. R. , Kellett R. G.
Published: August 2015

1. Case records were examined of 66 patients who died while being treated for high blood pressure.

2. The possibility that benzothiadazine diuretics may have some deleterious as well as beneficial effects was investigated.

3. It is possible that the thiazides may have some adverse clinical effects, at least in females, with regard to the incidence of myocardial infarction in hypertensive patients.
The Role of Nurse Practitioners in Hypertension Care
Authors: Soghikian Krikor
Published: August 2015

1. Two groups of hypertensive patients, randomly assigned to either physician or nurse practitioner care, were compared, after two years of follow up, with respect to diastolic blood pressure reduction and utilization and costs of medical services. In addition, satisfaction with hypertension care was evaluated.

2. There was no statistical difference in mean diastolic blood pressure reduction between the physician and nurse practitioner groups.

3. Patients in the nurse practitioner group made more visits for hypertension care than those in the physician group; thus, even though the cost per nurse practitioner visit was lower than the cost per physician visit, the total annual cost of care per patient was higher in the nurse practitioner group.

4. Patients followed by nurse practitioners were very satisfied with their care.

5. Nurse practitioners provide excellent hypertension care and thereby save valuable physician time.
Improvement in Foetal Growth with Treatment of Maternal Hypertension in Pregnancy
Authors: Gallery E. D. M. , Saunders D. M. , Hunyor S. N. , Györy A. Z.
Published: August 2015

1. A highly significant inverse relationship was found between blood pressure in untreated hypertensive subjects in late pregnancy and birth weight.

2. Reversal of this intrauterine growth retardation was achieved in 19 patients by treatment of hypertension with oxprenolol.

3. No adverse effects from oxprenolol were found in the patients or in their babies.
Biochemical Correlates of the Increase in Blood Pressure with Age
Authors: Grim C. E. , Weinberger M. H. , Henry D. P. , Luft F. C. , Fineberg N. S.
Published: August 2015

1. Blood pressure, plasma renin activity, plasma aldosterone, urinary noradrenaline during sleep (UNA-S) and several estimates of sodium intake were determined in 379 normotensive subjects (age 13–70) to investigate the relationship of these variables to blood pressure.

2. Blood pressure was correlated with age, weight, plasma renin activity UNA-S, and estimates of sodium intake. These variables were frequently intercorrelated.

3. Multiple-correlation analysis revealed that after removal of the effects of age, blood pressure was related to weight, plasma renin activity, UNA-S and estimates of sodium intake.

4. However, multiple-regression analysis failed to demonstrate an effect of plasma renin activity, UNA-S, or estimates of sodium intake on blood pressure when the effects of age, weight, race and sex were removed.

5. Careful matching of subjects by age, weight, race and sex in studies of blood pressure and biochemical factors in normal subjects is crucial to proper interpretation of such data.
The Effect of Mental Arithmetic on Blood Pressure Variability and Baroreflex Sensitivity in Man
Authors: Sleight P. , Fox P. , Lopez R. , Brooks D. E.
Published: August 2015

1. Baroreflex sensitivity was tested in three normal, three borderline and one hypertensive subject before and during mental arithmetic, the prolongation of pulse interval caused by a provoked rise in blood pressure being used as a measure of baroreflex sensitivity.

2. Baroreflex sensitivity was significantly decreased during mental arithmetic.

3. During mental arithmetic the arterial pressure fluctuated markedly.

4. These findings suggest that in man, as well as animals, the defence of alerting reaction depresses baroreflex control and thus contributes to the rise in blood pressure seen at this time.
Time-dependent Changes in Prostaglandin Excretion in Response to Frusemide in Man
Authors: Scherer B. , Weber P. C.
Published: August 2015

1. To evaluate in man by a non-invasive technique the possible role of prostaglandin (PG) compounds in initial renal haemodynamic effects after frusemide we studied the urinary excretion of PGE2 and of PGF2α before and at 15 min and 120 min after intravenous injection of this drug.

2. An increase of PGE2 and of PGF2α excretion was found in all 19 volunteer subjects within 15 min after frusemide, and PG excretion had returned towards control values at 120 min. The stimulation of PGF2α excretion by frusemide was markedly lower in men than in women, but this difference was statistically not significant.

3. No clear-cut relation was found between urinary PG compounds, on the one hand, and urinary volume, urinary sodium and urinary potassium, on the other hand, during the study.

4. The results support the assumption that the rapid increase of urinary PG compounds after frusemide, which parallels the changes in renal haemodynamics, may be an indicator of an activation of the PG system, in part or predominantly, in the vascular compartment.
Inactive Renin in Rabbit Plasma: Effect of Haemorrhage
Authors: Richards H. K. , Grace S. A. , Noble A. R. , Munday K. A.
Published: August 2015

1. Renin activity in rabbit plasma increases after acidification (pH 3·3), probably due to activation of an inactive form of renin.

2. Both active and inactive renin in plasma increase after haemorrhage. This stimulus does not change the relative proportions of the two forms.

3. After ligation of the renal blood vessels neither form of renin increases in response to haemorrhage.

4. One day after bilateral nephrectomy no inactive renin could be demonstrated in plasma.

5. In the rabbit, therefore, the kidney is a major source of the inactive renin in plasma.
Hypertension with Mineralocorticoid Administration to the Long-Evans Rat
Authors: Holland O. B. , Gomez-Sanchez C. , Ziegler T.
Published: August 2015

1. The Carworth Long-Evans rat has been reported to develop adrenal-regeneration hypertension but not deoxycorticosterone acetate (DOCA) hypertension. Deficiency of a hypothalamic receptor for deoxycorticosterone which mediates saline polydipsia has been postulated to underlie this resistance. Since a mineralocorticoid etiology for adrenal-regeneration hypertension has been postulated and all mineralocorticoids are thought to act on common receptors, these previous reports are difficult to reconcile.

2. To determine if an absolute or relative resistance to mineralocorticoids is present, Charles River Long-Evans and Sprague-Dawley rats were given 40 mg (107 μmol) of DOCA pellets/rat or 250 μg (0·65 μmol) of 2α-methyl-9α-fluorocortisol/day subcutaneously.

3. Saline polydipsia occurred with both steroids with both rat strains, though significantly less with the Long-Evans rats. Both types of rats became hypertensive and developed cardiac and renal enlargement with both steroids. Hypertension developed more rapidly with 2α-methyl-9α-fluorocortisol.

4. Thus mineralocorticoid hypertension can be produced in the Charles River Long-Evans rat, and the development of adrenal-regeneration hypertension in this rat strain is not incompatible with a mineralocorticoid etiology for adrenal-regeneration hypertension.
Evidence for Activation of Circulating Inactive Renin by the Human Kidney
Authors: Derkx F. H. M. , Wenting G. J. , In't Veld A. J. Man , Verhoeven R. P. , Schalekamp M. A. D. H.
Published: August 2015

1. In eight patients with essential hypertension (EHT) and six patients with renovascular hypertension (RVHT) peripheral venous enzymatically active and inactive renin values were followed after acute stimulation of renin release by the vasodilating agent diazoxide (300 mg intravenously). Active renin rose during the first hour after diazoxide and remained high during the following 15 h, but inactive renin fell during the first hour and rose thereafter. Peripheral venous active and inactive renin were not different from arterial values both before and after diazoxide.

2. Sixteen patients with EHT received propranolol, 80 mg, four times a day. Six of them had a first injection of diazoxide the day before propranolol was started and a second one after 10–14 days of propranolol treatment. Peripheral vein active renin was lowered by propranolol, but inactive renin was raised. Both the diazoxide-induced rapid rise of active renin and the fall of inactive renin observed in untreated patients were absent during treatment with propranolol.

3. In four patients with EHT and seven patients with RVHT renal vein sampling was performed before and 30 min after diazoxide. Increased release of active renin from kidneys that were not markedly contracted was associated with a fall of the renal vein to peripheral vein ratio of inactive renin to a value less than one.

4. It is concluded that under certain circumstances stimulated release of active renin is associated with removal of inactive renin from the circulation by the kidney. This may in fact be due to intrarenal transformation of circulating inactive renin into its active counterpart. The findings suggest that a β-adrenoreceptor might be involved in this activation process.
Glycerol-Induced Acute Renal Failure in Brattleboro Rats with Hypothalamic Diabetes Insipidus
Authors: Konrads A. , Hofbauer K. G. , Bauereiss K. , Möhring J. , Gross F.
Published: August 2015

1. During the development of glycerol-induced acute renal failure in Sprague-Dawley rats, plasma concentrations of vasopressin rise and probably induce an increase in blood pressure.

2. In the present studies the role of vasopressin in acute renal failure was further analysed by experiments in Brattleboro rats homozygous for hereditary hypothalamic diabetes insipidus which were injected intramuscularly with 10 ml of glycerol/kg (61 mmol/l).

3. After the injection of glycerol plasma osmolality increased transiently and packed cell volume was elevated. The rats became anuric and plasma urea concentrations rose progressively. Plasma renin concentration increased significantly within 2 h. Plasma renin substrate concentration rose progressively and had almost doubled by 8 h.

4. In contrast with previous observations in Sprague-Dawley rats, blood pressure did not rise in rats with diabetes insipidus after the injection of glycerol.

5. When 2 h after the injection of glycerol kidneys were taken from rats with diabetes insipidus and perfused with an electrolyte solution in a single-pass system for 1 h, renal vascular resistance was 30% higher than in control kidneys 10 min after the start of the perfusion and remained elevated thereafter. In similar experiments with kidneys from Sprague-Dawley rats with acute renal failure, renal vascular resistance was increased fivefold immediately after the start of the perfusion, but decreased subsequently.

6. These data support the idea that in glycerol-induced acute renal failure of Sprague-Dawley rats an increased release of vasopressin is responsible for the elevation of blood pressure and suggest that this hormone also participates in renal vasoconstriction. However, a rise of plasma vasopressin concentrations alone cannot fully explain the increase in renal vascular resistance and the development of acute renal failure.
Inhibition of Mitochondrial Electron Transfer in Rats by Ethanethiol and Methanethiol
Authors: Vahlkamp T. , Meijer A. J. , Wilms J. , Chamuleau R. A. F. M.
Published: August 2015

1. We have investigated the effects of ethanethiol, methanethiol and dimethyl sulphide on some metabolic processes of isolated rat hepatocytes, isolated mitochondria from liver and brain and ox-heart submitochondrial particles.

2. Ethanethiol, but not dimethyl sulphide, inhibited both gluconeogenesis and ureogenesis from various substrates in rat hepatocytes, depressed cellular ATP content and caused an increased reduction of the mitochondria.

3. Ethanethiol inhibited respiration in isolated rat-liver mitochondria with several substrates, both in the presence of ADP and phosphate or in the presence of an uncoupling agent. Ethanethiol also inhibited respiration in isolated rat-brain mitochondria. Dimethyl sulphide was much less effective in inhibiting mitochondrial respiration.

4. In ox-heart submitochondrial particles ethanethiol inhibited electron transfer between cytochrome c and oxygen.

5. Purified cytochrome c oxidase was inhibited by ethanethiol in a non-competitive manner.

6. Methanethiol inhibited cytochrome c oxidase and was an effective inhibitor of mitochondrial electron transfer, both in liver and brain.

7. The difference in inhibitory properties between ethanethiol, methanethiol and dimethyl sulphide observed in our experiments coincides with the difference in potency to elicit coma in rats. We suggest that inhibition of mitochondrial electron transfer by mercaptans may be relevant to the mechanism by which energy production in brain is depressed during hepatic coma.
The Role of the Baroreceptor Reflex in the Cardiovascular Effects of Propranolol in the Conscious Spontaneously Hypertensive Rat
Authors: Struyker-Boudier H. A. J. , Smits J. F. , Van Essen H.
Published: August 2015

1. The role of baroreceptors in the cardiovascular mechanism of action of dl-propranolol has been studied by comparing the acute effects of subcutaneous injection of 1 and 5 mg/kg (3·3 × 10−6 and 16·5 × 10−6 mol/kg) of this drug in conscious baroreceptor-denervated spontaneously hypertensive (SH) rats with those in sham-operated control SH rats.

2. At 5 mg/kg (16·5 × 10−6 mol/kg) propranolol caused a small, but significant, increase in blood pressure in sham-operated SH rats, whereas both after 1 and 5 mg/kg (3·3 × 10−6 and 16·5 × 10−6 mol/kg) immediate hypotension was observed in baroreceptor-denervated animals.

3. Heart rate dropped rapidly after injection of 1 or 5 mg/kg (3·3 × 10−6 and 16·5 × 10−6 mol/kg) propranolol both in the baroreceptor-denervated and sham-operated SH rats. Bradycardia was significantly larger in the baroreceptor-denervated animals after an injection of 5 mg/kg (16·5 × 10−6 mol/kg).

4. It is concluded that the lack of an early hypotensive effect of propranolol in intact animals is caused by an increased baroreceptor reflex activity as a consequence of the fall in cardiac output.
Kallikrein—Kinin System in One- and Two-Kidney Goldblatt Hypertensive Rats
Authors: Albertini R. , Rosas R. , Croxatto H. R. , Roblero J.
Published: August 2015

1. Urinary kallikrein, renal tissue kininogenase activity, and plasma kininogen were measured during the development of hypertension in rats, either with left renal artery clamped and contralateral kidney intact (Goldblatt 2-kidney) or removed (Goldblatt 1-kidney). Plasma urea, plasma volume and blood volume were also measured.

2. In Goldblatt 2-kidney rats, urinary kallikrein was not significantly different from that of sham-operated rats up to the 5th post-operative week even though at this time the Goldblatt 2-kidney animals were hypertensive. Urinary kallikrein started to decrease at week 8. Plasma kininogen was significantly elevated 5 and 10 weeks after surgery and returned to normal by week 15. No changes in renal tissue kininogenase activity were observed. Plasma urea and plasma and blood volumes were normal 5 weeks after, but significantly increased at 10 and 15 weeks after surgery.

3. In Goldblatt 1-kidney rats from the fifth week urinary kallikrein and renal kininogenase activity were significantly decreased compared with unilaterally nephrectomized rats, whereas plasma kininogen, plasma urea and plasma and blood volumes were significantly elevated.

4. These results show important differences in the kallikrein system between the Goldblatt 1-kidney and 2-kidney models of renovascular hypertension in rats.
Inhibition of Rat Liver Mitochondrial 3-hydroxy-3-methylglutaryl-CoA Lyase by Succinyl-CoA
Authors: Deana Renzo , Rigoni Fernanda , Galzigna Lauro
Published: August 2015

1. Succinyl-CoA inhibits 3-hydroxy-3-methylglutaryl-CoA lyase (EC 4.1.3.4) when added to purified preparations of the enzyme.

2. The apparent Ki value is 2·1 × 10−4 mol/l and the inhibition has the features of a partially competitive inhibition.

3. The effect of succinyl-CoA both added and enzymically produced on the lyase activity of sonically disrupted rat liver mitochondria results in decreased acetoacetate formation.

4. This occurs with mitochondria obtained from normal, starved and streptozotocin-diabetic rats.

Riassunto

1. Il succinilCoA inibisce la 3-idrossi-3-metilglutarilCoA liasi (EC 4.1.3.4) se viene aggiunto a preparazioni di enzima purificato.

2. Il valore della Ki è 2·1 × 10−4 mol/l ed i dati indicano una inibizione parzialmente competitiva.

3. Il succinilCoA, aggiunto o prodotto enzimaticamente, provoca una diminuzione nella produzione di acetoacetato nei mitocondri sonicati di fegato di ratto.

4. Lo stesso fenomeno si verifica con mitocondri di ratti normali, digiuni e diabetici da streptozotocina.
Correlation of Ethanol Concentrations in Blood and Saliva
Authors: McColl K. E. L. , Whiting B. , Moore M. R. , Goldberg A.
Published: August 2015

1. The concentrations of ethanol in blood, mixed saliva obtained before and after rinsing and drying the mouth and parotid saliva have been monitored in 12 healthy subjects after the ingestion of alcohol.

2. A highly significant linear correlation was found between blood and the three types of saliva examined from 20 min after completion of drinking.

3. Blood and mixed saliva samples were obtained from 20 patients attending the Casualty Department with evidence of ethanol intoxication. A similar correlation was obtained.

4. These results show that salivary ethanol may be used as an index of blood ethanol concentrations, provided that the salivary sample is not obtained within 20 min of the ingestion of alcohol.
Effect of Sodium Depletion on the Steroidogenic and Pressor Actions of Angiotensin in the Rat
Authors: Campbell W. B. , Schmitz J. M. , Itskovitz H. D.
Published: August 2015

1. To investigate the relative roles of angiotensin II (AII) and des-Asp1-angiotensin II (angiotensin III) in the control of blood pressure and aldosterone release, the effects of seven angiotensin agonists on mean arterial blood pressure and serum aldosterone concentrations were compared in normal and sodium-depleted, conscious rats.

2. In normal rats, angiotensin I, α-Asp1-angiotensin II, β-Asp1-angiotensin II, and angiotensin II-amide were equipotent in elevating mean arterial blood pressure. Angiotensin III, des-Asp1-angiotensin I, and poly-O-acetylserine-angiotensin II were 25%, 25%, and 41% as potent as angiotensin II, respectively. After sodium depletion, pressor responses to these angiotensin peptides were reduced approximately 60–80% when compared with control responses. In contrast, pressor responses to noradrenaline were not significantly affected by sodium depletion.

3. Angiotensin II, β-Asp1-angiotensin II, angiotensin II-amide, and angiotensin III were equipotent in increasing serum aldosterone concentrations in normal animals. Angiotensin I was 59% and des-Asp1-angiotensin I only 5% as potent as angiotensin II in their abilities to release aldosterone. After sodium depletion, control serum aldosterone concentrations increased as did the slope of the dose—response curve for each angiotensin peptide. Angiotensin II was the most potent steroidogenic peptide in sodium-depleted rats with angiotensin III and β-Asp1-angiotensin II being 27%, angiotensin I 7%, angiotensin II-amide 3%, and des-Asp1-angiotensin I 1% as potent as angiotensin II in releasing aldosterone. Poly-O-acetylserine-angiotensin II has less steroidogenic effect than angiotensin II or III in both normal and sodium-depleted animals.

4. Infusions of the angiotensin II antagonist, Sar1-Ile8-angiotensin II, and the angiotensin III antagonist, Ile7-angiotensin III, enhanced aldosterone release in normal rats without altering blood pressure. After sodium depletion, Sar1-Ile8-angiotensin II decreased blood pressure without affecting aldosterone release whereas Ile7-angiotensin III diminished aldosterone release without altering blood pressure.

5. These data suggest that angiotensin II, independent of its conversion into angiotensin III, is an important regulator of steroidogenesis in the rat in normal sodium states. In sodium depletion, the octapeptide retains significant steroidogenic activity; however, the contribution of angiotensin III to its steroidogenic effects is increased.
Increased Turnover of Muscle Contractile Proteins in Duchenne Muscular Dystrophy as Assessed by 3-Methylhistidine and Creatinine Excretion
Authors: Ballard F. J. , Tomas F. M. , Stern L. M.
Published: August 2015

1. Myofibrillar protein degradation has been measured in patients with Duchenne muscular dystrophy, normal boys, adult males and Duchenne carriers by the rate of 3-methylhistidine excretion after transfer of subjects to a meat-free diet.

2. Although absolute rates of protein breakdown are lower in Duchenne patients, expression of the data to allow for differences in muscle mass gives fractional degradation rates 2–3 times higher than in age-matched controls.

3. Fractional rates of muscle protein synthesis are increased in the Duchenne patients to almost the same extent as protein breakdown.

4. Rates of muscle protein breakdown in obligate and presumed carriers of the Duchenne gene are not different from controls.
Studies on Mineralocorticoid ‘Escape’ in Cirrhosis
Authors: Wilkinson S. P. , Smith I. K. , Moodie Helen , Poston Lucilla , Williams R.
Published: August 2015

1. The mineralocorticoid 9α-fluorohydrocortisone was given to 12 patients with cirrhosis without ascites. In seven an ‘escape’ from its sodium-retaining effects was observed, the other five continuing to retain sodium.

2. Changes in plasma renin activity (PRA) and inulin clearance (Cinulin) were used in the assessment of possible changes in the ‘effective’ extracellular fluid volume. PRA fell and Cinulin increased to a similar extent in each of the two groups of patients. These findings do not support the concept that the failure to show the mineralocorticoid escape in some patients with cirrhosis is due to a failure of expansion of the effective extracellular fluid volume.

3. Sodium reabsorption in the different segments of the nephron as estimated by clearance techniques under conditions of maximal water diuresis showed that the greatest changes to account for both mineralocorticoid escape and sodium retention were in the part of the nephron beyond the diluting segment.