bluuebunny/crossref_metadata_2025_split huggingface dataset:
STIMULATION BY ANGIOTENSIN OF PROSTACYCLIN BIOSYNTHESIS IN RATS AND DOGS
Authors: Dusting G. J. , Mullins Elizabeth M. 
Published: June 2007

SUMMARY1. Stimulation of prostanoid release by angiotensins (AI and All) in rat isolated mesenteric vasculature and in the circulation of anaesthetized dogs has been investigated by bioassay.2. AI and All released a PGI2‐like substance into rat mesenteric effluent and arterial blood of dogs; PGE2, PGF2α or TXA2 were not detected.3. AI stimulated PGL release in both systems largely as a result of its conversion to All, since PGI2 release was much reduced after treatment with captopril.4. Intravenous AII (0‐2‐1.0μg kg−1min−1) in dogs released PGI2 mainly from the lungs since right atrial blood contained much less than arterial blood.5. Indomethacin (1 μg/ml) abolished All‐induced PGI2 release from the mesentery preparation, but intravenous indomethacin (10 mg/kg), meclofena‐mate (2 mg/kg) or aspirin (100 mg/kg) did not eliminate the pulmonary source of PGI2 in dogs. These findings highlight the dangers of assuming in vivo treatment with cyclo‐oxygenase inhibitors abolishes biosynthesis of all prostanoids.
EFFECT OF β‐ADRENORECEPTOR BLOCKADE ON THE RENIN RESPONSE TO ACUTE NATRIURESIS
Authors: Vandongen Robert , Barden Anne , Tunney Anne 
Published: June 2007

SUMMARY1. The response of plasma renin activity to frusemide 40 mg given intravenously, was examined before and after oral propranolol 160 mg daily for 7 days in normal and hypertensive subjects.2. Although basal renin levels were often reduced, the increase following frusemide was essentially unaltered by propranolol therapy.3. These findings indicate that enhanced renin activity associated with diuretic use may not be prevented by concurrent propranolol administration. Limitation of the hypotensive action of combined β‐blocker diuretic therapy can therefore be anticipated.4. Preservation of the renin stimulatory effect of frusemide during beta blockade confirms the value of this procedure in the investigation of mineralo‐corticoid and renovascular hypertension where discontinuation of treatment may be undesirable.
EFFECTS OF MEXILETINE ON TRANSMEMBRANE ACTION POTENTIALS AS AFFECTED BY EXTERNAL POTASSIUM CONCENTRATION AND BY RATE OF STIMULATION IN GUINEA‐PIG PAPILLARY MUSCLES
Authors: Sada Hideaki , Ban Takashi , Oshita Shuzo 
Published: June 2007

SUMMARY1. The effects of mexiletine and quinidine were compared on transmembrane potentials in guinea‐pig papillary muscles, using conventional microelectrode techniques.2. Mexiletine (23–1 μ mol/1) decreased the maximum rate of rise of the action potential (V̇max) and increased the ratio of the effective refractory period to the action potential duration at 90% repolarization level (ERP/APD90); these effects were prominent with elevation of the external potassium concentration ([K]o) from 2–7 to 5–4, 81 and 100mmol/1.3. The percentage decrease in V̇max induced by 5 and 10 μmol/1 of quinidine was approximately constant in 2–7, 5–4 and 100 mmol/1 [K]o solutions.4. The decrease in V̇max produced by mexiletine was progressively increased as the driving rate was raised from 0–25 to 5H z. This rate‐dependent change was pronounced when the concentration was raised from 23–1 to 46–2 and 92–4 /μmol/1.5. Mexiletine in concentrations of 23–1 and 92–4 μ miol/1 delayed the recovery of V̇max in a premature action potential to the level of V̇max in the conditioning action potentials at the driving rate of 0–25 Hz.6. It appears that mexiletine exerts its anti‐arrhythmic action by a selective depressant effect on depolarized cells (high [K]o) and cells with high frequency discharges, as is the case with lignocaine.
THE CARDIAC AND VASCULAR EFFECTS OF SODIUM GLUTAMATE
Authors: Kirkendol Paul L. , Pearson James E. , Robie Norman W. 
Published: June 2007

SUMMARY1. The cardiovascular effects of sodium glutamate were investigated in anaesthetized dogs with bolus injections, intravenous infusions and rabbit isolated papillary muscles.2. The intravenous bolus injections of sodium glutamate resulted in slight, transient decreases in contractile force at doses of 58 and 117 mg/kg, which were followed by brief increases in blood pressure.3. Sodium glutamate had no effect on contractile responses of isolated papillary muscles at any of the concentrations used.4. Infusions of glutamate produced no change in blood pressure, an increase in cardiac output, and a decrease in heart rate, total peripheral resistance and femoral vascular resistance.5. The infusion of sodium glutamate into animals with no renal function resulted in an increased plasma osmolality and a decreased haematocrit.6. The results from this study show that sodium glutamate had minimal cardiovascular effects. The results from the infusion data suggest that glutamate increases intravascular volume by an osmotic effect.
ORTHOSTATIC HYPOTENSION AFTER THE FIRST ADMINISTRATION OF PRAZOSIN IN HYPERTENSIVE PATIENTS: ROLE OF THE PLASMA VOLUME
Authors: Semplicini A. , Pessina A. C. , Palatini P. , Hlede M. , Dal Palù C. 
Published: June 2007

SUMMARY1. Prazosin (2 mg, p.o.) was administered to nine patients with essential hypertension while intra‐arterial pressure was recorded by an Oxford portable apparatus. In all patients, 30 min‐3 h after the administration, systolic and diastolic pressure fell on assuming the upright posture and four patients fainted. No correlation was found between the degree of fall in pressure and the plasma concentration of the drug. Acute expansion of the plasma volume by means of 6% Dextran infusion reduced the orthostatic blood pressure fall in all cases and a significant inverse correlation was found between plasma volume and orthostatic fall of pressure.2. After ten days of continuous treatment with prazosin, 2 mg daily, a significant decrease in blood pressure was observed while orthostatic hypotension disappeared, probably due to the plasma volume expansion induced by the drug.
ADRENALINE DEPLETION IN THE HYPOTHALAMUS OF THE RAT AFTER CHRONIC α‐METHYLDOPA
Authors: Beart P. M. , Prosser Denise , Louis W. J. 
Published: June 2007

SUMMARY1. Individual anterior hypothalamic‐preoptic nuclei were dissected from the brains of control and α‐methyldopa treated (2 × 40 mg/kg, 5 days) rats, and the concentrations of adrenaline and other catecholamines were estimated.2. By a combination of radioenzymatic assay and paper chromatography the concentrations of adrenaline, noradrenaline, dopamine, α‐methylnoradrenaline and α‐methyldopamine were determined concurrently in the same sample.3. α‐Methyldopa reduced the adrenaline levels of the hypothalamic nuclei by 47–68% of control concentrations.4. A differential displacement of the parent catecholamines was observed and the depletions were ranked: adrenaline < dopamine < noradrenaline.5. α‐Methylnoradrenaline and α‐methyldopamine were found in all hypothalamic nuclei.6. The depletion of hypothalamic adrenaline by α‐methyldopa could represent a pharmacological mechanism contributing to the antihypertensive action of the drug.
EFFECTS OF ISOPRENALINE, LEVODOPA AND A PHOSPHODIESTERASE INHIBITOR (ICI 63,197) ON CYCLIC AMP LEVELS AND CONTRACTIONS OF SOLEUS MUSCLES IN ANAESTHETIZED CATS
Authors: Merican Zainuddin , Nott M. W. 
Published: June 2007

SUMMARY1. Cyclic AMP levels have been determined in the soleus muscles of anaesthetized cats in the absence of drugs, and during depression of incomplete tetanic contractions produced by (‐)‐isoprenaline, ICI 63,197 (a phosphodiesterase inhibitor) or levodopa.2. Cyclic AMP levels were elevated at the peak of tension depression produced by isoprenaline. Effects of isoprenaline on cyclic AMP and on contractions were dose dependent and statistically significantly related one to the other. Both effects were blocked by propranolol.3. ICI 63,197 and levodopa produced isoprenaline‐like effects on contractions but times to peak effect and recovery were longer. Cyclic AMP levels estimated during the depressant action were elevated.4. The results support the involvement of cyclic AMP in the depressant effect of β‐adrenoreceptor agonists on slow‐contracting mammalian skeletal muscle.
EFFECT OF DEPLETION OF SPINAL NORADRENALINE BY 6‐HYDROXYDOPAMINE ON THE DEVELOPMENT OF RENAL HYPERTENSION IN RATS
Authors: Bosland M. C. , Versteeg D. H. G. , van Put J. , de Jong W. 
Published: June 2007

SUMMARY1. A single injection in rats of 250 μg of 6‐hydroxydopamine HCl (6‐OHDA) into the subarachnoidal space of the spinal cord of rats resulted in a lasting, selective depletion of spinal noradrenaline. Dopamine levels in the spinal cord and catecholamine levels in various brain regions were not markedly affected.2. When ether anaesthesia was used spinal noradrenaline was found to be almost completely depleted by the administration of 6‐OHDA. Only partial depletion was achieved when pentobarbitone anaesthesia or neuroleptic analgesia was used.3. The blood pressure rise caused by electrical stimulation of the posterior hypothalamus was not affected by 6‐OHDA treatment 7 days previously.4. 6‐OHDA administration did not influence the development of two‐kidney Goldblatt hypertension. When 6‐OHDA was administered 7 days before clipping, a slight delay of the development was observed, but this did not occur when 6‐OHDA treatment was given 3–4 h before clipping.5. It is concluded that intact spinal noradrenergic neurotransmission is neither a prerequisite for the development of two‐kidney Goldblatt hypertension, nor for the pressor response to hypothalamic stimulation.
STUDIES IN THE RAT ON ENDRALAZINE, A NEW ANTIHYPERTENSIVE DRUG STRUCTURALLY RELATED TO HYDRALAZINE
Authors: Oates Helen F. , Stoker Lynette M. 
Published: June 2007

SUMMARY1. The effects on blood pressure, heart rate and plasma renin activity of a new hydralazine congener, endralazine, were evaluated in anaesthetized rats. Dose‐response relationships for endralazine, hydralazine and diazoxide, administered intravenously, were compared, and the interactions of endralazine with the ganglionic blocking agent, pentolinium, or with adrenaline, noradrenaline and angiotensin II were examined.2. In the dose range 0.05 to 1.0 mg/kg, endralazine produced prompt dose‐related reductions in systolic and diastolic blood pressure, with relatively little effect on heart rate. The drug had a pronounced dose‐related renin stimulating effect.3. Endralazine retained approximately 80% of its hypotensive activity after pretreatment with pentolinium, and caused no significant attenuation of pressor responses to adrenaline, noradrenaline or angiotensin II.4. Endralazine was an effective hypotensive agent, with a prompt onset of action, a prolonged and stable effect, and a potency at least twice that of hydralazine and 20 to 25 times that of diazoxide. The data are consistent with a predominantly direct vasodilator mode of action.
THE EFFECTS OF GABA‐ERGIC DRUGS ON ENKEPHALIN‐INDUCED MOTOR SEIZURE PHENOMENA IN THE RAT
Authors: Dzoljic M. R. , Poel‐Heisterkamp A. L. v. d. 
Published: June 2007

SUMMARY1. The relationship between the effects of GABA‐ergic drugs and D‐ala2 ‐met‐enkephalinamide (DALA)‐induced myoclonic contractions of inframandibular muscles has been studied in the rat.2. GABA‐ergic drugs altered enkephalin‐induced myoclonic contractions in the following manner:(a) The GABA‐mimetic drugs, muscimol, gabaculine and baclofen, decreased DALA‐induced myoclonic contractions.(b)The GABA antagonist, bicuculline and the anticonvulsant substance, sodium valproate (dipropylacetic acid, DPA) potentiated DALA‐induced myoclonic contractions. The potentiating effect of DPA is probably due to its opiate‐like activity, since naloxone abolished this effect.3. The modulatory effect of the GABA‐mimetic drug on enkephalin‐induced myoclonic contractions may give grounds for further study to test the possible use of other GABA‐mimetic drugs and possibly opiate antagonists for the treatment of myoclonic syndromes.
CARDIAC β‐ADRENORECEPTORS IN THE THYROXINE‐TREATED DOG
Authors: Ho K. , Lloyd B. L. , Taylor R. R. 
Published: June 2007

SUMMARY1. Myocardial β‐adrenoreceptors, assessed in membrane preparations of left ventricle by 3 H‐dihydroalprenolol binding, were compared in dogs following thyroxine administration (n= 6), aortocaval fistula (n= 12), and in normal dogs (n= 7).2. Left ventricular hypertrophy occurred in response to both aortocaval fistula and thyroxine treatment. Yield of myocardial membrane between the different groups was not significantly different.3. Binding site concentration (pmol/mg membrane protein) in dogs with aortocaval fistulae was similar to that in normal dogs and was not significantly influenced by the presence or absence of cardiac failure, degree of hypertrophy or duration of fistula.4. Thyroxine‐treated dogs had an increased concentration of binding sites (c. 1.8‐fold) compared with both fistula and normal groups, while binding affinities were similar in all groups.5. The data suggest that β‐adrenoreceptor concentrations in myocardium increase as a direct result of thyroid hormone action rather than as a result of secondary haemodynamic changes or ventricular hypertrophy.
IMPORTANCE OF CIRCULATING ANGIOTENSIN II FOR ELEVATION OF ARTERIAL PRESSURE DURING ACUTE HYPERCAPNIA IN ANAESTHETIZED DOGS
Authors: Staszewska‐Barczak Janina , Dusting Gregory J. 
Published: June 2007

SUMMARY1. In anaesthetized dogs acute hypercapnia produced by ventilation with 10% CO2 in air caused release of vasoactive substances and changes of arterial pressure. Catecholamines, angiotensin II, bradykinin and prostaglandin‐like substances were bioassayed continuously in arterial blood using the blood‐bathed organ technique of Vane.2. Acute hypercapnia in control dogs causes responses of rat stomach strip, chick rectum and rat colon indicating initial release of noradrenaline, followed by angiotensin II, and occasionally release of prostaglandin‐like substances into the circulation.3. The initial transient, pressor response to hypercapnia coincided with the appearance of noradrenaline, and the secondary progressive rise in arterial pressure was accompanied by increased circulating angiotensin II.4. In dogs treated with the angiotensin converting enzyme inhibitor SQ 20881 (1–2 mg/kg, i.v.), hypercapnia did not cause the secondary elevation of arterial pressure despite pronounced elevation of noradrenaline levels in the circulation. Increased arterial concentrations of bradykinin of less than 1 ng/ml, assayed by a strip of cat jejunum, were detected during hypercapnia in four out of six dogs treated with SQ 20881, but not in untreated dogs.5. Intravenous infusion of the angiotensin antagonist [Sar1‐Ile8]‐angiotensin II (0.5–1.0 μg/kg per min) attenuated the secondary pressor response to hypercapnia and abolished the contractions of rat colon produced by hypercapnia and angiotensin II.6. The results indicate that adrenergic stimulation may be responsible for the transient pressor response on induction of hypercapnia, but elevation of angiotensin II activity in the circulation is of major importance for mediating the secondary progressive rise in arterial pressure during the later stage of acute respiratory acidosis.7. After inhibition of angiotensin converting enzyme, hypercapnia reduces arterial pressure, not only because the vasoconstrictor effect of angiotensin has been removed, but also because inhibition of pulmonary kininase may allow vasodilator kinins to reach the arterial circulation.
SODIUM‐DEPENDENT RELAXATION IN ARTERIAL SMOOTH MUSCLE *
Authors: Gillespie Mark N. , Niehaus Karl E. , Rodger Ian W. , Diamond Louis 
Published: June 2007

SUMMARY1. The effects of isosmotic substitution of choline for sodium on resting tension and on relaxation after noradrenaline‐induced contraction was studied in rabbit isolated aortic strips immersed in Hepes‐buffered physiologic salt solution (PSS) warmed to 37°C and gassed with 100% O2.2. Isosmotic substitution of choline for sodium produced a sustained increase in resting tension which effectively prevented any evaluation of the influence of sodium on relaxation. The increase in resting tension was insensitive to 10−8 mol/1 atropine but was abolished by 10 min exposure to calcium‐free PSS prior to replacement of sodium.3. Under sodium‐calcium free conditions which eliminated the increase in resting tension observed in sodium‐free PSS, stimulation with 10−5 mol/1 noradrenaline initiated contractions that were 55 ± 7.5% of the control response in normal PSS. Washout of noradrenaline with sodium‐calcium‐free PSS failed to produce any decrement in tension. However, restoration of the normal sodium resulted in gradual relaxation.4. These results suggest that sodium is required for relaxation after noradrenaline‐induced contraction of arterial smooth muscle.
SYSTEMIC AND REGIONAL HAEMODYNAMIC RESPONSES TO ISOPRENALINE IN CONSCIOUS RENAL HYPERTENSIVE RABBITS
Authors: van Boom Martin , Saxena Pramod R. 
Published: June 2007

SUMMARY1. Using the electromagnetic flow probe and the radioactive microsphere technique, systemic and regional haemodynamic variables were measured in conscious normotensive and hypertensive rabbits. The rabbits were made hypertensive by unilateral nephrectomy combined with cellophane‐wrapping of the remaining kidney and systemic and regional haemodynamic effects of isoprenaline infusions (0.5 μg‐kg−1 .min−1) were compared in the two groups of animals.2. Isoprenaline evoked increases in heart rate and cardiac index while the total peripheral resistance decreased. In the hypertensive rabbits the effects were similar, except for a significantly more pronounced decrease in blood pressure.3. Isoprenaline increased the fraction of the cardiac output delivered to the heart, skin and fat, at the expense of the fractions to the brain, stomach, small intestine, pancreas, liver and kidney(s) in both normotensive and hypertensive animals. Local peripheral resistance was decreased, most prominently, in the heart, skin, skeletal muscle and fat.4. In the normotensive rabbits pretreatment with propranolol (4 mg.kg−1 infused in 1 h) effectively blocked the cardiovascular responses following isoprenaline infusion.5. Since the systemic and regional haemodynamic effects of isoprenaline were not less (if anything, slightly more) in the hypertensive than in the normotensive rabbits, our results provide no evidence for subsensitivity of β‐adrenoceptors as a contributory factor in the development of hypertension in this model.
THE β‐ADRENORECEPTOR IN HUMAN LYMPHOCYTES
Authors: Watanabe Yasuhiro , Lai Rong‐Tsan , Yoshida Hiroshi 
Published: June 2007

SUMMARYThe β‐adrenoreceptors of human lymphocytes were investigated by binding assays using a radiolabeled β‐adrenoreceptor agonist, 3H‐hydroxybenzylisoproterenol, in an intact cell system. Intact human lymphocytes had binding sites for the ligand, which seemed to represent physiological β‐adrenoreceptors. Thus, assay of binding of the β‐adrenergic agonist, 3H‐HBI, by intact lymphocytes can be used to study β‐adrenoreceptors in human tissue and to elucidate possible β‐adrenoreceptor disorders in human diseases.
DIRECT VASODILATOR ACTIVITY OF ATROPINE IN THE RAT PERFUSED HINDLIMB PREPARATION
Authors: Merrick B. Alex , Holcslaw Terry L. 
Published: June 2007

SUMMARY1. The autoperfused hindlimb technique in the rat was used to determine the effects of atropine upon the peripheral vasculature.2. Injection of atropine (0.1–0.8 μmoles) into the hindlimb perfusion circuit resulted in a dose‐dependent decrease in perfusion pressure which was immediate in onset and always preceded systemic pressure changes. The duration of vasodilation lengthened with increasing doses of atropine and ranged from 1.5 to 9 min.3. During atropine‐induced vasodilation, challenging doses of acetylcholine did not alter the perfusion pressure.4. These experiments suggest that atropine is capable of direct vasodilator activity upon the peripheral vasculature in which a muscarinic mechanism appears unlikely.
THE INFLUENCE OF HEART RATE ON DIGOXIN‐INDUCED INHIBITION OF MYOCARDIAL NA+‐K+‐ATPASE ACTIVITY IN THE DOG
Authors: Marsh A. J. , Lloyd B. L. , Taylor R. R. 
Published: June 2007

SUMMARY1. Groups of sedated dogs were studied at spontaneous heart rates (HR), 55–100/min, or at paced HR 200/min, with or without intravenous digoxin administration. After 60 min, active rubidium uptake (86Rb+) of ventricular samples was determined in vitro.2. Untreated fast and slow HR groups had similar uptakes. Following digoxin, 0.08 mg/kg, uptake was less at fast than slow HR (63.8, s.e.m. = 4.5 v. 87.5, s.e.m. = 5.0 pmol/mg LV/15 min, P< 0.01). After 0.125 mg/kg, values were again lower in the fast HR group in which five of seven developed ventricular tachycardia.3. Heart rate does not alter in vitro activity of myocardial Na+‐K+‐ATPase but does influence inhibition of the enzyme resulting from digoxin administration.
RAT MYOCARDIAL PROTEIN DEGRADATION
Authors: Steer J. H. , Hopkins B. E. 
Published: June 2007

SUMMARY1. Myocardial protein degradation rates were determined by following tyrosine release from rat isolated left hemi‐atria in vitro.2. After two 20 min preincubations the rate of tyrosine release from hemi‐atria was constant for 4 h.3. Skeletal muscle protein degradation was determined by following tyrosine release from rat isolated hemi‐diaphragm (Fulks, Li & Goldberg, 1975).4. Insulin (10‐7M) inhibited tyrosine release from hemi‐atria and hemi‐diaphragm to a similar extent. A 48 h fast increased tyrosine release rate from hemi‐diaphragm and decreased tyrosine release rate from hemi‐atria. Hemi‐diaphragm tyrosine release was inhibited by 15 mmol/1 D‐glucose but a variety of concentrations of D‐glucose (0, 5, 15 mmol/1) had no effect on tyrosine release from hemi‐atria. Five times the normal plasma levels of the branched‐chain amino acids leucine, isoleucine and valine had no effect on tyrosine release from either hemi‐atria or hemi‐diaphragm.
THE KETOTIC RATIO (KB/NEFA) IN MAN
Authors: Schade David S. , Eaton R. Philip 
Published: June 2007

SUMMARY1. The ‘ketotic ratio’, which is defined as the plasma ketone‐body concentration divided by the plasma nonesterified fatty acid concentration, is potentially useful in predicting the magnitude of the ketone response to a given increment in plasma fatty acid concentration.2. Two parameters of the ketotic ratio were studied. First, a comparison of the basal plasma ketotic ratio with the ketotic ratio following an acute heparin‐induced increase in nonesterified fatty acid concentration was made. Second, the effect upon the ketotic ratio of noradrenaline which has been reported to increase the plasma ketone‐body concentration independent of the change in plasma nonesterified fatty acid concentration, was determined.3. The results suggest that the basal ketotic ratio has predictive value in estimating the rise in plasma ketone‐body concentration following an acute increase in plasma nonesterified fatty acid concentration. When noradrenaline was given to increase plasma nonesterified fatty acid concentration, this predictive value was still valid, although a steeper regression line was obtained. Thus, the ketotic ratio is a non‐invasive in vivo technique which provides insight into the direct ketotic activity of hormones independent of their lipolytic effects.