bluuebunny/crossref_metadata_2025_split huggingface dataset:
CONTRACTILE RESPONSES TO α1‐ADRENOCEPTOR STIMULATION DURING MATURATION IN THE AORTA OF THE NORMOTENSIVE AND SPONTANEOUSLY HYPERTENSIVE RAT: RELATION TO STRUCTURE
Authors: Sudhir Krishnankutty , Angus James A. 
Published: June 2007

SUMMARY1. The significantly greater rise in blood pressure during the first 20 weeks of life in spontaneously hypertensive rats (SHR) when compared with normotensive Wistar‐Kyoto rats (WKY) may be related to increased vasoconstrictor responses caused by enhanced transmitter release or post‐junctional receptor changes.2. The reactivity of rat isolated aorta to post‐junctional α1‐adrenoceptor stimulation by methoxamine and to transmural sympathetic nerve stimulation was studied in ring segments suspended at equivalent transmural pressures in organ baths.3. Wall stress in the SHR aorta was significantly higher at 4 weeks, but lower at 9 and 20 weeks when compared with the WKY aorta, a possible adaptation to the higher pressures seen in the SHR at the latter ages.4. The sensitivity (location of EC50) to methoxamine was similar at all ages in both strains, but the SHR aortae at 9 and 20 weeks generated higher maximal contractile force to this agent compared with the WKY aorta.5. The increase in force to methoxamine parallelled the medial hypertrophy of the SHR aorta, determined from computerized morphometric analysis.6. There was an enhanced response to transmural field stimulation in the SHR aortae at 9 weeks, that was not accounted for by medial hypertrophy or altered neuronal uptake of noradrenaline.7. These studies suggest that enhanced maximal contractile force in the SHR aorta to α1‐adrenoceptor stimulation is accounted for by medial hypertrophy. However, there is an additional enhanced reactivity at 9 weeks in response to nerve stimulation in the SHR aorta that may be related to increased innervation density.
DAILY VARIATION IN INFLUENCE OF LITHIUM ON SERUM CALCIUM CONCENTRATION: A PRELIMINARY REPORT
Authors: Fujimura Akio , Ohashi Kyo‐ichi , Ebihara Akio 
Published: June 2007

SUMMARY1. One millilitre of 5% glucose (vehicle, n= 10) or 1 mL solution of lithium chloride (LiCl) (0.5 or 2.0 mmol/kg per day, n= 10 for each) was injected intraperitoneally in Wistar rats at 10:00 or 22:00 h for 6 days. Blood samples for ionized and total calcium were taken on day 7.2. Mild elevations in ionized, but not non‐ionized (total‐ionized) calcium were observed following LiCl treatment in both administration times.3. The increment in ionized calcium was greater when LiCl was injected at 22:00 h than when it was given at 10:00 h.4. These data indicate that: (1) the influence of lithium on calcium metabolism varies with its administration time; and (2) mild hypercalcaemia induced by the agent mainly depends on the elevation in the ionized fraction of calcium.
EFFECTS OF CHRONIC CONVERTING ENZYME INHIBITION ON THE VASCULAR RENIN‐ANGIOTENSIN SYSTEM
Authors: Saito Hiroshi , Nakamaru Mitsuaki , Rakugi Hiromi , Mikami Hiroshi , Ogihara Toshio , Inagami Tadashi 
Published: June 2007

SUMMARY1. The effects of chronic oral administration of inhibitors of angiotensin converting enzyme (ACE) on the vascular renin–angiotensin system were studied.2. Male Sprague‐Dawley rats were treated orally with five ACE inhibitors, captopril, enalapril, ramipril, cilazapril and CS‐622 (10 mg/kg per day), for periods of 1–2 weeks. Their mesenteric arteries were then isolated and perfused in vitro with Krebs'‐Ringer solution, and the angiotensin II (AII) released into the perfusate was measured under unstimulated and isoproterenol‐stimulated conditions. The vascular renin activity was also determined after treatments with ACE inhibitors.3. Treatment with captopril for 1 week suppressed the isoproterenol‐stimulated increase in All release, but had little effect on the baseline release. Oral treatment with captopril for 2 weeks or with other ACE inhibitors for 1 week markedly inhibited both the unstimulated and stimulated release of AII from the mesenteric vasculature.4. Both the vascular renin activity and the plasma renin activity increased on captopril treatment, but their changes with time were different.5. These results indicate that virtually complete inhibition of the vascular renin–angiotensin system can be achieved after prolonged treatment with ACE inhibitors, and suggest that the chronic antihypertensive action of ACE inhibitors is not solely due to inhibition of the plasma renin–angiotensin system.
INTRACEREBROVENTRICULAR INFUSIONS OF INSULIN INCREASE VASOPRESSIN RELEASE IN RATS
Authors: Nishimura Masato , Takahashi Hakuo , Matsusawa Makoto , Ikegaki Iwao , Nakanishi Tadashi , Hirabayashi Masami , Yoshimura Manabu 
Published: June 2007

SUMMARY1. The role of cerebral insulin or insulin‐like immunoreactive substance (ILI) on arginine–vasopressin (AVP) release using rats was investigated. Feeding rats with a high salt diet for 4 weeks significantly decreased the contents of ILI in both the hypothalamus and pituitary gland. Intracerebroventricular infusions of insulin (4 and 40 μg/min for 30 min) increased plasma AVP concentrations dose‐dependently without hypoglycaemia, but decreased hypothalamic and pituitary contents of AVP.2. These results indicate that ILI in the brain may play a role in the secretion of AVP, and that this mechanism could be operated to control a water–sodium balance.
DOES VERAPAMIL LIMIT MYOCARDIAL INFARCT SIZE IN A HEART DEFICIENT IN XANTHINE OXIDASE?
Authors: Adachi Takeo , Miura Tetsuji , Noto Tetsuya , Ooiwa Hitoshi , Ogawa Takashi , Tsuchida Akihito , Iwamoto Toshihiro , Goto Mahiko , Iimura Osamu 
Published: June 2007

SUMMARY1. The delay of ischaemic myocardial necrosis by verapamil has been reported in the dog heart, which contains a high level of xanthine oxidase, a potential source of cytotoxic free radicals. To test whether the retardation of ischaemic myocyte death by verapamil is not an isolated phenomenon in the xanthine oxidase rich heart, we assessed the effect of verapamil in the rabbit heart, which lacks xanthine oxidase.2. Verapamil (200 μg/kg, i.v. bolus plus 40 μg/kg per min) was administered in a group of rabbits (n= 5) to test the haemodynamic response to this agent. The heart rate, blood pressure and left ventricular dp/dt max were reduced by 11, 25 and 57%, respectively, and the plasma concentration of verapamil was maintained at 300–400 ng/mL during the infusion.3. In other groups of rabbits, the effect of the same dosage of verapamil on the size of myocardial infarct after 20 or 30 min ischaemia and 72 h reperfusion was examined. The verapamil was administered for 45 min, starting 15 min prior to ischaemia. The percentage of area at risk infarcted (%I/AAR) was 15.2±3.9% in the 20 min ischaemia control group and 15.4±4.5% in the 20 min ischaemia verapamil group, 49.1±3.4% in the 30 min ischaemia control group and 41.2±3.3% in the 30 min ischaemia verapamil group. The %I/AAR was significantly smaller in the 20 min ischaemia control groups and 15.4±4.5% in the 20 min ischaemia there was no difference in %I/AAR between the control and verapamil treated animals in either the 20 or the 30 min ischaemia groups.4. These results suggest that verapamil does not delay the transition from reversible to irreversible myocardial injury during coronary occlusion in the rabbit, which like the human, lacks myocardial xanthine oxidase.
EFFECTS OF HALOTHANE, KETAMINE, PROPOFOL AND ALFENTANIL ANAESTHESIA ON CIRCULATORY CONTROL IN RABBITS
Authors: Van Leeuwen Andrew F. , Evans Roger G. , Ludbrook John 
Published: June 2007

SUMMARY1. We have made a within‐rabbit comparison of the effects of four general anaesthetic regimens on the haemodynamic response to acute reduction in central blood volume and on baroreflex control of heart rate.2. Acute haemorrhage was simulated by gradually inflating a cuff on the inferior vena cava in order to cause cardiac output to fall at a constant rate of 8.5%/min while the responses of systemic vascular resistance, arterial pressure and heart rate were measured. The full range of the baroreceptor–heart rate reflex was elicited by inflating aortic and vena caval cuffs. These indices of circulatory control were repeatedly measured within five protocols, to which each rabbit was exposed in randomized order.3. In each protocol the rabbit was first studied unanaesthetized. Then a small dose of thiopentone sodium was given (16 mg/kg). In the four main protocols the rabbit was then intubated and ventilated, first with 100% oxygen and then with 50% nitrous oxide, during administration of one of four anaesthetic agents. These were halothane (2.0 and 2.5%), ketamine (2.5 mg/kg per min), propofol (0.83 and 1.25 mg/kg per min) and alfentanil (2.5 and 3.33 μg/kg per min). In a sham protocol the effects of 100% oxygen, then those of 50 and 75% nitrous oxide, were studied while the rabbit remained conscious.4. In unanaesthetized rabbits, in the presence or absence of nitrous oxide, the normal biphasic haemodynamic response to simulated haemorrhage occurred. The first, vasoconstrictor, phase was attenuated by halothane, ketamine and propofol, so that arterial pressure fell more steeply than normal. Not only was the vasoconstrictor phase unaffected by alfentanil but it was extended, so that arterial pressure remained at a normal level even when cardiac output had fallen by 59%. This effect of alfentanil appeared to be mediated centrally, since it could be reproduced by injecting small doses (1.5–7.5 μg) into the fourth ventricle. All four anaesthetic agents and nitrous oxide attenuated the baroreceptor control of heart rate. The effect was least with nitrous oxide and alfentanil, greatest with halothane.
LACK OF EFFECT OF GRANULOCYTE‐MACROPHAGE COLONY STIMULATING FACTOR ON THE RAT AORTA OR HUMAN SAPHENOUS VEIN
Authors: Watabe T. , Moulds R. F. W. 
Published: June 2007

SUMMARY1. In order to assess whether the observed hypotensive response in some patients given human granulocyte‐macrophage colony stimulating factor (GM‐CSF) is caused by a direct vascular effect of the GM‐CSF, the effects of mouse and human GM‐CSF were examined in rat aortic rings and human saphenous veins respectively.2. No effects of GM‐CSF were observed, either in the presence or absence of endothelium, on responses to the α‐adrenoceptor agonist phenylephrine.3. These data suggest that GM‐CSF does not have direct effects on either vascular endothelium or smooth muscle, and that a direct vascular effect of GM‐CSF is not the explanation for the observed clinical response.
THE EFFECT OF PRAZOSIN THERAPY ON PLATELET ACTIVATION IN ESSENTIAL HYPERTENSION
Authors: Okrucká A. , Pechán J. , Mikulecký M. 
Published: June 2007

SUMMARY1. Plasma levels of β‐thromboglobulin, initial and total platelet aggregation (induced by adrenaline or adenosine diphosphate [ADP]) were determined in 26 normotensive subjects and 26 patients with untreated essential hypertension. Groups of 18 essential hypertensive patients and 18 age‐ and sex‐matched normotensives were compared.2. After 7 days of treatment with prazosin in a dose of 2–8 mg daily the above measures were repeated in 18 essential hypertensive patients. A significant increase in plasma levels of β‐thromboglobulin, initial and total adrenaline‐induced as well as ADP‐induced platelet aggregation was found in hypertensives. Prazosin restored the mean arterial blood pressure in hypertensives to normal, but it had no significant influence either on increased β‐thromboglobulin levels or on initial and total aggregability.3. The results confirm increased platelet aggregation and in vivo platelet activation in patients with essential hypertension; however there is a discrepancy with previous reports about those results obtained after prazosin therapy. The results suggest that increased platelet aggregation and in vivo activation need not be restored to normal after effective antihypertensive therapy alone. They give reason for the combination of antihypertensive together with anti‐aggregatory therapy in essential hypertension.
SODIUM INTAKE MODULATES RENAL VASCULAR REACTIVITY TO ENDOTHELIN‐1 IN DAHL RATS
Authors: Grossman Ehud , Hoffman Aaron , Keiser Harry R. 
Published: June 2007

SUMMARY1. The systemic and renal haemodynamic responses to endothelin‐1 (ET1) were evaluated and compared to Angiotensin II (AII) in anaesthetized Dahl salt‐sensitive (DS) and salt‐resistant (DR) rats on either low (0.1% NaCl in diet) or high (8% NaCl in diet) salt intake.2. Baseline mean arterial pressure on low salt diet was similar in both strains, while on high salt diet it was 73 ± 4 mmHg in DR rats and 119 ± 8 mmHg in DS rats (P<0.05). Baseline renal blood flow (RBF) and renal vascular resistance (RVR) were similar in all groups.3. AII in bolus injection induced a short, dose‐dependent increase in blood pressure and renal vascular resistance and a fall in renal blood flow. The maximal pressure increase was significantly greater in DS rats on high salt diet than that in each of the other groups (P<0.05). The fall in renal blood flow and the increase in renal vascular resistance were attenuated in both strains on low salt diet.4. ET1 induced an initial decrease followed by a prolonged increase in blood pressure; both phases were similar in all groups. However, renal vascular reactivity to ET1 was markedly modulated by salt intake. On low salt diet, following a bolus injection of ET1 (1 nmol/kg), RBF decreased by 34% in DR and by 20% in DS rats, while on high salt diet RBF decreased by 34% in DR and by 80% in DS rats (P<0.05 high vs low salt). RVR increased only by 98% and 72% on low salt diet in DR and DS rats, respectively (P<0.05 vs baseline), whereas on high salt diet RVR increased by 584% and 554% in DR and DS rats respectively (P<0.05 high vs low salt).5. It is concluded that DS rats are not hypersensitive to ET1 as they are to other pressor agents, and that salt intake, rather than blood pressure, modulates substantially the renal vascular reactivity to ET1.
SELECTIVE DEPRESSION OF MAXIMUM RATE OF DEPOLARIZATION OF GUINEA‐PIG VENTRICULAR ACTION POTENTIALS BY AMIODARONE AND LIGNOCAINE IN SIMULATED ISCHAEMIA: COMPARISON WITH ENCAINIDE
Authors: Campbell Terence J. , Hemsworth Paul D. 
Published: June 2007

SUMMARY1. Standard microelectrode techniques were used to record intracellular action potentials from guinea‐pig ventricular myocardium superfused with either control physiological saline (pH 7.5; pO2 500 mmHg; [K+] 5.6 mmol/L) or ‘simulated ischaemic’ solution (pH 6.4; pO2 90 mmHg; [K+] 11.2 mmol/L).2. The effects on action potential parameters of therapeutic concentrations of lignocaine, amiodarone and encainide were studied under both conditions.3. Simulated ischaemia, in the absence of drugs, produced marked reductions in resting potential (‐ 86.6 ± 2.3 to ‐ 64.7 ± 3.5 mV), maximum rate of depolarization (V̇max; 263 ± 66 to 106 ± 36 V/s) and action potential duration (164 ± 24 to 97 ± 26 ms). No drug produced any additional effect on resting potential.4. All three drugs produced enhanced depression of Vmax in ischaemia compared to control conditions (class I effect). This was much more marked for lignocaine and amiodarone (inactivated channel blockers) than for encainide (open channel blocker).5. In addition the prolongation of action potential duration seen with acute exposure to amiodarone (174 ± 12 to 192 ± 17 ms; class III effect) was abolished under simulated ischaemic conditions.6. It is concluded that lignocaine and amiodarone exert greater selectivity for ischaemic tissue than does encainide and that amiodarone may function primarily as a class I agent under ischaemic conditions.
EFFECTS OF ENDOTHELIAL CELL REMOVAL ON α‐ADRENOCEPTOR‐MEDIATED RESPONSES OF AORTAE OF PREGNANT RATS
Authors: Jansakul C. , King R. G. , Boura A. L. A. 
Published: June 2007

SUMMARY1. The possibility that changes in sensitivity of the aorta occurring during pregnancy in the rat are due to changes in uptake mechanisms, α‐ and/or β‐adrenoceptor‐mediated responses was investigated.2. Thoracic aortic rings from 20 day pregnant rats showed increased sensitivity to the constrictor effects of phenylephrine, with increased maximum responses when compared with those from non‐pregnant animals. Removal of endothelium caused leftward shifts of the log concentration‐response curves with further increases in maxima to the same extent in rings of both non‐pregnant and 20 day pregnant rats.3. Propranolol, β‐oestradiol, and nisoxetine did not significantly alter the CR‐curves to phenylephrine of endothelium‐intact or denuded thoracic aortic rings obtained from either non‐pregnant or 20 day pregnant rats.4. BHT‐920 failed to cause marked constriction of endothelium‐intact rings. After removal of endothelium, significant constrictor responses to BHT‐920 occurred which were of similar magnitude for rings from both non‐pregnant and 20 day pregnant rats.5. Relaxant responses to BHT‐920 of endothelium‐intact rings preconstricted with phenylephrine were not significantly different between those from non‐pregnant and 20 day pregnant rats. Removal of endothelium resulted in rightward shifts of the curves together with decreased maximum responses.6. These results support earlier suggestions that the endothelium plays a role in controlling vascular reactivity to phenylephrine. The increased maximum response of thoracic aortic rings to phenylephrine seen during pregnancy does not appear to be due to marked changes in amine uptake mechanisms or β‐ or α2‐adrenoceptor‐mediated responses.
SUPPRESSOR CALCIUM INFUSION RAISES PLASMA ATRIAL NATRIURETIC PEPTIDE CONCENTRATIONS IN HUMANS
Authors: Finn Wendy L. , Tunny Terry J. , Klemm Shelley A. , Thompson Robyn E. , Gordon Richard D. 
Published: June 2007

SUMMARY1. Calcium was infused in normal subjects in subpressor dosage to examine the effects of raised calcium levels on atrial natriuretic peptide (ANP) concentrations.2. Calcium infusion progressively raised serum ionized and total calcium concentrations significantly, without raising mean arterial pressure or heart rate.3. Plasma ANP concentrations increased significantly by 5 min of infusion and increased further by 15 min (approximately 40%) to levels which were maintained to 60 min.4. Urinary sodium excretion increased by 140% during calcium infusion.5. Calcium may affect secretory as well as contractile functions of the atrial myocyte.
BIOCHEMICAL CORRECTION IN THE SYNDROME OF HYPERTENSION AND HYPERKALAEMIA BY SEVERE DIETARY SALT RESTRICTION SUGGESTS RENIN‐ALDOSTERONE SUPPRESSION CRITICAL IN PATHOPHYSIOLOGY
Authors: Klemm Shelley A. , Gordon Richard D. , Tunny Terry J. , Finn Wendy L. 
Published: June 2007

SUMMARY1. Plasma potassium and chloride concentrations were raised and plasma renin activity, aldosterone, bicarbonate and arterial pH were reduced in two brothers with the syndrome of hypertension and hyperkalaemia with normal glomerular filtration rate (Gordon's syndrome), on unrestricted or moderately restricted sodium diets.2. These abnormalities were corrected in both patients within 10 days of severe sodium restriction.3. Pressor sensitivity to cold and angiotensin II decreased on low sodium diet, associated with a fall in blood pressure.4. Increasing distal tubular sodium delivery by infusion of normal saline increased fractional excretion of potassium when aldosterone had been stimulated by severely restricted sodium diet, but not when aldosterone levels were low on unrestricted sodium diet.5. These findings are consistent with excessive sodium reabsorption as the primary renal lesion in Gordon's syndrome, leading to volume expansion and suppression of renin and aldosterone. Severe dietary sodium restriction leading to volume contraction, by stimulating renin and aldosterone and promoting kaliuresis, corrects the abnormalities.
VASOCONSTRICTION IN THE RENAL VASCULAR BED DURING EXERCISE: STUDIES IN CONTROL AND HEART FAILURE RABBITS
Authors: Langton David , Way Diana , Trigg Lisbeth , Blake Duncan , McGrath Barry 
Published: June 2007

SUMMARY1. The effects of graded treadmill exercise on renal blood flow (RBF) were examined in seven rabbits, in which congestive heart failure (CHF) was produced by the administration of doxorubicin, 1 mg/kg, twice weekly for 8 weeks, and in seven controls. A third group of five rabbits underwent doxorubicin treatment with the addition of surgical section of the left renal sympathetic nerve.2. During submaximal exercise, there was a small reduction in RBF in controls, which was greatly exaggerated in CHF.3. In both control and heart failure rabbits, there was a precipitous fall in RBF as exercise fatigue developed.4. Renal sympathectomy ablated these changes in RBF during exercise.5. It is concluded that in heart failure there is an exaggerated, sympathetically mediated, diversion of blood flow away from the kidney. The onset of exercise fatigue in both normal and heart failure rabbits is accompanied by a marked intensification of this process.
HYPERLIPIDAEMIA INCREASES ALBUMINURIA IN HYPERTENSIVE AND NORMOTENSIVE RATS
Authors: Cooper M. E. , Vranes D. A. , Panagiotopoulos S. , Allen T. J. , Goodall I. , Jerums G. 
Published: June 2007

SUMMARY1. The effects of a high cholesterol diet on urinary albumin excretion were examined in spontaneously hypertensive (SHR) and Wistar‐Kyoto (WKY) rats over 36 weeks.2. Cholesterol feeding resulted in an increase in total‐cholesterol and a decrease in HDL‐cholesterol without influencing triglyceride levels in both strains.3. Urinary albumin excretion was significantly elevated in cholesterol‐fed SHR and WKY rats.4. These results suggest that hyperlipidaemia may be important in acceleration of experimental nephropathy.
EFFECT OF FISH OIL FEEDING ON BLOOD PRESSURE AND VASCULAR REACTIVITY IN SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Yin K. , Chu Z. M. , Beilin L. J. 
Published: June 2007

SUMMARY1. To examine possible antihypertensive mechanisms of fish oil feeding, we have studied vascular reactivity of aortic rings and blood pressure of spontaneously hypertensive rats (SHR).2. SHR were fed a synthetic diet supplemented with either (10% by weight) ‘Max EPA’ fish oil or hydrogenated coconut oil (saturated fat) for 4 weeks.3. Mean systolic blood pressure of fish oil fed rats was 9 mmHg lower than saturated fat fed controls.4. Aortic rings of control SHR had a biphasic response to acetylcholine (ACh), relaxing at lower concentrations but contracting at concentrations higher than 3X10‐7 mol/L. No such contractions were seen in tissues of fish oil fed rats. The contractions were abolished by indomethacin, suggesting that they were caused by a cyclo‐oxygenase product.5. Tissue analysis showed that both aortic and serum generation of thromboxane B2 (TxB2) was approximately three times less in fish oil fed rats than in control tissues.6. These results indicate that the lowering of blood pressure in fish oil fed SHR could in part be due to decrease in production of thromboxane (TxA2), a potent vasoconstrictor, hence influencing vascular tone and compliance of the aorta.
MECHANISMS OF THE EFFECTS OF ENDOTHELIN ON RESPONSES TO NORADRENALINE AND SYMPATHETIC NERVE STIMULATION
Authors: Wong‐Dusting H. K. , La M. , Rand M. J. 
Published: June 2007

SUMMARY1. The effects of endothelin (0.1–1 nmol/L) and the phorbol ester, phorbol 12‐myristate 13‐acetate (PMA, 0.1–100 nmol/L) have been studied on vasoconstrictor responses to sympathetic nerve stimulation and noradrenaline in the rabbit isolated ear artery.2. Endothelin (0.1 nmol/L) significantly enhanced the biphasic response of the arteries to a prolonged period of sympathetic nerve stimulation (2 Hz for 60 s). Both the component of the response attributable to mobilization of intracellular calcium (phasic response) and the component due to the influx of extracellular calcium (tonic response) were enhanced.3. PMA (0.1 and 0.3 nmol/L), which activates protein kinase C, enhanced vasoconstrictor responses to noradrenaline but a higher concentration of PMA (100 nmol/L) inhibited responses to noradrenaline.4. It is concluded that the enhancement of responses to sympathetic nerve stimulation and noradrenaline produced by endothelin may be due to facilitation of the influx of extracellular calcium and to the activation of protein kinase C.