bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE α2‐ADRENOCEPTOR AGONISTS CLONIDINE TL99 AND DPI ENHANCE VASOCONSTRICTOR RESPONSES TO SYMPATHETIC NERVE STIMULATION AND NORADRENALINE IN THE RAT TAIL ARTERY PREPARATION
Authors: Xiao X‐H. , Medgett I. C. , Rand M. J. 
Published: June 2007

SUMMARY1. Clonidine (1–30 nmol/l) enhanced the vasoconstrictor responses to sympathetic nerve stimulation in isolated perfused artery preparations from the rat tail. Higher concentrations of clonidine produced vasoconstriction in most artery preparations and reduced the response to sympathetic nerve stimulation.2. The enhancing effect of clonidine was not affected by prazosin but was blocked by idazoxan, indicating that it was due to activation of α2‐adrenoceptors.3. The α2‐adrenoceptor agonists DPI and TL99, like clonidine, enhanced vasoconstrictor responses to sympathetic nerve stimulation.4. Vasoconstrictor responses to noradrenaline were enhanced by clonidine and TL99.5. The findings suggest that activation of postjunctional α2‐adrenoceptors results in facilitation of the contractile response elicited by activation of α1‐adrenoceptors.
EFFECTS OF NALOXONE ON GLUCOSE LEVEL IN THE HEPATIC VENOUS PLASMA IN THE RAT
Authors: Pacula Piotr , Janicki Piotr K. , Krząścik Pawel 
Published: June 2007

SUMMARY1. The effect of opioid receptor blockade by naloxone in vivo on hepatic venous plasma glucose concentration in rats was investigated.2. The plasma glucose levels in naloxone‐injected animals (10 mg/kg) were higher than in the control animals (P < 0.05).3. At the lower dose of naloxone (2 mg/kg) the resulting plasma glucose concentration did not differ significantly from control (P > 0.1).4. It is concluded that endogenous opioids may moderate the regulation of basal glucose levels in the rat.
EFFECTS OF ZSY‐27, A SYNTHESIZED PHOSPHODIESTERASE INHIBITOR, ON EXOCRINE SECRETION AND CYCLIC NUCLEOTIDE CONCENTRATION IN THE DOG PANCREAS
Authors: Iwatsuki K. , Horiuchi A. , Chiba S. 
Published: June 2007

SUMMARY1. Effects of intravenous injections of ZSY‐27, a synthesized phosphodiesterase inhibitor, on pancreatic exocrine secretion and on pancreatic cyclic AMP and cyclic GMP concentrations of dogs were investigated.2. ZSY‐27 (0.3 and 1 mg/kg) increased cyclic AMP concentration dose‐dependently, which preceded the increase in pancreatic secretion but did not affect cyclic GMP concentration.3. These results suggest that ZSY‐27 causes exocrine secretion from the dog pancreas mediated through an increase in intracellular cyclic AMP concentration.
INVOLVEMENT OF α1‐ADRENOCEPTORS IN CHRONOTROPIC RESPONSES TO ENDOGENOUSLY RELEASED AMINES IN THE PITHED RAT
Authors: Luca A. De , Rand M. J. 
Published: June 2007

SUMMARY1. In pithed rats, yohimbine (1 mg/kg i.v.) enhanced the positive chronotropic responses to spinal stimulation of cardiac sympathetic nerves with eight pulses delivered at 2 or 4 Hz, indicating that auto‐inhibition was operating, but did not increase responses to shorter lengths of trains of 8 pulses at 8, 16 or 32 Hz which did not allow sufficient time for auto‐inhibition to come into effect.2. The positive chronotropic response to cardiac sympathetic nerve stimulation with eight pulses at 8 Hz of about 60 beats/min was not affected by prazosin (1 mg/kg) or diltiazem (0.2 mg/kg), but was reduced to about 20% of the control value by propranolol (1 mg/kg).3. In the presence of propranolol, the residual positive chronotropic responses to cardiac sympathetic nerve stimulation were virtually abolished by prazosin (1 mg/kg) or diltiazem (0.2 mg/kg).4. The positive chronotropic response to tyramine (0.1 mg/kg i.v.) was reduced from 100 to 12 beats/min by propranolol (1 mg/kg), and the residual response was abolished by prazosin.5. The findings indicate that noradrenaline released from cardiac sympathetic terminals by nerve stimulation or by tyramine acts on α1‐adrenoceptors to produce a positive chronotropic response that is revealed when β‐adrenoceptors are blocked.
BLOOD PRESSURE, SALT APPETITE AND MORTALITY OF GENETICALLY HYPERTENSIVE AND NORMOTENSIVE RATS MAINTAINED ON HIGH AND LOW SALT DIETS FROM WEANING
Authors: Di Nicolantonio R. , Silvapulle M. J. 
Published: June 2007

SUMMARY1. Blood pressure, bodyweight, saline preference and mortality rate were examined in spontaneously hypertensive rats (SHR) of the Okamoto strain and normotensive control Wistar‐Kyoto (WKY) rats maintained on low (0.1% NaCl w/w), control (0.8% w/w) and high (3% w/w) salt diets from weaning until 6 months of age.2. The growth rate of SHR on high salt diet was not significantly different from that on control diet but SHR maintained on a low salt diet exhibited a markedly reduced growth rate. While the growth rate of WKY on low salt diet was not significantly different from that on control diet, the body weights of WKY on high salt diet were significantly greater than those of animals on control diet.3. While low salt diet markedly attenuated the development of hypertension in the SHR, high salt diet significantly exacerbated the blood pressure of this strain. Neither high nor low salt diet altered the blood pressure of WKY.4. SHR on high and low salt diets had an increased mortality rate compared with SHR on control salt diet but these differences were of slight statistical significance. Conversely, WKY on all three diets exhibited similar mortalities over the 6‐month observation period. There were no significant differences in mortalities between SHR and WKY on any diet.5. The preference for 0.9% saline, when offered as a choice with water, was not significantly different between SHR on the different diets. WKY on high salt diet, however, exhibited a significantly reduced preference for saline over the 10‐day test period compared with animals on control or low salt diet.6. Thus dietary salt modulates the hypertension of SHR but not the blood pressure of WKY. SHR would appear to require more dietary sodium for normal growth and perhaps full expression of its hypertension. The higher and lower blood pressures of the SHR on high and low salt diet, respectively, were associated with increased mortality, which was a trend not seen in the WKY.
EFFECT OF POTASSIUM LOADING ON BONE SODIUM AND TOTAL EXCHANGEABLE SODIUM IN SHEEP
Authors: Reid Amanda F. , Coghlan John P. , McDougall John G. , Whitworth Judith A. , Scoggins Bruce A. 
Published: June 2007

SUMMARY1. The effect of potassium (K) loading for 10 days on bone sodium (Na) and total exchangeable Na in sheep was examined.2. There were no significant changes in Na space or exchangeable Na after K loading.3. Bone Na concentration decreased by approximately 20% after K loading.4. The degree of mobilization of Na from both the non‐exchangeable and exchangeable pools in bone is sufficient to account to a large degree for the observed increase in extracellular fluid volume and the net negative sodium balance which is observed during K loading.
SHORT COMMUNICATION: CATECHOLAMINE CONCENTRATIONS DURING EXPOSURE OF RESTING MAN TO THE HEAT OF A STANDARD SWEAT TEST
Authors: Wilkinson Ruth , Johnson Ralph H. 
Published: June 2007

SUMMARY1. Normal subjects were heated for 45 min with a heat cradle under the conditions used to investigate sweating clinically.2. Skin temperatures on the chest and in the external auditory meatus rose but concentrations of noradrenaline and adrenaline decreased during heating.3. There was no change in adrenoceptor affinity or number as a result of the heat exposure.4. There was little change in blood pressure and heart rate and no dysrhythmias were observed with an electrocardiogram.5. It is concluded that heating with a heat cradle is generally not stressful and that there is a reduction in sympathetic nervous activity involving noradrenergic or adrenergic transmission during the procedure.
INFLUENCE OF BILE ACIDS ON THE BILIARY TRANSPORT MAXIMUM OF PHENOLSULPHONPHTHALEIN IN THE RAT
Authors: Collado P. S. , Muñoz M. E. , Esteller A. , González J. 
Published: June 2007

SUMMARY1. The effect of changes in bile acid secretion induced by cholestyramine treatment or taurocholate infusion on the biliary transport maximum (Tm) of phenolsul‐phonphthalein (PSP) was studied in Wistar rats.2. Five hours after oral administration of cholestyramine (1.5 g/kg bodyweight) the biliary output of bile acids decreased to 51% and bile flow to 76% of control values. The percentage of conjugated and unconjugated PSP excreted into bile and the Tm of the dye were not significantly modified by cholestyramine pretreatment.3. Administration of sodium taurocholate at increasing rates (60–480 nmol/100 g bodyweight per min) enhanced bile flow and the biliary output of bile acids in a linear dose‐related fashion. The Tm of PSP increased progressively until a maximum of 29% above the control values was reached at a taurocholate dose of 240 nmol/100 g body‐weight per min). The enhancement corresponded mainly to the unconjugated dye, the excretion of conjugated PSP not being significantly modified by the infusion of the bile acid.4. The results indicate that bile acids can influence to some extent biliary excretion of PSP in the rat, although this component is of minor importance at low bile acid secretory rates.
EFFECTS OF PROSTAGLANDIN D2 AND OMEPRAZOLE ON INDOMETHACIN‐INDUCED GASTRIC ULCERS IN RATS
Authors: Fukui Akira , Nakazawa Saburo , Goto Hidemi , Sugiyama Satoru , Ozawa Takayuki 
Published: June 2007

SUMMARY1. The mechanism of indomethacin‐induced gastric ulcers was investigated by measuring tissue prostaglandins (PG) levels.2. The effects of PGD2 and omeprazole, an H+ pump inhibitor, were also estimated.3. Four kinds of PG—6‐keto PGF1α, PGF2α, PGE2, and PGD2—in rat gastric mucosa were measured by high performance liquid chromatography.4. All PG levels decreased 1 h after oral administration of 2 mg/kg indomethacin, although they recovered considerably 24 h after administration. No gastric ulcers were observed throughout the experiments in rats treated with 2 mg/kg indomethacin.5. All PG were not detected 1 h, and even 24 h after administration of 12 mg/kg indomethacin. Over 6 h after administration, gastric ulcers were observed.6. Premedication with omeprazole prevented ulcer formation, although it did not improve gastric mucosal PG levels. Administration of PGD2 also reduced ulcer formation, and considerable amounts of PGD2 in gastric mucosa were detected.7. It can be concluded that H+ is a determining factor in the genesis of indomethacin‐induced gastric ulcers and that persistent decreases in tissue PG levels also participate in ulcer formation.
EFFECT OF FURAZOLIDONE AND NITROFURAZONE ON BRAIN GAMMA‐AMINO BUTYRIC ACID AND GLUTAMATE CONCENTRATIONS IN CHICKENS
Authors: Ali B. H. 
Published: June 2007

SUMMARY1. The concentrations of gamma‐amino butyric acid (GABA) and glutamate were measured in the brains of chickens which were treated with furazolidone (FZ) or nitrofurazone (NF) at oral doses of 12.5, 25 or 50 mg/kg for 5 days.2. At the end of the treatment, birds on the small dose of FZ or NF lost about 9% of their bodyweight, and those on the high doses lost about 18%.3. Both drugs produced dose‐dependent increases in the concentrations of GAA and glutamate which were statistically significant at doses of 25 and 50 mg/kg of NF and 50 mg/kg of FZ.
ENDOTHELIUM‐DERIVED RELAXING FACTOR RELEASED FROM CULTURED CELLS: DIFFERENTIATION FROM NITRIC OXIDE
Authors: Dusting G. J. , Read M. A. , Stewart A. G. 
Published: June 2007

SUMMARY1. Endothelium‐derived relaxing factor (EDRF) is an extremely labile mediator thought to be identical to nitric oxide (NO).2. A cascade superfusion technique was used to bioassay EDRF released from bovine aortic endothelial cells grown to confluence on microcarrier beads.3. Bradykinin (1–100 nmol/1), infused through a 1 cm column of endothelial cells on microcarriers, released an EDRF‐like substance that caused relaxations of de‐endothelialized strips of rabbit aorta (precontracted with phenylephrine). These relaxations diminished on successive tissues in the cascade, when compared with those produced by glyceryl trinitrate as a stable standard.4. Haemoglobin (1 μmol/1), infused directly over the bioassay tissues, abolished bradykinin‐induced relaxations and these were restored within 5 min after removal of haemoglobin. The infusion did not affect the relaxations produced by glyceryl trinitrate in this system.5. Methylene blue (20 μmol/1) inhibited bradykinin‐induced relaxations when infused over the rabbit aortae, and reduced those relaxations produced by glyceryl trinitrate. The effects of bradykinin, but not glyceryl trinitrate, were partially restored after removing methylene blue.6. These data are consistent with the known effects of these compounds on the activity of NO, and on EDRF in isolated blood vessels.7. The activity of EDRF (released by bradykinin) was compared directly with NO on strips of guinea‐pig trachea (de‐epithelialized) interposed in cascade between two rabbit aortae; all strips were precontracted with histamine and phenylephrine.8. A submaximal dose of NO that matched the relaxation produced by EDRF on the uppermost aorta, caused relaxation of the trachea, but EDRF had no effect on this tissue. In addition, the NO‐induced relaxation of the lower aorta was greater than that produced by EDRF.9. These data indicate that EDRF does not have identical biological activity to NO. EDRF could contain an NO moiety attached to a carrier molecule that is bound and stabilized in tracheal tissue.
SECONDARY SIGNALLING MECHANISMS IN ANGIOTENSIN II‐STIMULATED VASCULAR SMOOTH MUSCLE CELLS
Authors: Griendling Kathy K. , Berk Bradford C. , Socorro Lilian , Tsuda Terutaka , Delafontaine Patrick , Alexander R. Wayne 
Published: June 2007

SUMMARY1. Activation of vascular smooth muscle by angiotensin II results in the generation of two second messengers, inositol trisphosphate (IP3) and diacylglycerol (DG).2. IP3 is responsible for mobilizing calcium from endoplasmic reticulum. This signal is transient, most likely serving to initiate calcium events leading to contraction, and is attenuated by activation of protein kinase C.3. DG stimulates protein kinase C and ultimately Na+/H+ exchange, leading to intracellular alkalinization. Accumulation of DG/activation of protein kinase C is sustained, and may be enhanced by concurrent intracellular alkalinization. The delay in induction of the sustained response appears to be related to cellular processing of the angiotensin II‐receptor complex.4. Angiotensin II‐stimulated, phospholipase C‐mediated IP3 formation is also modulated by a pertussis toxin‐insensitive guanine nucleotide regulatory protein.5. The GTP binding protein, movement of the receptor‐ligand complex, and the signals generated by the two second messengers, IP3 and DG, interact in a complex manner to cause an integrated response of vascular smooth muscle cells to angiotensin II stimulation.
RELATIVE INHIBITORY POTENCY AND PLASMA DRUG LEVELS OF ANGIOTENSIN CONVERTING ENZYME INHIBITORS IN THE RAT
Authors: Johnston C. I. , Cubela R. , Jackson B. 
Published: June 2007

SUMMARY1. 125I‐351A, a tyrosyl derivative of the angiotensin converting enzyme (ACE) inhibitor lisinopril, was used as a radioligand, and radioinhibitor binding and displacement assays have been established.2. The in vitro potency of a range of ACE inhibitors against rat ACE was determined using the radioinhibitor binding displacement assay.3. The concentration of an ACE inhibitor needed to displace 50% of 125I‐351A bound to rat ACE (ID50) was closely correlated with the concentration needed to inhibit 50% of ACE enzymatic activity (IC50).4. Radioinhibitor binding displacement assay was used to measure the plasma concentrations of lisinopril, cilazapril and perindopril in rat plasma5. Plasma concentrations of lisinopril measured by radioimmunoassay were identical with that measured by radioinhibitor binding assays.
EFFECT OF ENALAPRIL TREATMENT ON PROGRESSION OF THE NEPHROTOXIC SERUM NEPHRITIS MODEL OF RENAL FAILURE IN THE RAT
Authors: Jackson B. , Debrevi L. 
Published: June 2007

SUMMARY1. Nephrotoxic serum nephritis was induced immunologically in uninephrectomized Sprague‐Dawley rats (n= 24). One‐half were assigned randomly to treatment with enalapril (5 mg/kg per 24 h).2. Untreated rats (n= 12) developed a progressive fall in creatinine clearance, a progressive rise in systolic blood pressure and marked proteinuria over a 6 week period. The mortality rate was 42% at 5 weeks and 66% at 6 weeks.3. Enalapril‐treated rats (n= 12) had no significant reduction in systolic blood pressure, and a similar reduction in creatinine clearance to that in untreated rats. Mortality was 50% at 5 weeks, and 92% at 6 weeks.4. Proteinuria but not the blood pressure rise was significantly reduced by enalapril treatment.5. Converting enzyme inhibitors may have a specific role in the treatment of nephritic diseases.
COMPARATIVE NEUROANATOMY OF ANGIOTENSIN II RECEPTOR LOCALIZATION IN THE MAMMALIAN HYPOTHALAMUS
Authors: Allen A. M. , McKinley M. J. , Mendelsohn F. A. O. 
Published: June 2007

SUMMARY1. The distribution of angiotensin II (AII) receptor binding sites in the hypothalamus of rat, rabbit, sheep and human was determined by in vitro auto‐radiography using 125I‐[Sar1, IIe8]‐AII as radioligand.2. High receptor binding levels were observed in the continuum of tissue comprising the anterior wall of the third ventricle, including the subfornical organ, the median pre‐optic nucleus and the organum vasculosum of the lamina terminalis.3. High levels of binding sites were also found in the paraventricular and supra‐optic nuclei, the median eminence and the arcuate nucleus.4. These findings demonstrate sites in the hypothalamus of rat, rabbit, sheep and human where AII could exert its known actions on fluid and electrolyte balance, pituitary hormone release and cardiovascular function.
ATRIAL NATRIURETIC FACTOR IN HUMAN PATHOPHYSIOLOGY
Authors: Crozier Ian G. , Richards A. Mark , Nicholls M. Gary , Espiner Eric A. , Ikram Hamid , Yandle Tim G. 
Published: June 2007

SUMMARY1. Evidence from numerous experiments incorporating central blood volume expansion and changes in sodium status supports atrial stretch as the prime determinant of ANF release.2. Plasma ANF levels are the result of both secretion and clearance of the peptide. Clearance is altered by a number of factors, including changes in posture in normal man and is probably impaired in disease states with diminished renal and hepatic blood flow.3. In normal subjects an inverse relationship exists between plasma ANF values and renin‐angiotensin‐aldosterone system activity. This relationship is lost and replaced by a positive association in heart failure, presumably reflecting the abnormal concurrence of increased atrial stretch and diminished renal perfusion in this condition. Plasma ANF values rise with increasing severity of heart failure and fall with effective treatment.4. Plasma ANF values are elevated in hypertension and cardiac tachyarrhythmias possibly reflecting raised central venous and atrial pressures.5. A variety of other disorders may be associated with abnormal plasma ANF values including cirrhosis and the syndrome of inappropriate ADH secretion.6. Evidence from low‐dose infusions of ANF in normal volunteers suggests that the variations in plasma ANF seen in health and disease are sufficient to exert biological effects.7. The advent of a specific antagonist is needed to provide further insight into the physiological and pathophysiological roles of ANF.
SPONTANEOUS OSCILLATIONS IN CYTOPLASMIC FREE CALCIUM CONCENTRATION IN VASCULAR SMOOTH MUSCLE: A POTENTIAL MECHANISM ASSOCIATED WITH MYOGENIC TONE
Authors: Bobik Alex , Weissberg Peter L. , Little Peter J. 
Published: June 2007

SUMMARY1. The cytoplasmic free calcium concentration was monitored in primary rat aortic smooth muscle cells, grown in culture and serum‐deprived for 24–48 h, with the calcium sensitive fluoroprobe, Fura‐2.2. In the absence of external stimuli, spontaneous increases in the cytoplasmic free calcium concentration were observed which averaged 60±11 nmol/l and lasted approximately 30s.3. The calcium transients were in part dependent on intracellular calcium and were abolished when the temperature was lowered to 10°C.4. It is concluded that vascular smooth muscle cells have an inherent ability to initiate spontaneous transient increases in cytoplasmic free calcium concentration via membrane calcium channels.
RESPONSE OF ATRIAL NATRIURETIC PEPTIDE TO ADRENALINE AND NORADRENALINE INFUSION IN MAN
Authors: Tunny Terry J. , Bachmann Anthony W. , Gordon Richard D. 
Published: June 2007

SUMMARY1. Atrial natriuretic peptide (ANP) levels were significantly increased during both adrenaline and noradrenaline infusions, in the physiological range, in normal subjects and in patients with essential hypertension.2. During adrenaline infusion significant increases in both circulating adrenaline and noradrenaline levels were observed. Mean arterial pressure was unaltered. Changes in heart rate were not significant.3. During noradrenaline infusion, significant increases in circulating noradrenaline and mean arterial pressure were also observed. Heart rate and plasma adrenaline levels were unaltered.4. Fluctuations in sympathetic nervous system activity may be involved in the regulation of ANP via adrenoceptor stimulated release of ANP. Other known regulators such as atrial stretch and increasing heart rate may modify this response.
EFFECTS OF INDOMETHACIN ON STEROID‐INDUCED CHANGES IN PRESSOR RESPONSIVENESS IN MAN
Authors: Whitworth Judith A. , Connell John M. C. , Gordon Deanna , Scoggins† Bruce A. 
Published: June 2007

SUMMARY1. It has been shown previously that hydrocortisone (F) increases pressor responsiveness in normal subjects. The present study examined the role of vasodilator prostanoids in determining these changes.2. Pressor responsiveness to angiotensin II (AII) (1–8 ng/kg per min) and phenylephrine (PE) (0.3–0.9 μg/kg per min) was examined in six normal men receiving: no treatment (day 1); 100 mg indomethacm p.o. (INDO) in three divided doses over 20 h (day 2); 200 mg F for 5 days, 50 mg 6 hourly p.o. (day 6); F plus 100 mg INDO (day 7).3. Blood pressure, body weight and plasma glucose rose with F and plasma potassium fell. F alone produced significant increases in response to AII at 2 ng/kg per min, for systolic pressure (SBP), diastolic pressure (DBP) and mean arterial pressure (MAP), and at 1 ng/kg per min for DBP. The threshold for SBP, DBP and MAP rises with AII was decreased by F. Responses to PE following F were greater at 0.6 μg/kg per min for SBP, DBP and MAP and the threshold for all parameters fell.4. INDO alone had no significant blood pressure or metabolic effects and no effect on the magnitude of the blood pressure rise with AII, but decreased the threshold dose for effects on MAP. INDO had no effect on the magnitude of the pressure rise with PE, but decreased the threshold dose for effects on SBP.5. INDO did not modify responsiveness or threshold to AII following F. Responsiveness to PE was unchanged and threshold fell for SBP only during INDO.6. These data do not suggest a major role for vasodilator prostanoids in modifying pressor responsiveness in F‐treated subjects.