bluuebunny/crossref_metadata_2025_split huggingface dataset:
REDUCED V1 VASOPRESSIN BINDING IN THE RAT NUCLEUS SOLITARII AFTER NODOSE GANGLIONECTOMY
Authors: Phillips P. A. , Widdop R. E. , Chai S‐Y. , Kelly J. , Mooser V. , Trinder D. , Johnston C. I. 
Published: June 2007

SUMMARY1. Anaesthetized male Sprague‐Dawley rats underwent unilateral nodose ganglionectomy or sham operation.2. One week later hindbrain V1 vasopressin binding site density was assessed by in vitro autoradiography with the selective V1 antagonist radiolgand [125I] [d(CH2)5, Sar7]AVP.3. Specific binding was observed in the nodose ganglion, nucleus tractus solitarius (NTS), area postrema, and inferior olive. Only binding in the medial subnucleus of the NTS was reduced by ipsilateral nodose ganglionectomy.4. These findings are consistent with V1 vasopressin receptors occurring pre‐synaptically on vagal primary viscerosensory afferent fibres.5. Such receptors may be involved in the effect of AVP on blood pressure and/or the baroreflex.
HAEMODYNAMIC EFFECT OF ENDOTHELIN, A NOVEL POTENT VASOCONSTRICTOR IN DOGS
Authors: Otsuka Atsuhiro , Mikami Hiroshi , Katahira Katsutoshi , Tsunetoshi Takeshi , Kohara Katsuhiko , Minamitani Kaori , Moriguchi Atsushi , Ogihara Toshio 
Published: June 2007

SUMMARY1. The effects of endothelin (40 and 400 pmol/kg, intravenous (i.v.), a novel vasoconstrictor, on haemodynamics were evaluated in normal dogs and dogs treated with hexamethonium.2. The lower dose of endothelin caused no significant changes in mean blood pressure (MBP), heart rate (HR), cardiac output (CO), or total peripheral resistance (TPR) in normal dogs. In dogs treated with hexamethonium MBP decreased transiently associated with decrease in TPR.3. In both dogs, the higher dose of endothelin caused MBP increase with CO increase in an early phase, and with TPR increase in a later phase. In normal dogs, the CO decreased 60 min after endothelin, but in dogs treated with hexamethonium the decrease in CO was not significant.4. Electrocardiograms showed ST changes and arrhythmias.5. Thus, endothelin has dual effects on both the vasculature and the heart, its effect depending on its dose and the time after its administration: initial vasodilation followed by prolonged vasoconstriction, and cardiostimulation followed by cardiosuppression. The cardiosuppression appears to be mediated in part by a neural mechanism.
EFFECTS OF ATRIAL NATRIURETIC PEPTIDE ON PHENYLEPHRINE‐INDUCED RENIN RELEASE IN DOGS
Authors: Tomura Y. , Hisa H. , Satoh S. 
Published: June 2007

SUMMARY1. The effect of atrial natriuretic peptide (ANP) on α‐adrenoceptor agonist‐induced renin release was examined in the de‐ennervated kidney of the anaesthetized dog pretreated with propranolol (1 mg/kg, intravenous).2. Phenylephrine (50 ng/kg per min) infused into the renal artery increased the renal secretion rate of renin (RSR) without affecting systemic blood pressure or renal blood flow.3. Although basal RSR was unaffected, the phenylephrine‐induced increase in RSR was abolished during intrarenal arterial infusion of ANP (10 ng/kg per min).4. The results suggests that exogenously administered ANP could suppress α‐adrenoceptor‐mediated renin release in the dog.
SERUM ANGIOTENSIN CONVERTING ENZYME ACTIVITY AND PLASMA RENIN ACTIVITY IN EXPERIMENTAL MODELS OF RATS
Authors: Ibarra‐Rubio María Elena , Cruz Cristino , Tapia Edilia , Peña José Carlos , Pedraza‐Chaverrí José 
Published: June 2007

ABSTRACT1. Serum angiotensin converting enzyme activity (ACEA) and plasma renin activity (PRA) were determined in rats under different experimental conditions such as: nephrotic syndrome (NS), bilateral nephrectomy (BN), renovascular hypertension (RH), dehydration (DEH), anaesthesia (AN), low sodium diet (LSD) and high sodium diet (HSD), and injection with propranolol (PRO) and isoprenaline (ISO).2. PRA increased in LSD, AN, NS, RH, DEH and IPT groups, and decreased in HSD, BN, and PRO groups. Serum ACEA did not change in RH, HSD, IPT, DEH, AN, and PRO groups, increased in NS group, and decreased in LSD and BN groups.3. Serum ACEA changed in the opposite direction to PRA only in the LSD group. This finding suggests that ACE may limit the full expression of the reninangiotensin system in the LSD group, but not in the other groups.
β‐ADRENOCEPTOR MEDIATED SECRETION OF ACTIVE AND INACTIVE RENIN IN CONSCIOUS SHEEP
Authors: Al Kattan A. H. K. , Parker J. C. , Noble A. R. 
Published: June 2007

ABSTRACT1. β‐Adrenoceptor linked regulation of plasma active and inactive renin was investigated in sheep with indwelling artery, vein and bladder catheters. Concurrent changes in renal function were also monitored.2. The β‐adrenoceptor agonist isoprenaline (bolus intravenous (i.v.) dose 0.5 mg/kg, 0.05 μg/kg per min) increased plasma active renin concentration within 15 min and reached a plateau increase of 306%. Initially plasma inactive renin remained unchanged but after 105 min it decreased.3. The non‐selective β‐adrenoceptor antagonist propranolol (bolus i.v. dose 4 mg/kg, 40 μg/kg per min) did not significantly alter basal plasma active renin but selectively reduced inactive renin. The absence of any change in active renin may reflect the relatively low level of stress‐induced sympathetic activation in these conscious animals compared to equivalent studies carried out on human subjects.4. Using the same dose schedules, propranolol completely blocked the isoprenaline‐induced increases in plasma active renin secretion even though it had no effect on the basal active renin levels.5. The selective β1‐adrenoceptor antagonist atenolol (bolus i.v. dose 5 mg/kg) decreased basal plasma active renin by 24% (+135 min) but reduced plasma inactive renin by 75% compared to control.6. Therefore, both a β‐adrenoceptor agonist (isoprenaline) and two β‐adrenoceptor antagonists (propranolol and atenolol) decreased plasma inactive renin concentration in conscious sheep.7. These results are discussed in relation to the accompanying changes in arterial blood pressure and aspects of renal function.
RELATIONSHIP BETWEEN SYSTEMIC AND CORONARY VASCULAR RESPONSES TO DIGOXIN AND CONCURRENT DRUG THERAPY WITH VERAPAMIL/β‐ADRENOCEPTOR ANTAGONISTS IN HUMANS
Authors: Powell A. C. , Horowitz J. D. , Hasin Y. , Louis W. J. 
Published: June 2007

ABSTRACT1. In 24 patients who were undergoing coronary arteriography for the assessment of ischaemic heart disease, the relationship between the systemic and coronary vascular responses to acute intravenous digoxin administration (500 μg) and concurrent drug therapy with the calcium antagonist verapamil (group I) or a β‐adrenoceptor antagonist (group II) or neither of these agents (group III) was examined.2. Systemic vascular resistance (SVR) tended to rise rapidly after digoxin injection in patients in groups II and III, and tended to decline initially in patients in group I; however, these differences were not statistically significant (variance ratio [VR] = 0.77).3. No significant differences were observed in coronary vascular responses to acute digoxin administration between the three groups of patients (VR = 0.34).4. For the entire group of 24 patients, no statistically significant digoxin‐induced effects on resistance could be demonstrated in either the systemic or coronary circulations, although in individual patients vasoconstrictor effects were observed.5. We conclude that acute intravenous administration of digoxin does not consistently cause systemic or coronary vasoconstriction in patients with ischaemic heart disease. Variability in vasomotor responses to digoxin is not clearly related to concurrent drug therapy with verapamil or a β‐adrenoceptor antagonist. The observation that systemic vascular resistance tends to increase in the first few minutes after digoxin injection should be addressed in future studies.
DENSITY DEPENDENCE OF RESPIRATORY INPUT IMPEDANCE IN NORMAL SUBJECTS
Authors: Wouters E. F. M. , Lándsér F. J. , Polko A. H. , Visser B. F. 
Published: June 2007

SUMMARY1. The forced oscillation technique is a non‐invasive and effort‐independent test used to characterize the mechanical impedance of the respiratory system. Total respiratory impedance was assessed from 4 to 52 Hz in 15 normal subjects breathing air and a helium‐oxygen mixture.2. Breathing helium‐oxygen reduced respiratory resistance and its frequency dependence as well as respiratory reactance very significantly. Resonant frequency during He‐O2 breathing was 1.88 times higher than during air breathing.3. It is concluded that by impedance measurement of the respiratory system in normal subjects a density‐dependent decrease of respiratory resistance due to decreased turbulence in the larger airways and a density‐dependent decrease in the inductive reactance can be found during breathing of low density gas mixtures.
ENZYME IMMUNOASSAY FOR METHIONINE‐ENKEPHALIN SULFOXIDE
Authors: Tiong George K. L. , Olley Jean E. 
Published: June 2007

SUMMARY1. An immunoassay technique employing an enzyme‐labelled ligand was developed for the sulfoxide derivative of the opioid peptide methionine‐enkephalin (MOE).2. The sensitivity of the enzyme immunoassay (EIA) was approximately twofold higher than that achieved in the radio‐immunoassay (RIA) using tritiated ligand. Cross‐reactivities of leucine‐enkephalin and β‐endorphin with the EIA were less than 0.1%, while that with Gly‐Gly‐Phe‐Met and oxidized Gly‐Gly‐Phe‐Met were 2.5% and 10.2%, respectively.3. These results indicate that the EIA is a useful alternative to the RIA for the assay of small peptides.
PERTUSSIS TOXIN ATTENUATES ANGIOTENSIN II BUT NOT β‐ADRENOCEPTOR FACILITATION OF NORADRENALINE RELEASE FROM RAT KIDNEY CORTEX
Authors: Murphy Timothy V. , Majewski Henryk 
Published: June 2007

SUMMARY1. Angiotensin II (AII; 0.01 and 0.1 μmol/L), angiotensin I (AI, 0.1 μmol/L) and the β‐adrenoceptor agonist isoprenaline (0.1 μmol/L) all facilitated the stimulation‐induced outflow of radioactivity from slices of rat kidney cortex incubated in [3H]‐noradrenaline.2. Treatment of rats with pertussis toxin (25 and 50 μg/kg i.v.) to inactivate G‐proteins attenuated the facilitation caused by AII and AI, but not that caused by isoprenaline.3. The hypothesis that isoprenaline enhances noradrenaline release by generating AII to activate facilitatory prejunctional AII receptors is not supported by the present study. The hypothesis predicts that pertussis toxin, by inactivating the G‐proteins associated with AII receptors, should have inhibited the facilitatory effect of isoprenaline. This did not occur.
RENAL AND MYOCARDIAL ADRENOCEPTORS IN STEROID CONTRACEPTIVE‐INDUCED HYPERTENSION IN RATS
Authors: Geraghty Dominic P. , Byrne K. Bruce , McPherson Grant A. , Burcher Elizabeth 
Published: June 2007

SUMMARY1. Systolic blood pressure (SBP), bodyweight, organ weight, renal β‐adrenoceptor and myocardial β‐ and myocardial α1‐adrenoceptor characteristics were investigated in female Sprague‐Dawley rats after chronic subcutaneous (s.c.) administration of ethynyloestradiol (EE2, 0.2 μg/day), levonorgestrel (NG, 2.0 μg/day) separately and in combination (EE2/NG).2. EE2 caused a sustained increase in SBP from 6 weeks (maximum at 14 weeks, +22 mmHg compared to control) which was accompanied by increased kidney and ventricle weight after 12 weeks. EE2/NG‐treated rats also demonstrated a gradual rise in SBP (maximum at 9 weeks, +18 mmHg compared with control) with renal and ventricular hypertrophy, but were normotensive by week 17 of treatment. In contrast, NG induced only transient SBP increases (maxima at 5 and 10 weeks, + 14 mmHg compared with control), unaccompanied by organ hypertrophy. Norethisterone (2 μg/day) also produced transient increases (weeks 6–8, + 13 mmHg) in SBP.3. α1‐ and β‐adrenoceptors were investigated using [3H]‐prazosin and (‐)‐ [125I]‐iodocyanopindolol (ICYP), respectively. Myocardial α‐ and β‐adrenoceptors were unaffected by steroid contraceptive administration for up to 12 weeks. Renal β‐adrenoceptor affinity was markedly reduced in 12 week EE2‐treated rats (equilibrium dissociation constant, KD, 53±7 pmol/L) compared with controls (KD, 31±4 pmol/L), an effect which was prevented by co‐administration of NG (KD, 34±8 pmol/L). Renal β‐adrenoceptor number was not altered by any treatment.4. The relatively late onset of organ hypertrophy and β‐adrenoceptor changes appear to result from, rather than cause, EE2‐induced hypertension.
SUBSENSITIVITY TO ATP AND SOME ANALOGUES IN PREPARATIONS OF RAT CAUDA EPIDIDYMIS AND VAS DEFERENS AFTER VASECTOMY
Authors: Ventura Sabatino , DeGaris Richard M. , Stead Cheryl K. , Pennefather Jocelyn N. 
Published: June 2007

SUMMARY1. The effects of ATP and some of its more stable analogues have been examined upon preparations of epididymal and prostatic halves of vasa deferentia and of cauda epididymides from rats that had undergone vasectomy by medial transection of the vas deferens.2. After unilateral vasectomy, the potencies of ATP, β, γ‐methylene ATP and 5’‐adenylylimidodiphosphate (AppNHp) in tissues ipsilateral to the vasectomy were decreased compared to tissues from the contralateral unoperated side of the animal.3. Tissues from bilaterally vasectomized rats were less responsive to ATP when compared to tissues taken from sham‐operated rats.4. Tissues taken from rats which had undergone vasovasostomies following unilateral vasectomy remained less responsive to these purines.5. Responses of cauda epididymides and epididymal halves of vasa deferentia taken from unilaterally and bilaterally vasectomized rats to α, β‐methylene ATP usually did not differ from those of respective controls.6. It is proposed that the subsensitivity which develops to ATP and some of its analogues on the epididymis and vas deferens following vasectomy may reflect increased breakdown, perhaps associated with changes in structural integrity of the tissues, rather than with the sympathetic denervation which is associated with vasectomy.
POSITIVE INOTROPIC AND VASOCONSTRICTOR RESPONSES TO 14β‐AMINOPREGNANE DERIVATIVES IN ISOLATED TISSUES FROM THE GUINEA‐PIG
Authors: Brown Lindsay 
Published: June 2007

SUMMARY1. The objective of this study was to compare the positive inotropic and vasoconstrictor responses in guinea‐pig isolated tissues of the aminosteroid derivatives LND 623 and LND 796 and the cardiac glycoside ouabain.2. Ouabain (‐ log EC50, 6.66±0.04, n= 11) was more potent as a positive inotropic agent on guinea‐pig right ventricular papillary muscles than either LND 623 (‐ log EC50, 6.26±0.08, n= 6) or LND 796 (‐ log EC50 5.66±0.05, n= 7). All compounds gave similar maximal increases in force of contraction. However, the ratio of the maximally effective concentration to the concentration giving 25% of the maximal response was approximately doubled for the aminosteroids compared with ouabain.3. Ouabain (‐ log EC50 6.27), LND 623 (‐ log EC50 6.24) and LND 796 (‐ log EC50 5.43) produced slowly developing contractions of guinea‐pig thoracic aortic rings.4. These results indicate that, while the aminopregnane derivatives and ouabain produce qualitatively similar results, the therapeutic range for the positive inotropic responses is greater for the aminosteroids.
FILTRATION FAILURE INDUCED BY pAMINOPHENOL IN RATS IS DUE TO RAISED INTRATUBULAR PRESSURE AND NOT CHANGES IN GLOMERULAR FUNCTION
Authors: Henry Mark A. , Harris Peter J. , Naughton Robert J. , Walker Lesley L. , Skinner Sandford L. , Tange John D. 
Published: June 2007

SUMMARY1. The p‐aminophenol (pAP) model of tubular necrosis displays elevated tubular pressures equivalent to ‘stop‐flow’, with low glomerular filtration rate (GFR) but maintained blood flow and urine output. Renal function, micropuncture, and morphological studies were performed in anaesthetized rats to examine the causes of filtration failure.2. At the height of pAP‐induced renal failure proximal tubular fluid reabsorption (Jv(a) was markedly reduced while proximal and distal free‐flow rates measured by tubular fluid collections during venting of the nephron were not significantly different from saline‐injected controls. Renal blood flow was maintained over the 4 h observation period despite extensive and selective proximal tubular necrosis. There was no temporal relationship between increased tubular pressure and cast formation.3. Maintained blood and tubular fluid flow rates indicate that activation of tubuloglomerular feedback plays little or no part in pAP‐induced renal failure, which is apparently due to high fluid flow resistance in the region of the connecting tubule, late distal convolution or collecting ducts. Morphological appearances were consistent with compression of these segments.
THE ACTIONS OF TULOBUTEROL ON ISOLATED PREPARATIONS OF GRAVID HUMAN MYOMETRIUM
Authors: Ziccone S. P. , Paull J. D. 
Published: June 2007

SUMMARY1. The effects of tulobuterol (Abbott 54173) on the contractile force developed by electrically stimulated strips of gravid (gestation 36–40 weeks) human uterine muscle were compared with those of isoprenaline and adrenalin.2. Isoprenaline produced inhibition of electrically evoked contractions of myometrium from 12 of 17 women at concentrations at or below 1 μmol/L (range 0.001–1 μmol/L). It enhanced contractions at concentrations of 10–50 μmol/L. In tissues from the remaining five women isoprenaline produced neither inhibitory nor excitatory effects. Adrenalin (0.1–50 μmol/L) was found to enhance contractile force in a concentration‐dependent manner (EC50= 0.30 μmol/L).3. In the presence of metoprolol (0.3 μmol/L), a selective antagonist at β1‐adrenoceptors, the isoprenaline concentration‐response relationship was shifted to the left, indicating that β‐adrenoceptors are present and that they mediate excitation in the human uterus.4. In contrast tulobuterol (in neither the presence nor absence of metoprolol), in the same concentration range as isoprenaline and adrenalin, (0.001–50 μmol/L) was found to have no effect on the electrically evoked contraction of gravid human uterine muscle strips.
ABNORMALITIES OF RESISTANCE VESSEL STRUCTURE IN ESSENTIAL HYPERTENSION: ARE THESE IMPORTANT?
Authors: Mulvany M. J. 
Published: June 2007

SUMMARY1. The relationship between essential hypertension and abnormalities of the proximal resistance vessels (small arteries) is reviewed, with particular emphasis on their structure.2. There seems to be good evidence that the media: lumen ratio of these vessels is increased, and this may account for the increased pressor response.3. Whether there is also growth is not clear, and it is possible that the altered structure is due to redistribution of existing cells.4. Regardless of the basis for the altered structure, it appears that in essential hypertension the altered vascular structure is in itself sufficient to explain the increased peripheral resistance.5. Paradoxically, the altered vascular structure does not seem to be the main determinant of blood pressure, but the altered vascular structure appears to allow it to perform its function in the most convenient fashion.6. It is suggested that the interest in vascular structure lies in connection with therapy, for correction of blood pressure without correction of vascular structure will probably not prevent all the consequences of the disease.7. Current therapies do not appear to be able, in the short‐term, to normalize vascular structure, indicating that there is a need to find other more specific ways of correcting vascular structure.
EFFECT OF LONG‐TERM TREATMENT WITH AN ANGIOTENSIN‐CONVERTING ENZYME INHIBITOR ON THE RENIN‐ANGIOTENSIN SYSTEM IN SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Morishita Ryuichi , Higaki Jitsuo , Okunishi Hideki , Kawamoto Tatsuhiko , Ishii Kenji , Nakamura Fumiaki , Katahira Katsutoshi , Nagano Masahiro , Mikami Hiroshi , Miyazaki Mizuo , Ogihara Toshio 
Published: June 2007

SUMMARY1. To obtain information on regulation of the brain renin–angiotensin system, the effect of long‐term administration of angiotensin‐converting enzyme (ACE) inhibitor on brain renin and angiotensinogen mRNA was studied.2. Spirapril (3 mg/kg) was orally administered daily for 8 weeks to spontaneously hypertensive rats (SHR) from 12 weeks after birth. Renin and angiotensinogen mRNA in the brain and kidney were then quantitated by Northern blot analyses with [32P]‐labelled rat renin and angiotensinogen cDNA as hybridization probes. Plasma renin activity (PRA), angiotensin II (AII) concentration, plasma ACE activity and brain tissue ACE activity were also measured.3. Compared with the control group, the Spirapril‐treated group had significantly lower blood pressure (P<0.01), significantly higher PRA (P<0.01), a not significantly different plasma AII concentration, and lower plasma and brain ACE activities (P<0.01). Interestingly, the brain renin and angiotensinogen mRNA levels of the two groups were similar, but the renal renin mRNA level was significantly higher in the Spirapril‐treated group (P<0.01).4. These results indicate that the mRNA levels of brain renin and angiotensinogen were not affected by chronic ACE inhibition in the circulation and suggest that AII in the brain might not be affected by systemic ACE inhibition.
STRESS IN MICE INCREASES INTRINSIC PENTOBARBITONE SENSITIVITY BY A PREDOMINANTLY PHARMACODYNAMIC MECHANISM
Authors: Carmody John J. , Graham Garry G. , Ruigrok Marielle A. 
Published: June 2007

SUMMARY1. Mice were swum for 3 min at room temperature.2. After this stress ‘sleeping time’ in response to pentobarbitone was increased by over 70%.3. Loss of ‘righting reflex’ occurred in these stressed animals at brain concentrations of pentobarbitone which were 40% lower than those needed for ‘sleep’ in the unstressed mice, indicating a true increase in sensitivity to the drug. ‘Waking’ (the return of the righting reflex) occurred at identical levels in both groups.4. Kinetic analysis showed that the rates of absorption, elimination and transfer between plasma and brain were slower in the swum than in the unswum mice, probably because of the reduced body temperatures produced by the swimming.
EFFECTS OF RESPIRATION ON BLOOD PRESSURE AND HEART RATE VARIABILITY IN HUMANS
Authors: Elghozi Jean‐Luc , Laude Dominique , Girard Arlette 
Published: June 2007

SUMMARY1. Non‐invasive continuous finger blood pressure (BP) measurement and a spectral technique based on the Fourier transform (FT) were recently combined to quantify short‐term fluctuations in haemodynamic variables.2. Systolic BP (SBP) recording combined low frequency (LF, Mayer waves) plus high frequency (HF, respiratory) oscillations. The presence of HF oscillations of SBP probably reflects fluctuations in cardiac output. Heart rate (HR) also exhibited a combination of low and HF (respiratory) oscillations. The vagus nerve mediates the efferent control of the respiratory sinus arrhythmia (RSA).3. During controlled breathing in a supine position, a change in SBP is associated with an opposite consequent change in HR. Respiratory sinus arrhythmia could therefore depend on the baroreceptor‐HR response to underlying SBP oscillations.4. The fast regulation of R‐R interval by SBP through the baroreceptor‐HR reflex may explain why the respiratory variations in the diastolic BP are small.