bluuebunny/crossref_metadata_2025_split huggingface dataset:
ROLE OF PLATELET CYTOSOLIC CALCIUM IN THE RESPONSE TO SALT INTAKE IN NORMOTENSIVE SUBJECTS
Authors: Yamakawa Hiroshi , Suzuki Hiromichi , Nakamura Makoto , Ohno Yoichi , Saruta Takao 
Published: June 2007

SUMMARY1. To investigate the role of cytosolic calcium in salt‐induced hypertension, a high salt diet was given to young normotensive subjects with or without a family history of hypertension.2. A high salt diet raised blood pressure significantly in normotensive subjects with a family history compared with the age and gender matched subjects without a predisposition to hypertension.3. Platelet cytosolic calcium was increased in predisposed subjects in a control period before salt intake.4. A positive correlation was observed between the changes in mean blood pressure and cytosolic calcium before high salt intake, although salt loading did not induce any significant change in cytosolic calcium.5. These results suggest that cytosolic calcium plays a role in elevation of blood pressure induced by salt loading in subjects with a family history of hypertension.
PHARMACOLOGICAL EVALUATION OF TWO NOVEL ANALOGUES OF MIANSERIN: 2‐N‐CARBOXAMIDINONORMIANSERIN(FCC5) AND 2‐N‐CARBOXAMIDONORMIANSERIN (FCC13)
Authors: Leitch Ian M. , Rawlow Andrew , Rechtman Mary P. 
Published: June 2007

SUMMARY1. The pharmacological properties have been examined of FCC5 (2‐N‐carboxamidinonormianserin) and FCC 13 (2‐N‐carboxamidonormianserin), two novel analogues of mianserin.2. FCC5 or FCC13 (100 μg/kg, i.v.) caused long‐lasting (>1 h) abolition of 5‐hydroxytry‐ptamine (5‐HT) and histamine‐induced bronchoconstriction in the anaesthetized guinea‐pig. Both analogues had no effect (up to 1 mg/kg, i.v.) on bronchoconstriction caused by acetylcholine (25–50 μg/kg, i.v.).3. The pressor effects of 5‐HT in pithed rats were significantly attenuated by FCC5 (0.1 mg/kg, i.v.) or FCC13 (0.5 mg/kg, i.v.).4. Oedema in the rat hind paw caused by intraplantar 5‐HT was inhibited by FCC5 (ID500.76 mg/kg, i.p.; 2.7 mg/kg, p.o.) or FCC13 (ID5100.65 mg/kg, i.p.; 5.8 mg/kg, p.o.).5. In the central nervous system (CNS), FCC 13 caused antagonism of 5‐HT activity. It inhibited: (i) l‐5‐hydroxytryptophan (l‐5‐HTP)‐induced head twitches in mice (ID501.85 mg/kg, i.p.), (ii) fenfluramine‐induced facilitation of flexor reflex activity (FRA) in spinalized decerebrate rats (SDR) (IC500.57 mg/kg, i.p.).6. FCC5 (≤30 mg/kg, i.p. and ≤3 mg/kg, i.p., respectively) had no effect in either test. In contrast to mianserin, it also had no overt central actions as (≤30 mg/kg, i.p.) had no effect on: (i) morphine‐induced catalepsy (MIC) or (ii) clonidine‐induced facilitation of FRA in SDR. However, high doses of FCC13 inhibited MIC (ID5020 mg/kg, i.p.), but had no effect on (ii) (≤10 mg/kg, i.p.).7. Thus, FCC5 and FCC13 are potent, orally active H1 and 5‐HT receptor antagonists. However, in contrast to FCC 13 and mianserin, FCC5 did not cause CNS‐mediated effects.
INHIBITORY EFFECT OF NEUROPEPTIDE Y ON STIMULATED RENIN SECRETION OF AWAKE RATS
Authors: Aubert Jean‐Francois , Walker Philippe , Grouzmann Eric , Nussberger Jürg , Brunner Hans R. , Waeber Bernard 
Published: June 2007

SUMMARY1. (1‐36)‐NPY is a vasoconstrictor peptide widely distributed in sympathetic nerve terminals. This peptide exerts an inhibitory action on renin release induced by various stimuli. Post‐synaptic neuropeptide Y (NPY) receptors show a high affinity for (1‐36)‐NPY as well as for the agonist (Pro34)‐NPY, while presynaptic receptors bind preferentially (13‐36)‐NPY.2. This study was undertaken to assess whether the NPY induced renin suppression in awake normotensive rats infused with the β‐adrenoceptor stimulant isoproterenol is mediated by activation of pre‐ or post‐synaptic receptors.3. Non‐pressor doses of (1‐36)‐NPY and (Pro34)‐NPY markedly attenuated the renin secretion triggered by isoproterenol whereas (13‐36)‐NPY had no effect. This suggests that the effect of NPY on renin release is due to the stimulation of post‐synaptic receptors. However it remains unknown whether NPY acts directly on juxtaglomerular cells or indirectly by modifying intraglomerular haemodynamics.
TIME COURSE OF REGIONAL FLOW DISTRIBUTION FOLLOWING REPERFUSION OF THE ISOLATED ISCHAEMIC RAT HEART
Authors: Sjöquist P‐O. , Abrahamsson T. , Johansson M. H. 
Published: June 2007

SUMMARY1. The regional distribution of flow was studied at different times after the onset of reperfusion in isolated rat heart preparations. The hearts were submitted to 30 min of global ischaemia followed by 60 min of reperfusion. Microspheres labelled with various nuclides were added to the perfusate before ischaemia and 1, 5, 20, and 60 min after the onset of reperfusion.2. One minute after the start of reperfusion, the flow to the left ventricular inner layer was restricted to 0.5 ± 0.2 mL/min per g (2–3% of the pre‐ischaemic flow). In this segment, the perfusion remained at the same low level during the entire reperfusion period studied. At the onset of reperfusion the flow to the outer layer of the left ventricle was 4.8 ± 1.7 mL/min per g (37% of the pre‐ischaemic flow), and 3.0 ± 1.3 mL/min per g (27% of the pre‐ischaemic value) to the free wall of the right ventricle. The flow was progressively reduced in the outer layer of the left ventricle in the course of reperfusion. After 60 min of reperfusion the flow to the left ventricular outer layer was 2.5 ± 0.9 mL/min per g (19% of pre‐ischaemic flow when compared with the onset of reperfusion [P < 0.05]).3. It is concluded that a ‘no‐reflow’ condition develops very early during reperfusion and becomes more marked during this period.
IS ISOLATED SYSTOLIC HYPERTENSION A WHITE COAT’ PHENOMENON IN THE ELDERLY?
Authors: Silagy C. A. , McNeil J. J. , McGrath B. P. , Farish S. 
Published: June 2007

SUMMARY1. Repeated clinic blood pressure measurement was compared with non‐invasive ambulatory blood pressure (ABP) monitoring in 10 elderly subjects with isolated systolic hypertension (ISH) and 11 normotensive controls (NT).2. Subjects were assessed on four occasions at weekly intervals. None was receiving antihypertensive or vasoactive medication.3. Mean clinic blood pressure was consistently higher than mean daytime ABP in both clinical groups. This effect was greater for systolic (SBP) than diastolic blood pressure (DBP) and in the ISH group compared with the NT group. The reproducibility of the clinic minus ABP difference was high in both groups; the mean±s.d. of the differences was 26± 15/9 ± 2 mmHg in the ISH group and 7 ± 18/8 ± 9 mmHg in the controls.4. ABP readings were normally distributed for both SBP and DBP in both groups. In the ISH group, the frequency distribution of SBP readings was shifted to the right whilst the distribution of DBP readings overlapped that of the NT subjects.5. These results suggest a pressor response may largely account for the elevated SBP seen in elderly subjects with sustained ISH based on casual readings.
NEUROVASCULAR FUNCTION DURING PREGNANCY IN THE SPONTANEOUSLY HYPERTENSIVE RAT
Authors: Yong E. M. , Mano M. T. , Head R. J. 
Published: June 2007

SUMMARY1. Blood pressure (BP) declines dramatically in the final week of gestation in the pregnant spontaneously hypertensive rat (SHR). This study investigated the hypothesis that alterations of vascular neuroeffector function in the pregnant SHR and normotensive Wistar‐Kyoto (WKY) rat are responsible for this decline.2. Pregnancy in SHR and WKY rats was associated with a significant drop in BP in the last week of gestation.3. Responses of the perfused mesenteric vasculature to bolus doses of noradrenaline (NA) and potassium chloride (KC1) were decreased in preparations from SHR rats 4 days before delivery. This decreased responsiveness was absent in preparations from SHR rats 1 day before delivery. Responses of the perfused mesenteric vasculature to sympathetic nerve stimulation were not influenced by pregnancy in the SHR.4. It is concluded that while there are dynamic changes occurring in neurovascular function just prior to delivery, it is unlikely that they are wholly responsible for the dramatic decline in blood pressure in the SHR rat.
Presynaptic α2‐adrenoceptor‐mediated modulation of norepinephrine release from vascular adrenergic neurons in reduced renal mass salt hypertensive rats
Authors: Tsuda Kazushi , Kimura Keizo , Shima Hiroki , Nishio Ichiro , Masuyama Yoshiaki 
Published: June 2007

SUMMARYThe present study was designed to investigate the presynaptic α2‐adrenoceptor function to inhibit norepinephrine (NE) release in blood vessels of reduced renal mass salt hypertensive rats (Na‐loaded HT). Isolated perfused mesenteric vasculatures were prepared from Na‐loaded HT and normotensive control rats (NT‐control), and the NE release and vascular responsiveness were examined. Periarterial nerve stimulation caused a significantly greater release of NE and pressor responses in Na‐loaded HT than in NT‐control. Yohimbine, a potent α‐adrenoceptor antagonist, demonstrated the facilitatory effects on NE release during nerve stimulation. The effects were significantly attenuated in Na‐loaded HT compared with NT‐control.These results demonstrate that vascular sympathetic nervous activity might be enhanced in Na‐loaded HT. Furthermore, the increased NE release from vascular adrenergic neurons in Na‐loaded HT could partially depend on impaired presynaptic α2‐adrenoceptor‐mediated modulation, which might contribute to the pathogenesis and maintenance of this form of salt‐dependent hypertension.
CHARACTERIZATION OF THE BARORECEPTOR HEART RATE REFLEX DURING DEVELOPMENT IN SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Head Geoffrey A. , Adams Michael A. 
Published: June 2007

SUMMARY1. We have examined the baroreceptor‐heart rate (HR) reflex in weight‐matched conscious spontaneously hypertensive rats (SHR) and normotensive Wistar‐Kyoto (WKY) rats during development.2. Graded steady‐state changes in mean arterial pressure (MAP) and the corresponding HR responses before and after vagal blockade with methylatropine were fitted to an S‐shaped logistic function.3. At 6 weeks of age, SHR had a 17% higher MAP than WKY and an increased baroreflex gain (slope) compared with WKY due to an increased curvature of the MAP‐HR relationship. The HR range (the difference between the upper and lower HR plateaus) was similar in the two strains at this time.4. From 9–14 weeks of age, the baroreflex gain progressively increased in WKY and decreased in SHR due to corresponding alterations in HR range.5. By 20 weeks the baroreflex gain was 23% lower in SHR than WKY due to a 37% lower HR range.6. There were no differences between the two strains in the sympathetic component of the baroreflex at any age, suggesting that the changes to baroreflex properties were confined to the cardiac vagus.7. Pretreatment with enalapril from 4–9 weeks reduced the hypertension of SHR at 14 and 20 weeks by 38% and abolished all baroreceptor‐HR reflex differences between the two strains.8. These studies suggest that the major alteration to the baroreceptor‐heart rate reflex in the SHR during development was a reduction in the maximum vagal capacity to respond to changes in blood pressure. This effect developed after the onset of hypertension and was prevented by antihypertensive treatment early in life. The lack of effect on the cardiac sympathetic component suggests that altered arterial baroreceptor afferents are not unlikely to be responsible.
XANTHINES INHIBIT HUMAN PLATELET AGGREGATION INDUCED BY PLATELET‐ACTIVATING FACTOR
Authors: Misso N. L. A. , Thompson P. J. 
Published: June 2007

SUMMARY1. Platelet‐activating factor (PAF) may be involved in the pathogenesis of asthma, and therefore the effects of the anti‐asthma drugs theophylline and enprofylline on human platelet aggregation and adenosine triphosphate (ATP) release induced by PAF and adenosine diphosphate (ADP) were studied.2. Enprofylline (50% inhibitory concentration [IC50] = 94.8±13.2 μmol/L) was more potent than theophylline (IC50= 934.1±40.1 μmol/L) as an inhibitor of PAF‐induced aggregation, and the xanthines were twice as potent as inhibitors of PAF‐induced aggregation when compared with ADP‐induced aggregation. ATP release was 1.4 times more sensitive to inhibition by the xanthines than aggregation.3. Although high concentrations of xanthines inhibited platelet aggregation and ATP release induced by PAF, therapeutic concentrations are unlikely to inhibit PAF‐induced effects.
A STUDY OF SERUM PROLACTIN LEVELS IN SCHIZOPHRENIA: COMPARISON OF MALES AND FEMALES
Authors: Kuruvilla Alice , Peedicayil Jacob , Srikrishna Geetha , Kuruvilla K. , Kanagasabapathy A. S. 
Published: June 2007

SUMMARY1. Serum prolactin levels were measured in large cohorts of schizophrenic patients (67 males and 42 females) and normal subjects (78 males and 42 females).2. There was no significant differences between the serum prolactin levels of patients and controls, except in the age group 15–29 years. There were no significant differences between the serum prolactin levels of males and females, either among the patients or the control subjects.3. The rise in serum prolactin levels after the commencement of neuroleptic medication in the patients was greater in females than in males even though the female patients received neuroleptics at lower doses.4. These data indicate that serum prolactin levels in unmedicated males and females are similar; however, the prolactin response to neuroleptic medication is greater in females than in males.
STUDIES ON THE EFFECT OF DOPAMINE ON THE HUMAN PLATELET RESPONSE
Authors: Anfossi Giovanni , Massucco Paola , Mularoni Elena , Cavalot Franco , Burzacca Serenella , Mattiello Luigi , Trovati Mariella 
Published: June 2007

SUMMARY1. The present study investigated the in vitro effect of dopamine on platelet responses in healthy subjects.2. Dopamine concentrations over 5 μmol/L induced a primary aggregating response and a slight release of α‐granule proteins, β‐thromboglobulin and platelet factor‐4 in all subjects. In 25% of investigated subjects a delayed secondary aggregation was observed with dopamine concentrations over 100 μmol/L.3. Low dopamine concentrations (5–7.5 nmol/L) increased the platelet sensitivity to other aggregating agents (adenosine diphosphate, collagen and sodium arachidonate). The effect of subaggregating concentrations of serotonin was potentiated by dopamine.4. The effect of dopamine on platelet responses was prevented by low concentrations of α‐adrenoceptor antagonists (phentolamine and yohimbine); antagonists of dopamine receptors (haloperidol and domperidone) were able to decrease the extent of the dopamine‐induced secondary aggregating wave in the responders, but they failed to prevent the primary aggregation and the effects on platelet response to other aggregating agents.5. The present data demonstrated that the effects of dopamine on human platelets are mainly mediated by interactions with α‐adrenoceptors.
DOES THE HAEMODYNAMIC RESPONSE TO ACUTE CENTRAL HYPOVOLAEMIA DEPEND ON THE RATE OF FALL OF CARDIAC OUTPUT?
Authors: Evans Roger G. , Hayes Ian P. , Ludbrook John 
Published: June 2007

SUMMARY1. In published studies of the effects of acute blood loss in conscious rabbits, the rates of haemorrhage have ranged for 3–9% of blood volume/min. This is potentially a confounding factor when it comes to comparing the results of different studies. We have therefore tested whether the haemodynamic response to acute central hypovolaemia depends on the rate of fall of cardiac output.2. Cardiac output in six conscious rabbits was reduced by 4, 8 and 12% of baseline levels per min by gradual inflation of a cuff around the thoracic inferior vena cava. These rates correspond approximately to blood loss at rates of 3, 6 and 9% of blood volume/min.3. The haemodynamic responses were biphasic. In Phase I (compensatory) there was progressive systemic vasoconstriction and tachycardia, and only a small fall in blood pressure. In Phase II (decompensatory), systemic vasoconstriction failed abruptly, arterial pressure plummeted and heart rate declined.4. We could detect no effect of rate of fall of cardiac output on the pattern of the haemodynamic responses in either Phase I or Phase II.5. We conclude that the rate of blood loss in different studies of haemorrhage in conscious rabbits, within the range 3 to 9 per cent of blood volume per minute, need not be regarded as a confounding factor when it comes to interpreting the results. It is likely that this conclusion can be generalized to studies of haemorrhage in other mammalian species.
ACUTE AND CHRONIC EFFECTS OF ANGIOTENSIN‐CONVERTING ENZYME INHIBITORS ON TISSUE ANGIOTENSIN‐CONVERTING ENZYME
Authors: Chai Siew Y. , Perich Rose , Jackson Bruce , Mendelsohn Frederick A. O. , Johnston Colin I. 
Published: June 2007

SUMMARY1. The effects of angiotensin‐converting enzyme (ACE) inhibitors on the tissue ACE were assessed by quantitative in vitro autoradiography after acute and chronic administrations of the drugs.2. Following acute administration of lisinopril, perindopril or benazepril, ACE was markedly inhibited in the lung, kidney and blood vessels but not in the testis. In the brain, ACE was inhibited mainly in structures with a deficient blood brain barrier.3. High doses of perindopril progressively inhibited ACE in other brain structures. Tissue ACE inhibition persisted after serum levels of the enzyme had returned to control levels. In the case of perindopril, the time course of tissue ACE inhibition correlated with the inhibition of the pressor responses to exogenous angiotensin I.4. After chronic administration of lisinopril or perindopril for 14 days, a similar pattern of ACE inhibition was observed in the kidney, lung and blood vessels. In the lung, however, lisinopril was found to increase total ACE by 30%, while plasma ACE was increased two‐threefold by both lisinopril and perindopril. Testicular ACE remained unaltered by chronic lisinopril treatment.5. Overall, the changes in tissue ACE after the administration of inhibitors more closely parallel the drugs' biological effects than changes in plasma ACE or drug levels. ACE in the testis and brain is protected by permeability barriers that limit access of the drugs.
EFFECT OF PERINDOPRIL ON THE DEVELOPMENT OF ATHEROSCLEROSIS IN THE CHOLESTEROL‐FED RABBIT
Authors: Campbell Julie H. , Fennessy Paul , Campbell Gordon R. 
Published: June 2007

SUMMARY1. The aim of the study was to examine the effect of the angiotensin‐converting enzyme inhibitor perindopril on the development of atheroma in the cholesterol‐fed rabbit.2. The normal human carotid artery, like most large human arteries, has a preformed diffuse intimal thickening. To model this thickening, the right carotid artery of the 12‐week‐old rabbit had an expanded balloon catheter passed down it to remove the endothelium and partially damage the media.3. Fourteen weeks after this operation, a myointimal thickening similar in almost all respects to the human intimal thickening had developed. The rabbits were then divided into six groups of six rabbits fed on: (i) a 1% cholesterol diet; (ii) a 1% cholesterol diet plus a hypotensive dose of perindopril (0.3 mg/kg per day); (iii) a 1% cholesterol diet plus a non‐hypotensive dose of perindopril (0.01 mg/kg per day); (iv) a normal diet; (v) a normal diet plus a hypotensive dose of perindopril (0.3 mg/kg per day); and (vi) a normal diet plus a non‐hypotensive dose of perindopril (0.01 mg/kg per day).4. After 6 weeks of treatment the animals were sacrificed. There were ameliorating effects of both hypotensive and non‐hypotensive doses of perindopril on the development of plaques, as determined by the area of intima covered by Oil Red‐O‐staining plaque and light microscopy.5. Cell culture studies indicated that perindopril has no effect on smooth muscle proliferation, but increases collagen and non‐collagen synthesis by smooth muscle cells and decreases their binding of the atherogenic lipoprotein beta‐very low density lipoprotein (β‐VLDL).6. The results suggest that perindopril has a beneficial effect in decreasing the severity of atherosclerotic lesions in the cholesterol‐fed rabbit, possibly by affecting lipoprotein metabolism.
EFFECTS OF AE0047 ON RENAL HAEMODYNAMICS AND FUNCTION IN ANAESTHETIZED DOGS
Authors: Hayashi K. , Uchida T. , Kido H. , Shinyama H. , Watanabe M. 
Published: June 2007

SUMMARY1. The effects of AE0047, a newly developed calcium channel blocker, on renal haemodynamics and function were investigated and compared with those of nicardipine in anaesthetized dogs.2. Intravenous injection of AE0047 (10 and 30 μg/kg) caused a dose‐related fall in blood pressure (BP). The AE0047‐induced fall in BP was of slow onset and long lasting. AE0047 at 10 μg/kg elicited a slight increase in renal blood flow (RBF) and urine formation.3. When AE0047 was infused intrarenally at non‐hypotensive doses (25 and 50 ng/kg per min), there was no significant increase in RBF. However, the glomerular filtration rate increased significantly after drug infusion. Intrarenal arterial (i.r.a.) infusion of AE0047 led to dose‐related increases in urine flow (UF), urinary excretion of electrolytes (Na+, K+ and Cl‐) and fractional excretion of electrolytes. The AE0047‐induced increase in urine formation was of very slow onset and progressed even after the cessation of the AE0047 infusion.4. The intrarenal arterial infusion of nicardipine at same doses as AE0047 produced significant increases in urine formation, but these effects were immediately restored to the control values after cessation of the nicardipine infusion.5. It was shown that AE0047 has a long‐lasting diuretic effect and that AE0047‐induced diuresis may be due to inhibitory effects on sodium and water reabsorption in the renal tubules.
EFFECTS OF HYDROXOCOBALAMIN AND HAEMOGLOBIN ON NO‐MEDIATED RELAXATIONS IN THE RAT ANOCOCCYGEUS MUSCLE
Authors: Li C. G. , Rand M. J. 
Published: June 2007

SUMMARY1. The effects of hydroxocobalamin (Vitamin B12a) on relaxations produced by nitric oxide (NO), some NO‐donating compounds and nitrergic nerve stimulation in isolated preparations of the rat anococcygeus muscle were compared with the effects of haemoglobin.2. Hydroxocobalamin (30 μmol/L) significantly reduced relaxations induced by NO (0.1–3 μmol/L) and sodium nitroprusside (SNP; 0.01–0.3 μmol/L) but did not affect relaxations induced by glyceryl trinitrate (GTN; 0.01–1 μmol/L), S‐nitrosocysteine (0.1–0.3 μmol/L) or stimulation of nitrergic nerves. A higher concentration of hydroxocobalamin (100 μmol/L) slightly reduced nitrergic nerve stimulation‐induced relaxations.3. Haemoglobin (10 μmol/L) blocked relaxation induced by NO and reduced relaxations induced by SNP, GTN, S‐nitrosocysteine and nitrergic nerve stimulation.4. When nitrergic nerve stimulation‐induced relaxations had been partially reduced by the NO synthase inhibitor l‐NAME (5–10 μmol/L), hydroxocobalamin had only a weak and transient inhibitory effect.5. Noradrenergic contractions induced by field stimulation were not affected by hydroxocobalamin (30 μmol/L), but were enhanced by haemoglobin (10 μmol/L).6. The results suggest that the transmitter released from nitrergic nerves in anococcygeus muscles resembles NO‐releasing compounds such as S‐nitrosocysteine and GTN but not SNP or free NO.