摘要:

SUMMARY1. Sequential bilateral carotid artery ligation (BCL) separated by a 1 week interval was performed on 5 month spontaneously hypertensive rats (SHR) (i.e. SHRSR‐B1/Izm) and the developmental course of hypertension and cerebrovascular lesions in advanced age were analysed as compared with those in age‐matched sham‐operated controls.2. Behavioural activity and behavioural reaction to light were also investigated in the above‐mentioned SHR, young and adult stroke‐prone SHR (i.e. SHRSP‐A3/Izm), SHR (i.e. B1/Izm) and Wistar‐Kyoto rats (i.e. WKY/Izm).3. All of the control SHR developed severe hypertension resulting in cerebral stroke with focal oedema due to cerebral haemorrhage and infarction as a result of arterionecrosis 18 months after birth.4. SHR usually die within a few days of BCL. In the present study, however, they successfully survived without cerebrovascular damage for a long time, although they developed a similar severe hypertension in a significantly shorter period of time (P<0.05) and showed behavioural abnormalities that were probably due to severe cerebral ischaemia.5. These experimental results suggest an ischaemic tolerance phenomenon in a hypertensive model that was exposed to mild ischaemic stress by unilateral carotid artery ligation (UCL) before the subsequent induction of severe ischaemia by BCL. The results also suggest that an aggravation of hypertensive cerebrovascular changes due to long‐lasting ischaemia after BCL was prevented through a possible cumulative effect of i

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb00577.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARY1. The responsiveness of aortic rings from 4 and 12 week streptozotocin‐induced diabetic rats to D600 (Gallopamil) and nifedipine was studied.2. The sensitivity and responsiveness to D600 were significantly enhanced (P<0.05; 5‐test, ANOVA; 9 d.f.) only in the 4 week diabetic preparations precontracted with noradrenaline.3. Nifedipine‐induced relaxations were significantly enhanced (P<0.05–0.01;t‐test, ANOVA; 8–12 d.f.) in all the diabetic (4 and 12 weeks) aortic preparations precontracted with both noradrenaline (10‐7mol/L) and KCl (40 mmol/L) when compared with controls.4. D600, unlike nifedipine, did not produce significant relaxation of diabetic aortic preparations precontracted with KCl (40 mmol/L) at both week 4 and 12 of the disease when compared with controls.5. These results suggest that there is differential responsiveness of streptozotocin diabetic rat aorta to D600 a

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb00578.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARY1. Plasma renin activity (PRA), plasma angiotensin I concentration (ANG I), plasma angiotensinogen concentration (PAC) and the plasma levels of active, total and inactive renin (prorenin) were measured in rats with carbon tetrachloride (CCl4)‐induced acute renal failure. Rats were treated with a single oral dose of CCl4(2.5 mL/kg) and killed 1, 2, 3 and 7 days later.2. On days 1–3 PRA, ANG I and PAC decreased and increased on day 7. Active renin fell on days 2 and 3, total renin (trypsin treatment) augmented on day 1 and diminished on day 3, prorenin and per cent prorenin increased on days 1 and 2. Angiotensin I concentration paralleled PRA and PAC. The CCl4‐induced decrease in PRA was secondary to the fall in active renin and in PAC. Total renin augmented as a consequence of the elevation of prorenin. Renal function, evaluated by serum urea, serum creatinine and creatinine clearance, decreased on days 1 and 2 when PRA was low and plasma prorenin was high.3. These data do not support the involvement of the circulating active renin‐angiotensin system (RAS) in the pathophysiology of acute renal failure induced by CCl4, however, increased prorenin levels were associated with the decrease in renal f

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb00579.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARY1. The effects of adenosine and its analogues on actin polymerization in human polymorphonuclear leucocytes (PMN) induced by three different chemotactic stimulants, platelet‐activating factor (PAF),N‐formyl‐methionyl‐leucyl‐phenylalanine (FMLP) and an activated fragment of C5 (C5a) were investigated.2. Adenosine and its analogues inhibited the actin polymerization induced by these three agents in a concentration‐dependent manner and theophylline, a competitive antagonist at adenosine receptors, abolished these inhibitory effects.3. The adenosine analogue 5′‐N‐ethylcarboxamideadenosine (NECA) was a more potent inhibitor of actin polymerization than eitherl‐N6‐phenylisopropyladenosine (PIA) or adenosine itself; the rank order of potency of these agonists was characteristic of adenosine A2 receptors.4. Adenosine deaminase (ADA) abolished the inhibitory effect of adenosine and augmented PAF‐induced actin polymerization.5. It was concluded that, at physiological concentrations, adenosine inhibits actin polymerization in PMN via activation of PMN surface membrane adenosine A2 receptors and thus modulates chemotactic stimul

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb00580.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARY1. To determine whether morphine modulates the development of cardiac arrhythmias through mu opioid receptors by an action within the central nervous system (CNS). Catecholamine‐induced ventricular arrhythmias were produced, in the rat, by continuous infusion of epinephrine at incremental doses until the development of fatal arrhythmias, usually ventricular fibrillation.2. Morphine, 0.1 mg/kg i.v., significantly suppressed (P<0.05) the development of epinephrine‐induced arrhythmias compared with the control group. This was opposed by the mu opioid antagonist naloxone (1 or 2 mg/kg) in a dose‐dependent manner.3. To determine whether these effects were operative in the brain, rats received an injection of either morphine 50 μg/kg or its diluent (control) into the lateral cerebral ventricle intracerebroventricularly (i.c.v.). Morphine significantly increased (P<0.05) the threshold for the development of arrhythmias.4. To further explore whether this effect was operative at the mu opioid receptor, a more specific mu opioid receptor agonist morphiceptin (50 mUg/kg) was administered i.c.v. and produced a significant increase (P<0.05) in the threshold for cardiac arrhythmias compared with controls.5. The action of morphine was further established to be operating through mu opioid receptors from experiments with the i.c.v. administration of naloxone (+) and naloxone (—) followed by morphine showing that the action of morphine in the brain was prevented by the opioid antagonist naloxone but not by its stereo‐isomer that is not a mu opioid receptor antagonist.6. These data suggest a role for morphine to modulate cardiac arrhythmias, specifically to increase arrhythmia threshold, through an action within the CNS at mu opioid

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb00581.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

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

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb00582.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARY1. The antidiuretic, pressor and electrolyte transport effects of arginine vasopressin (AVP) were simultaneously evaluated in the anaesthetized water diuretic rat. Increasing concentrations of AVP (7.5, 75 and 750 ng/kg bolus and per h), were used to produce plasma levels which approximate the physiological range (4.8 ± 2.4, 35.7 ± 12.5, 85.2 ± 16.1 pg/mL respectively).2. Administration of a minimally effective antidiuretic dose (7.5 ng) increased mean urine osmolality (from 101 ± 7 to 312 ± 89 mosmol/kg) without altering mean arterial pressure (MAP), renal plasma flow (RPF) or glomerular filtration rate (GFR). A maximal antidiuretic dose of AVP (75 ng) increased mean urine osmolality to 2002 ± 109 mosmol/kg and was associated with significant mean increases in MAP (9 mmHg), RPF and GFR (25%) by 30–60 min. A further ten‐fold increase in AVP (750 ng) produced a greater increase in MAP (116 ± 6 to 134 ± 7 mmHg;P<0.01) as well as increasing RPF and GFR by 35.5 and 38.9% respectively.3. Increasing concentrations of AVP also progressively increased the fractional excretion of sodium, potassium and phosphate. However, fractional calcium and magnesium excretion was significantly decreased with maximal and supramaximal concentrations.4. These studies support evidence that AVP is a pressor hormone in physiological concentrations in baroreceptor intact animals. Its role in renal electrolyte transport is unclear. Measured increases in RPF and GFR with the maximal and supramaximal AVP concentrations appear to be correlated with the incr

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb00583.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARY1. Adrenocorticotrophic hormone (ACTH) and corticosteroids stimulate salt appetite in laboratory animals. The hypothesis tested was that cortisol administration increases salt preference in humans.2. Sodium taste studies (detection and recognition thresholds, taste intensity and preference tests) were conducted before, during and after cortisol administration (200 mg/day for 5 days) in normal men on a free diet.3. Cortisol significantly increased systolic blood pressure (SBP), 113 ± 3–130±4 mmHg,P<0.05; diastolic blood pressure (DBP), 65±3–81±2 mmHg,P<0.05; mean arterial pressure (MAP), 81± 2–97± 3 mmHg,P<0.05; and bodyweight, 72.9±3.0–75.4±3.3 kg,P<0.05.4. Salt detection and recognition thresholds, taste intensity and preference for sodium chloride were unchanged fol

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb00584.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARY1. Crude venom gland extracts (VGE) were prepared from femaleDelena canceridesandIsopeda montanaspiders. The VGE were tested in isolated rat atrial, caudal artery and pithed rat preparations for pharmacological activity.2. In rat isolated atrial preparations,D. canceridesandI. montanaVGE, each in a concentration of 2 glands/mL, produced increases in atrial rate which were abolished by propranolol (1 μmol/L) but not by ketanserin (0.1 μmol/L) or reserpine pretreatment (2.5 mg/kg s.c. 24 h prior to experimentation) indicating a direct action on atrial β‐adrenoceptors.3. In rat caudal artery preparations each VGE produced an increase in perfusion pressure, which was taken as an index of vasoconstriction. Pressor responses toD. canceridesVGE (1 gland/mL) were abolished in the presence of prazosin (1 mol/L) but not by reserpine pretreatment, indicating an action of the VGE on vascular α1‐adrenoceptors. Neither prazosin nor reserpine pretreatment had any effect on pressor responses of rat caudal artery preparations toI. montanaVGE. Ketanserin (6 nmol/L) produced a small reduction in the degree of vasoconstriction produced by the VGE. This demonstrates a lack of α1‐adrenoceptor agonist activity of the VGE.4. Both VGE produced dose‐dependent increases in mean arterial pressure and heart rate in pithed rat preparations. The use of relatively selective receptor antagonists indicated that the increases in mean arterial pressure (MAP) produced by both VGE were mediated by an action on α2

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb00585.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY