摘要:

SUMMARY1. The effect of chemical sympathectomy with 6‐OH‐dopamine (6‐OHDA) on the onset of adrenocorticotrophin (ACTH)‐induced hypertension was examined in Sprague–Dawley rats (n= 23).2. 6‐OHDA injection produced a fall in systolic blood pressure (SBP) from 100±5 mmHg control to 74±4 mmHg post‐6‐OHDA Treatment Day 1 (P<0.001), but did not alter food or water intake, urine volume or electrolyte excretion.3. Compared with sham injection, ACTH‐treated rats showed an increase in blood pressure (sham: 98±7 mmHg; ACTH: 123±9 mmHg on Treatment Day 10;P<0.01), loss of bodyweight, and increases in water intake and urine volume.4. The magnitude of the blood pressure rise on ACTH was greater in 6‐OHDA‐treated rats than in intact control rats. Metabolic changes were similar.5. Chemical sympathectomy with 6‐OHDA did not delay or block the onset of A

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01432.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. In the present study we examined thein vitroeffect of vasoactive intestinal peptide (VIP) on spontaneous contractions in both inner and outer layers of non‐pregnant human myometrium. A dose‐dependent relaxation was observed, but with a marked difference in sensitivity to VIP between the two layers, with an IC50value of 1 X 10−8and 1 X 10−5mol/L in the outer and inner layers, respectively.2. We also established that VIP did not directly stimulate the adenylate cyclase activity. The only slight stimulations were observed in non‐initial rate conditions. The maximal response of this indirect effect was obtained for VIP concentrations between 1 X 10−9and 1 X 10−8mol/L and this occurred to the same extent (an approximately 1.4‐fold increase) in both layers. However this response is specific, since structurally related peptides such as glucagon, gastric inhibitory polypeptide (GIP), secretin, or human growth hormone‐releasing factor (hGRF) had no effect in our preparations.3. Autoradiographic studies revealed that specific VIP binding sites were located on the vascularization of the intermediate vascular layer and on arterioles and venules distributed in the inner and outer myometrial layers. They were also present in the endometrium, but not on smooth muscle cells of either layer.4. Such observations could provide evidence for another signal transduction pathway to mediate the biological effect of VIP. An additional intermediate step on the vascularization distributed in all of the muscle c

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01433.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. The influence of myocardial noradrenaline depletion on the incidence and severity of reperfusion arrhythmias in closed‐chest anaesthetized rats was investigated. Five‐minute left coronary artery occlusion was carried out via an implanted occluder. Four groups of rats were studied: controls, rats treated with reserpine (5 mg/kg, intraperitoneally) 24 h before occlusion, and rats receiving 0.2 mg/kg gallopamil intravenously 5 min before occlusion either with or without reserpine pretreatment.2. In the control group all animals had ventricular tachycardia (VT) and fibrillation (VF) immediately after reperfusion. Gallopamil reduced VT to 50% and VF to 25% (P<0.05 versus control). In the reserpine group all had VT, and 67% had VF, this being not significantly different from controls. Additional treatment with gallopamil markedly reduced VT and totally prevented VF (P<0.05 versus control).3. Thus, total depletion of myocardial noradrenaline stores neither prevented the occurrence nor reduced the severity of reperfusion arrhythmia in rats, while gallopamil treatment was effect

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01434.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. Blood pressure and pulse rate responses to intravenously (i.v.) administered nifedipine were studied in chloralose‐anaesthetized rats subjected to hypoxaemia, hyperoxaemia, alkalosis, acidosis, hypocarbia with alkalosis, or hypercarbia with acidosis, or hypercarbia with acidosis.2. Ventilation with a gas mixture of 17% O2, 28% O2, or 23% O2with 5% CO2at a fixed stroke volume (10 mL/kg) and rate (80 strokes/min) induced hypoxaemia, hyperoxaemia or hypercarbia, respectively. Hypocarbia was induced by ventilation with 17% O2at 160 strokes/min. Acidosis or alkalosis was produced by intravenous infusion of 1 mol/L HCl or 1 mol/L NaHCO3, respectively, in animals ventilated with room air.3. There were significant decreases in blood pressure and pulse rate during acidosis, and increases in pulse rate during alkalosis and hypercarbia. No marked changes in these parameters were observed under the other experimental conditions.4. The control animals showed a dose‐dependent decrease in blood pressure without marked changes in pulse rate in response to nifedipine injection.5. Significant reductions in the hypotensive effect of nifedipine were observed in rats subjected to alkalosis, acidosis, or hypercarbia. A similar tendency was also found during hypocarbia while the responses to nifedipine during hypoxaemia and hyperoxaemia were statistically the same as those in the controls.6. It is concluded that alterations of blood pH reduce the hypotensive effect of nifedipine, and we suggest that blood pH changes probably play a more important role thanPO2orPCO2abnormalities in altering the cardiovascular responses to nifedipine in hypoventilated or hyperventilated r

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01435.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. In anaesthetized intact Sprague‐Dawley rats, the angiotensin‐converting enzyme inhibitor enalaprilat, 1 mg/kg, had no significant effect on the pressor responses to the α1‐adrenoceptor agonist phenylephrine (PE). Doxazosin 1 mg/kg was found to be a potent α1‐adrenoceptor antagonist.2. The combination of enalaprilat 1 mg/kg plus doxazosin 1 mg/kg was 3.3‐fold more potent in antagonizing α1‐adrenoceptors than doxazosin 1 mg/kg alone.3. After treatment of rats with deoxycorticosterone acetate (DOCA) twice weekly for 5 weeks, the α1‐adrenoceptor antagonist action of doxazosin in anaesthetized rats was not potentiated by enalaprilat 1 mg/kg.4. Since DOCA treatment suppresses renin activity, these findings strongly support the hypothesis that angiotensin II can modulate the functional activity of α1‐adrenoceptor in va

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01436.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. Dose‐response curves were obtained to bolus injections of 5‐hydroxytryptamine (5‐HT) in Krebs'‐perfused hindquarters of male Wistar rats. Vasoconstrictor responses to 5‐HT (5.7–363 nmol/kg) were significantly attenuated in hindquarters of alloxan‐treated 14 day diabetic rats compared with non‐diabetics.2. Infusion of the thromboxane A2(TxA2)‐mimetic U46619 (317 and 31.7, but not 3.17 nmol/L) significantly potentiated vasoconstrictor responses to 5‐HT in Krebs'‐perfused hindquarters of non‐diabetic and diabetic rats. The degree of potentiation was similar for both groups.3. In Krebs'‐perfused hindquarters of non‐diabetic rats, infusion of the α1‐adrenoceptor agonist methoxamine (8.96 μmol/L, which caused a rise in perfusion pressure intermediate in magnitude to that produced by infusion of 31.7 and 317 nmol/L U46619) did not significantly affect responses to bolus injections of 5‐HT.4. The same concentration of methoxamine did not cause a significant potentiation of vasoconstrictor responses to 5‐HT (except for the two highest 5‐HT doses, 182 and 363 nmol/kg) in hindquarters of diabetic rats. This potentiation was significantly less than that due to 317 nmol/L U46619, although there was no significant difference between the rise in basal perfusion pressures produced by these concentrations of methoxamine and U46619.5. Infusion of the TxA2receptor antagonist AH23848 (111 nmol/L) inhibited the potentiating effect of U46619 (317 nmol/L) on responses to 5‐HT in both non‐diabetic and diabetic rats.6. These results indicate that the potentiation of constrictor responses to 5‐HT by U46619 is mediated by activation of TxA2/prostaglandin H2(PGH2) receptors, and suggest that a synergistic interaction of TxA2and 5‐HT could be of impor

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01437.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. We have characterized in unanaesthetized rabbits the reflex effects of injecting nicotine into the pericardial sac or left atrium on heart rate, arterial pressure, systemic vascular resistance and the amplitude and frequency of respiration. These effects were compared with those of atrial administration of nicotine and veratridine, and intrapericardial administration of veratridine and bradykinin.2. Injection of nicotine (6.25–400 μg) into the pericardial sac caused dose‐dependent falls of heart rate and arterial pressure, and a brief period of hypopnoea. The fall in arterial pressure was mainly due to a fall in systemic vascular resistance. The threshold dose was 25 μg. Near maximal falls in heart rate (108 beats/min) and arterial pressure (47 mmHg) occurred at a dose of 200–400 μg. The latency between injection and the onset of bradycardia was 3.0 s.3. The effects of intrapericardial nicotine on arterial pressure and respiration were antagonized in a dose‐dependent fashion by intrapericardial mecamylamine (1–100 μg/kg) but were unaffected by intrapericardial hyoscine methylbromide (10 μg/kg) or vecuronium (1–10 μg/kg). The haemodynamic and respiratory effects were abolished by intrapericardial procaine. The haemodynamic effects were increased, though not significantly, by sino‐aortic baroreceptor denervation. In decerebrate, artificially ventilated rabbits, bilateral cervical vagotomy converted the hypotensive and bradycardic response into a slowly developing tachycardia without change in arterial pressure.4. Left atrial injection of nicotine (6.25–100 μg) caused bradycardia, a rise in arterial pressure, and prolonged hyperpnoea preceded by transient hypopnoea. After sino‐aortic barodenervation it caused profound falls in heart rate and arterial pressure and transient hypopnoea, which were abolished by intrapericardial procaine.5. Intrapericardial injection of veratridine (50–100 μg) had no consistent effect under control conditions. After sino‐aortic barodenervation it caused falls in heart rate and arterial pressure which were abolished by intrapericardial procaine. Left atrial injection of veratridine caused highly variable haemodynamic effects.6. Intrapericardial bradykinin (2.5–25 μg) caused rises in both arterial pressure and heart rate. These were abolished by intrapericardial procaine.7. We conclude that when nicotine is injected into the pericardial sac of conscious rabbits the reflex haemodynamic and respiratory effects are due to the selective activation of neuronal‐type nicotinic cholinoceptors on vagal afferents that originate in the epicardium. The reflex effects of left atrial nicotine are probably due to the excitation of a combination of carotid chemoreceptors and cardiac receptors.SUMMARY8. The effects of nicotine, veratridine and bradykinin that we observed in conscious rabbits were profoundly different from those

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01438.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. Effects of 8‐(N,N‐diethylamino)octyl‐3,4,5‐trimethoxybenzoate hydrochloride (TMB‐8), an inhibitor of intracellular calcium release, on renal function were examined in anaesthetized dogs.2. Intrarenal arterial infusion of TMB‐8 (0.03 and 0.1 mg/kg per min) increased urine flow rate, urinary sodium excretion and fractional excretion of sodium without affecting blood pressure, renal blood flow or glomerular filtration rate.3. The results suggest that TMB‐8 inhibits tubular sodium reabsorption to induc

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01439.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. The left anterior descending coronary artery (LAD) was completely ligated for 90 min (i.e. myocardial ischaemia was produced) in the dog anaesthetized with pentobarbital.2. Bevantolol, a β1‐adrenoceptor antagonist, was injected (1 mg/kg, intravenously) 5 min before LAD occlusion. The bevantolol injection decreased heart rate without affecting blood pressure.3. The myocardial samples were taken from the LAD area immediately after the end of LAD occlusion, and were subjected to analysis of the myocardial levels of non‐esterified fatty acids (NEFA).4. In dogs in which saline was injected, ischaemia produced accumulation of NEFA, especially arachidonic and palmitoleic acids, in the myocardium.5. In dogs in which bevantolol was injected, the accumulation of NEFA induced by ischaemia was almost completely inhibited.6. It is concluded that bevantolol inhibits ischaemia‐induced accumulation of NEFA in the myocardium, and that stimulation of the β1‐adrenoceptors is probably responsible for NEFA accumulation induced by

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01440.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY