摘要:

SUMMARY1. The present review discusses evidence in support of the concept that alterations in sympathetic neurotransmitter release might contribute to the pathogenesis of hypertension.2. Studies suggest that changes in sympathetic nervous activity in both the central and peripheral nervous systems participate in blood pressure control.3. In the periphery increased release of norepinephrine from vascular adrenergic neurons might lead to the enhanced vasoconstrictor responses and thus to an elevation in systemic blood pressure.4. The amount of neurotransmitter release from sympathetic nerve endings can be regulated by autoregulatory systems by presynaptic receptors located on nerve terminals.5. It has been proposed that alterations to sympathetic nervous activity of hypertension might be partially due to abnormalities in presynaptic modulation of neurotransmitter release in central and peripheral tissues.6. This article summarizes the results of studies to evaluate presynaptic receptor functions and sympathetic neurotransmitter release in hypertension.

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01478.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. The proposition that stimulation of the secretomotor nerve to the ovine parotid gland might involve co‐release of vasoactive intestinal peptide (VIP) was tested by studying responses to infusion of VIP directly into the gland's arterial blood supply and by assay of VIP in parotid venous blood.2. In unstimulated glands, an arterial blood concentration of 1.5–2.5 X 10−9mol/L VIP did not evoke fluid secretion but it increased K+ and phosphate secretion and glandular blood flow. The same blood concentration of VIP potentiated the stimulation of salivary flow rate caused by intraarterial infusion of bethanechol but nerve stimulation was not potentiated. VIP increased glandular blood flow in both conditions of stimulation.3. Atropine blocked neurally stimulated salivary secretion but an increase in glandular blood flow was still detectable. There was therefore no evidence for a non‐cholinergic neural mechanism for salivary secretion.4. Furthermore, VIP concentrations in glandular venous blood were not increased by nerve stimulation.5. The results indicate that exogenous VIP can affect the flow and composition of ovine parotid secretion but was not involved in the response to secretomotor nerve stim

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01479.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. The effects of neurotensin on pancreatic exocrine secretion were investigated both in the intact whole pancreas and in the isolated, blood‐perfused pancreasex vivoin anaesthetized dogs.2. Intravenous (i.v.) injections of neurotensin (0.01‐1 nmol/kg) elicited dose‐dependent increases in the secretory rate of pancreatic juice without changes in plasma levels of cholecystokinin (CCK). The concentration of bicarbonate in the pancreatic juice induced by neurotensin was increased, but the protein concentration was scarcely changed.3. The neurotensin‐induced secretion was inhibited by SCH23390, a dopamine D‐1 antagonist, but not by domperidone, phentolamine, propranolol, atropine, cimetidine, or L‐364,718, a CCK antagonist.4. Intra‐arterial (i.a.) injections of neurotensin (0.1‐3 nmol/kg) also elicited dose‐dependent increases in the secretory rate of pancreatic juice flow, but did not change bicarbonate or protein concentration. The secretory activities were less effective and 1 nmol/kg of neurotensin i.a. was approximately equal to that of 0.03 nmol/kg of neurotensin i.v.5. These results suggest that neurotensin mainly stimulates pancreatic secretion by acting indirectly. Neurotensin‐induced secretion is, at least in part, mediated by endogenously released dopamine which activates dopamine D‐1 receptors on the pancreas. In addition to its indirect action, neurotensin has a weak direct action to stimulate

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01480.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. Catecholamine‐induced water transport was measured using an everted gut sac technique. Adrenaline, noradrenaline and isoprenaline induce dose‐dependent increases in water transport by the proximal intestinal sacs. Use of selective adrenergic agents revealed the possible involvement of α1‐ and β2‐receptors in mediation of catecholamine stimulation of water transport in this segment.2. Inhibition of glycolysis reduced the effect mediated through α1‐receptors, while the inhibition of oxidative phosphorylation blocked the β2‐receptor mediated increase in water transport.3. Basal transport of water was also significantly reduced by inhibition of glycolysis but was significantly elevated by blockage of oxidative phosphorylation.4. Suppression or stimulation of glycolysis was paralleled by similar changes in lactic acid release from the gut wall.5. It is concluded that the energy for the catecholamine‐induced water transport is contributed by glycolysis and oxidative phosphorylation coupled to α1‐ and β2‐receptors, respectively. Under basal conditions water transport is mainly dependent on glycolysis in the segmen

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01481.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. Azumolene sodium is a new water‐soluble derivative of dantrolene sodium that also acts as a skeletal‐muscle relaxant.2. Azumolene (6 μmol/L) inhibited the hypercontractility induced separately by 3% halothane, 2 mmol/L caffeine and 80 mmol/L potassium chloride in isolated malignant hyperpyrexia (MH)‐susceptible muscle. Azumolene was equipotent with dantrolene in inhibiting the abnormal responses.3. Like dantrolene, azumolene (6 μmol/L) not only prevented but reversed the abnormal contractures induced by halothane and caffeine. Contracture responses to caffeine were also modified by azumolene in control preparations.4. In the presence of maximal effective concentrations of dantrolene, azumolene failed to further relax caffeine‐induced contractures, and the converse was also true. This was observed in both MH‐susceptible and control preparations.5. Sarcoplasmic reticulum Ca2+‐dependent ATPase activity from MH‐susceptible and control muscle was not affected by azumolene.6. Like dantrolene, azumolene may inhibit Ca2+release directly from the sarcoplasmic reticulum and be of therapeutic value for the

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01482.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. We examined the effects of torasemide (0.3 and 1 mg/kg i.v.) on renal haemodynamics and function employing renal clearance and stop‐flow techniques in anaesthetized dogs and compared these with furosemide (1 and 3 mg/kg i.v.).2. Torasemide and furosemide did not influence renal haemodynamics, in the renal clearance study, but caused a dose‐related and significant increase in urine flow and urinary excretion of sodium and potassium. Torasemide and furosemide increased fractional excretion of sodium in the distal tubules with a relatively small increase in the fractional excretion of lithium (index of sodium excretion at the proximal tubules,FELi). The diuretic profile of torasemide was of long duration, compared with that of furosemide.3. Torasemide and furosemide inhibited sodium reabsorption at the distal portion of the tubules in the stop‐flow study.4. It is suggested from these results, that the main diuretic site of action of torasemide is the ascending limb of the loop of

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01483.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. The effects of sodium‐loading on releases of endogenous digitalis‐like substance were investigated by measuring digoxin‐like immunoreactivity (DLI) during intravenous infusions of isotonic (0.15 mol/L) and hypertonic (1 mol/L) saline in anaesthetized rats. Plasma DLI was measured after death by a digoxin‐radioimmunoassay.2. The infusion of isotonic saline and hypertonic saline elevated the central venous pressure to similar levels. The plasma DLI concentration in both the infused groups rose significantly compared with that in the control rat not receiving the intravenous infusion.3. The difference in the hypothalamic concentrations of DLI was not significant among the three groups, however, there was a significant inverse relationship between the plasma and hypothalamic concentrations of DLI.4. Results indicate that the central venous pressure, but not sodium concentration, is essentially involved in the release of DLI, possibly from the hypot

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01484.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. The distribution of binding sites for [125I]‐labelled endothelin‐1 ([125I]‐ET‐1) and [125I]‐labelled sarafotoxin S6B ([125I]‐SRT) was visualized in rat tissues usingin vitroautoradiography.2. A high density of endothelin‐1 (ET‐1) binding was found in the heart. In the kidney, ET‐1 binding occurred in association with glomeruli, proximal tubules, the inner stripe and inner medulla. In the adrenal, a high density of ET‐1 binding occurred in the medulla as well as the zona glomerulosa.3. The binding affinity constant (KA) for ET‐1 binding in these sites ranged from 1 to 10 X 109/mol per litre.4. Although sarafotoxin S6B (SRT) was 10–100‐fold weaker than ET‐1 in displacing [125I]‐ET‐1 from these sites, 1 μmol/L unlabelled SRT completely abolished [125I]‐ET‐1 binding in all sites. Other venom peptides did not affect [125I]‐ET‐1 binding.5. The pattern of [125I]‐SRT receptor binding in rat tissues byin vitroautoradiography was identical to that for ET‐1 receptor binding, and both unlabelled SRT and unlabelled ET‐1 fully competed with [125I]‐SRT for binding.6. These results provide evidence that SRT binds to the ET receptor in a range of rat tissues. The results suggest that there may be subclasses of ET receptors which can be distinguished by the relat

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01485.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. Basal and stimulated guanylate cyclase activity during ADP‐induced human platelet aggregation in comparison with the actions of sodium nitroprusside (SNP) on platelets was investigated.2. Sodium nitroprusside exhibited bothex vivoandin vitroantiplatelet effects, as assessed by inhibition of subsequent ADP‐induced aggregation in platelet‐rich plasma. A strong correlation between decrease in aggregation and increase in platelet guanylate cyclase activity in the presence of SNP was obtained.3. When SNP was administered after the induction of aggregation, it caused acceleration of disaggregation (in reversible aggregation) and produced disaggregation (under conditions of otherwise irreversible aggregation) which was time‐dependent.4. Platelet aggregation was accompanied by a transient increase in platelet cyclic GMP content and guanylate cyclase activation by the nitric oxide (NO) donor SNP. Changes in guanylate cyclase activity were haem‐associated and probably reflected saturation of enzyme by haem.5. Maximal SNP disaggregating effect coincided with peak guanylate cyclase responsiveness to SNP.6. The present investigation provides evidence that increased responsiveness of platelet guanylate cyclase to NO during aggregation facilitates disaggregation in the presence of SNP. Thus, availability of NO (endogenous or exogenous) at sites of incipient platelet aggregationin vivomay play a pivotal role regarding limitation of thi

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01486.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY