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1. |
REGULATION OF PROXIMAL TUBULE FUNCTION BY ANGIOTENSIN |
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Clinical and Experimental Pharmacology and Physiology,
Volume 19,
Issue 4,
1992,
Page 213-222
Peter J. Harris,
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摘要:
SUMMARY1. Independent of its effects on renal haemodynamics and glomerular filtration, angiotensin II (All) has direct actions on the proximal tubule involving transepithelial Na+, H+, HCO3‐, and water reabsorption, ammoniagenesis, gluconeogenesis and renal growth.2. The effects of AH on water and electrolyte transport are biphasic and dose‐dependent, such that low concentrations (10‐12–10‐9mol/L) stimulate reabsorption whereas high concentrations (10‐7‐10‐6mol/L) inhibit reabsorption. Similar dose‐response relations have been obtained for luminal and peritubular addition of AIL3. The cellular responses to All are mediated via an AT‐1 receptor coupled via G‐regulatory proteins to several parallel signal transduction pathways. Low doses inhibit the basolateral adenylate cyclase, lower intracellular cAMP and withdraw the inhibitory effect of protein kinase A on the luminal Na/H exchanger. Stimulation of this exchanger may also occur due to All‐receptor activation of phospholipase C to release diacyl glycerol, or by local transduction in the brush‐border membrane involving phospholipase A2.4. Inhibition of proximal fluid reabsorption is associated with increased intracellular Ca2+released from intracellular stores, or entering via voltage‐sensitive channels in response to the release of inositol‐l,4,5,‐trisphosphate, or following Ca2+channel opening induced by the arachidonic acid metabolite 5,6,‐epoxy‐eicosatrienoic acid.5. The stimulatory actions of peritubular All on proximal transport are inhibited by physiological concentrations of atrial natriuretic factor (ANF) and by parathyroid hormone (PTH).6. It is concluded that intrarenal All acts to maintain optimal matching of fluid reabsorption and filtered load in response to changes in sodium balance, as well as to promote acidification of the urine during acidosis and perhaps to potentiate tu
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1992.tb00441.x
出版商:Blackwell Publishing Ltd
年代:1992
数据来源: WILEY
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2. |
INHIBITORY EFFECT OF NEUROPEPTIDE Y ON STIMULATED RENIN SECRETION OF AWAKE RATS |
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Clinical and Experimental Pharmacology and Physiology,
Volume 19,
Issue 4,
1992,
Page 223-228
Jean‐Francois Aubert,
Philippe Walker,
Eric Grouzmann,
Jürg Nussberger,
Hans R. Brunner,
Bernard Waeber,
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摘要:
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 mod
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1992.tb00442.x
出版商:Blackwell Publishing Ltd
年代:1992
数据来源: WILEY
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3. |
FAILURE OF THE NITROUS OXIDE TISSUE EQUILIBRATION METHOD FOR THE DETERMINATION OF BRAIN AND MYOCARDIAL BLOOD FLOW UNDER CONTROLLED CONDITIONS |
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Clinical and Experimental Pharmacology and Physiology,
Volume 19,
Issue 4,
1992,
Page 229-233
Michael A. Reid,
William B. Runciman,
Colin F. McLean,
Laurence E. Mather,
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摘要:
SUMMARY1. Two adult merino ewes were prepared with intravascular cannule for sampling aortic root blood, sagittal sinus blood and coronary sinus blood.2. One week after preparation the animals were anaesthetized then ventilated with a gas mixture containing 10% nitrous oxide (N2O) for 60 min. Serial measurements of brain and myocardial blood flow were made using the N2O tissue equilibration method of Kety and Schmidt.3. N2O failed to achieve matching arteriovenous blood concentration equality and saturation of the relevant tissues. Valid use of the Kety‐Schmidt method, therefore, could not be confirmed.4. Because of the failure of the arteriovenous equilibration, serially determined brain and myocardial blood flows were found to decrease with time.5. The use of this method in circumstances where tissue saturation with the indicator gas cannot be ascertained is arbitrar
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1992.tb00443.x
出版商:Blackwell Publishing Ltd
年代:1992
数据来源: WILEY
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4. |
SODIUM AND NORADRENALINE IN CEREBROSPINAL FLUID AND BLOOD IN SALT‐SENSITIVE AND NON‐SALT‐SENSITIVE ESSENTIAL HYPERTENSION |
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Clinical and Experimental Pharmacology and Physiology,
Volume 19,
Issue 4,
1992,
Page 235-241
Yuhei Kawano,
Kaoru Yoshida,
Minoru Kawamura,
Hiroki Yoshimi,
Terunao Ashida,
Hitoshi Abe,
Masahito Imanishi,
Genjiro Kimura,
Shunichi Kojima,
Morio Kuramochi,
Teruo Omae,
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摘要:
SUMMARY1. The effects of dietary sodium on blood pressure and levels of sodium, other electrolytes and noradrenaline (NA) in the cerebrospinal fluid (CSF) and blood of 15 patients with essential hypertension were studied. The CSF and blood sampling was carried out after 7 days of a high salt intake (16–18 g/day) and after 7 days of a low salt intake (1–3 g/day).2. Blood pressure and sodium concentrations in CSF and serum were significantly higher in the high salt period than the low salt period (CSF Na+concentration: 147.7 ± 0.4 mmol/Lvs145.3 ± 0.5 mmol/L;P<0.001). Levels of CSF pressure and potassium or calcium concentrations were not different between the two periods. Plasma NA and plasma renin activity (PRA) were lower and CSF NA levels tended to be lower in the high salt period.3. The levels and the changes in sodium and NA in CSF were not significantly different between the salt‐sensitive (n= 8) and the non‐salt‐sensitive (n= 7) subjects, but the changes in plasma NA and PRA were smaller in the salt‐sensitive subjects.4. These results indicate that the sympathetic nervous system is less suppressed in salt‐sensitive subjects during high salt intake. This may be due to altered neural responsiveness to sodium loading rather than being greater increases in sodium concentration in the central
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1992.tb00444.x
出版商:Blackwell Publishing Ltd
年代:1992
数据来源: WILEY
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5. |
POTASSIUM CHANNEL ACTIVATION IMPROVES BLOOD FLOW PATTERN OF CONSCIOUS RATS IN CUTANEOUS MICROCIRCULATION |
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Clinical and Experimental Pharmacology and Physiology,
Volume 19,
Issue 4,
1992,
Page 243-248
RolfF. Hertel,
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摘要:
SUMMARY1. A dose‐dependent mean arterial blood pressure reduction (tailcuff method) to an intravenously administered potassium channel activator (22 or 24 μg/ kg bw) was found in conscious rats.2. Intravital microscopic analysis of skin microcirculation in conscious rats was performed with respect to erythrocyte flow velocity and diameters of capillaries. There was a dose‐dependent increase of erythrocyte flow velocity; diameters of capillaries were dilated following a dosage of 6 and 12 Mg/kg bw, but constricted following a dosage of 24 μg/kg bw.3. Frequency distributions of velocity ranges in capillaries under observation (real time video recordings) proved that the increase of microvascular perfusion is manifested by a shift of maximal values to increasing velocity ranges.4. It is concluded that potassium channel activation plays an important role in the local regulation of perfusion on the peripheral circul
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1992.tb00445.x
出版商:Blackwell Publishing Ltd
年代:1992
数据来源: WILEY
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6. |
TIME COURSE OF REGIONAL FLOW DISTRIBUTION FOLLOWING REPERFUSION OF THE ISOLATED ISCHAEMIC RAT HEART |
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Clinical and Experimental Pharmacology and Physiology,
Volume 19,
Issue 4,
1992,
Page 249-252
P‐O. Sjöquist,
T. Abrahamsson,
M. H. Johansson,
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摘要:
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
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1992.tb00446.x
出版商:Blackwell Publishing Ltd
年代:1992
数据来源: WILEY
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7. |
ISOLATION AND CHARACTERIZATION OF THE RAT LIVER AVP RECEPTOR USING [125I][d(CH2)5′SARCOSINE7]AVP1 |
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Clinical and Experimental Pharmacology and Physiology,
Volume 19,
Issue 4,
1992,
Page 253-260
Deborah Trinder,
Janice M. Kelly,
Ross Fernley,
Vincent Mooser,
Paddy A. Phillips,
Colin I. Johnston,
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摘要:
SUMMARY1. A vasopressin (AVP) binding protein was purified from rat liver membranes by an improved method using [125I][d(CH2)5′Sarcosine7]AVP, a selective Vi AVP radioligand and a combination of CHAPS solubilization, gel filtration, lectin affinity and FPLC ion exchange chromatography.2. The purified protein exhibited a maximum binding activity of 2480 pmol/ mg protein with a KDof 4.5 nmol/ L, which corresponds to a purification of approximately 26 700‐fold. The molecular weight of this protein was 70 000 Da.3. The binding of [125I][d(CH2)5′Sarcosine7]AVP to the solubilized membranes was dependent on the protein concentration, and was inhibited by the unlabelled peptides [d(CH2)5′Sarcosine7]AVP, AVP, and to a lesser degree by peptides with high V2receptor affinity, such as 1‐desamino‐D‐AVP and [d(CH2)5′D‐Ileu2‐Ileu4]AVP.4. In addition, an AVP anti‐idiotypic monoclonal antibody bound to both the partially purified and purified lectin affinity AVP binding protein in a concentration‐dependent manner. These results indicate that the purified protein displays similar characteristics to the liver membra
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1992.tb00447.x
出版商:Blackwell Publishing Ltd
年代:1992
数据来源: WILEY
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8. |
INCREASED SENSITIVITY TO ENDOTHELIN‐1 IN ISOLATED KREBS‐PERFUSED KIDNEYS OF STREPTOZOTOCIN‐DIABETIC RATS |
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Clinical and Experimental Pharmacology and Physiology,
Volume 19,
Issue 4,
1992,
Page 261-265
Paul J. Tammesild,
Wayne C. Hodgson,
Roger G. King,
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摘要:
SUMMARY1. Vascular responses to endothelin‐1 (ET‐1) and noradrenaline (NA) were measured in isolated Krebs'‐perfused kidneys of 2 week old streptozotocin‐diabetic and non‐diabetic rats.2. Bolus injections of either ET‐1 or NA caused dose‐dependent increases in perfusion pressure. Responses to ET‐1 (10–60 ng/g kidney), but not to NA (0.001–10 μg/g kidney), were significantly potentiated in kidneys of diabetic rats compared with non‐diabetics.3. Indomethacin significantly attenuated responses to NA (0.3–10 μg/g kidney) in kidneys of both diabetic and non‐diabetic rats.4. Neither indomethacin (1 μmol/L) nor the cyclo‐oxygenase/lipoxygenase inhibitor BW755C (1 μmol/L) had any significant effect on the log dose‐response curve to ET‐1 in either group of kidneys.5. Perfusion with N‐nitro‐L‐arginine (NOLA; 10 μmol/L) had no effect on basal perfusion pressures, but potentiated responses to ET‐1 in both groups of kidneys. However, the difference in responses to ET‐1 between kidneys from diabetic and non‐diabetic rats remained significant in the presence of NOLA.6. ET‐1 responses were inhibited in Ca2+‐free Krebs’ solution (plus 1 mmol/L EGTA).7. The results of the present study indicate an increased sensitivity to ET‐1 in isolated Krebs'‐perfused kidneys of diabetic rats. Responses to ET‐1 were unaffected by cyclo‐oxygenase and/ or lipoxygenase inhibitors, but were potentiated by an
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1992.tb00448.x
出版商:Blackwell Publishing Ltd
年代:1992
数据来源: WILEY
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9. |
MEASUREMENT AND IDENTIFICATION OF PRORENIN AND RENIN IN OVARIAN FOLLICULAR FLUID FROM CATTLE AND PIG |
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Clinical and Experimental Pharmacology and Physiology,
Volume 19,
Issue 4,
1992,
Page 267-273
Arne Hagemann,
Arne Høj Nielsen,
Vibeke Dantzer,
Birthe Avery,
Knud Poulsen,
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摘要:
SUMMARY1. In previous studies we have demonstrated and solved several methodological problems in relation to the measurement of prorenin by trypsin activation in rat, bovine, hog and horse plasma.2. The aim of the present study was to develop a method for the measurement of prorenin in bovine and porcine ovarian follicular fluid.3. Trypsin activation of follicular fluid generated angiotensin I immunoreactive material (AI IM) in both species.4. The AI IM interfered with the renin assay, but could be completely removed by a cation exchange resin in a batch‐wise technique.5. The enzymatic activity of trypsin‐activated prorenin and pre‐existing active renin was completely inhibited by a specific inhibitor of renin.6. The reactions were optimized and an accurate measurement of prorenin in ovarian follicular fluid was developed.7. The existence of prorenin and renin in bovine ovarian follicular fluid was established. Prorenin and renin in porcine ovarian follicular fluid was demonstrated for the first time.8. The ratio between ovarian follicular fluid and plasma was 43 for prorenin and 19 for active renin in cattle. The same ratios in pigs were 1.3 and 0.4, respectively. These findings indicate a species difference with respect to the amount of prorenin or active renin present in ovarian follicular
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1992.tb00449.x
出版商:Blackwell Publishing Ltd
年代:1992
数据来源: WILEY
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10. |
LETTERS TO THE EDITOR |
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Clinical and Experimental Pharmacology and Physiology,
Volume 19,
Issue 4,
1992,
Page 275-276
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ISSN:0305-1870
DOI:10.1111/j.1440-1681.1992.tb00450.x
出版商:Blackwell Publishing Ltd
年代:1992
数据来源: WILEY
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