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1. |
USE OF SYNTHETIC OLIGONUCLEOTIDE AND RECOMBINANT DNA PROBES TO STUDY RENIN GENE EXPRESSION |
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Clinical and Experimental Pharmacology and Physiology,
Volume 12,
Issue 3,
1985,
Page 199-203
Ian A. Darby,
G. Peter Aldred,
John P. Coghlan,
Ross T. Fernley,
Jennifer D. Penschow,
Graeme B. Ryan,
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摘要:
SUMMARY1. Using hybridization histochemistry renin gene expression has been localized in the juxtaglomerular apparatus (JGA) of the renal cortex in both mouse and sheep kidney.2. This technique also located renin gene expression in afferent arterioles and interlobular arteries distant from the glomerular tuft in lamb renal cortex.3. A short (30 mer) synthetic oligonucleotide probe, complementary to a region of the mouse submaxillary gland renin gene, specifically labelled mouse submaxillary gland and kidney.4. Hybridization histochemistry and Northern blot analysis using both the synthetic oligonucleotide (mouse) probe and a 700 base pair recombinant (sheep) probe showed differences in renin gene expression in the kidney in response to Na restriction in the mouse and Na depletion in the sheep.
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1985.tb02631.x
出版商:Blackwell Publishing Ltd
年代:1985
数据来源: WILEY
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2. |
ROLE OF CARDIAC AND VASCULAR AMPLIFIERS IN THE MAINTENANCE OF HYPERTENSION AND THE EFFECT OF REVERSAL OF CARDIOVASCULAR HYPERTROPHY |
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Clinical and Experimental Pharmacology and Physiology,
Volume 12,
Issue 3,
1985,
Page 205-209
P. I. Korner,
G. L. Jennings,
M. D. Esler,
A. Broughton,
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摘要:
SUMMARY1. Changes in amplifying capacities of the hypertrophied heart and resistance vessels account for the characteristic evolution of haemodynamic patterns in the course of essential hypertension.2. Reversal of hypertrophy in established essential hypertension requires prolonged control of blood pressure. Redevelopment of hypertension on stopping drug therapy is slowest if there has been reversal of both vascular and cardiac hypertrophy. It may be possible to subsequently maintain normal blood pressure in a proportion of patients by non‐pharmacological means following the initial period of drug therapy.3. Preliminary findings suggest that in a majority of patients the sympathetic nervous system may be overactive, whilst a smaller subset may have dysfunction of volume regulatio
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1985.tb02632.x
出版商:Blackwell Publishing Ltd
年代:1985
数据来源: WILEY
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3. |
MIGRATION‐INDUCED CHANGES IN BLOOD PRESSURE: A CONTROLLED LONGITUDINAL STUDY |
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Clinical and Experimental Pharmacology and Physiology,
Volume 12,
Issue 3,
1985,
Page 211-216
N. R. Poulter,
K. T. Khaw,
M. Mugambi,
W. S. Peart,
P. S. Sever†,
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摘要:
SUMMARY1. A longitudinal study of the effects of migration on blood pressure and related factors is being carried out in members of a black Kenyan population who migrate from a traditional rural community to an urban environment.2. Data on the first 139 migrants (78 male, 61 female) and 204 control non‐migrants (126 male, 78 female) who have been followed up for a period of 6 months are presented.3. Blood pressure changes rapidly on migration (within the first 2 months); thereafter trends between migrants and controls differ. Significant differences in systolic pressure between migrants and controls are found at all examinations during the 6 month follow‐up in both sexes. Diastolic pressure falls in controls but rises in migrants, the greatest difference being seen at the 6 month examination.4. Migration is associated with a marked increase in dietary sodium and a fall in potassium demonstrated by measurements of urinary electrolyte excretion in 3 × 12 h or 3 × 24 h urine collections.5. Analysis of covariance shows that the blood pressure differences between migrants and controls are partly explained by urinary sodium/potassium ratios and in some instances by body w
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1985.tb02633.x
出版商:Blackwell Publishing Ltd
年代:1985
数据来源: WILEY
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4. |
BLOOD PRESSURE, SALT TASTE AND SODIUM EXCRETION IN RATS EXPOSED PRENATALLY TO HIGH SALT DIET |
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Clinical and Experimental Pharmacology and Physiology,
Volume 12,
Issue 3,
1985,
Page 217-220
J. B. Myers,
V. J. Smidt,
S. Doig,
R. Di Nicolantonio,
T. O. Morgan,
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摘要:
SUMMARY1. Blood pressure, sodium excretion and salt taste were examined in Sprague Dawley (SD) and Munich Wistar (MW) rats exposed prenatally to either a high salt (2.3% NaCl w/w) or control diet.2. There was no significant difference in blood pressure at 2, 6 or 12 months between high salt and control groups in either strain. Similarly there was no significant difference in sodium excretion following a saline load by gavage (150 mmol/l, 1.5% BW).3. Munich Wistar rats which received high salt diet prenatally exhibited a reduced saline preference when offered a choice between water and 150 mmol/l NaCl as drinking fluid. There was no significant difference in saline preference between Sprague Dawley rats which received the high salt or control diet.4. Prenatal exposure to high salt diet failed to alter the blood pressure or excretion of a salt load in either SD or MW rats. In MW rats but not SD high salt diet prenatally resulted in a reduced saline preference at 3 months of age.
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1985.tb02634.x
出版商:Blackwell Publishing Ltd
年代:1985
数据来源: WILEY
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5. |
IMPORTANCE OF ENDOGENOUS VASOPRESSIN IN THE HYPERTENSIVE AND BRADYCARDIC RESPONSE TO CENTRAL α1‐ADRENERGIC STIMULATION |
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Clinical and Experimental Pharmacology and Physiology,
Volume 12,
Issue 3,
1985,
Page 221-225
Masao Hiwatari,
Colin I. Johnston,
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摘要:
SUMMARY1. To determine the interaction between α1‐adrenergic and vasopressinergic mechanisms in the central regulation of cardiovascular functions, the effects of intracerebroventricular (i.c.v.) administration of the α1‐agonists, methoxamine and phenylephrine, were examined in conscious Long‐Evans (LE) rats and Brattleboro rats with hereditary hypothalamic diabetes insipidus (DI).2. In LE rats, i.c.v. methoxamine and phenylephrine (3–30 μg/kg) increased blood pressure and decreased heart rate in a dose‐related manner, while they had no detectable cardiovascular effects in DI rats.3. Neither i.c.v. (0.5 ng/kg per min, 1 h) nor intravenous (i.v., 2 ng/kg per min, 2 h) infusion of vasopressin (AVP) restored the cardiovascular response to i.c.v. phenylephrine in DI rats.4. In LE rats, however, i.v. pretreatment with the specific antagonist to the pressor effect of AVP, d(CH2)5Tyr(Me)AVP (10 μg/kg), attenuated the hypertensive and bradycardic effects of i.c.v. phenylephrine, while i.c.v. pretreatment with AVP antagonist (300 ng/kg) did not alter the cardiovascular response to i.c.v. α1‐agonist.5. The cardiovascular response to i.c.v. phenylephrine was blocked by i.c.v. pretreatment with the α1‐antagonist, prazosin (2 μg/kg).6. Intracerebroventricular phenylephrine increased plasma AVP levels 14‐fold without affecting plasma angiotensin II levels.7. The present study clearly demonstrated that endogenous AVP plays a significant role in the cardiovascular respons
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1985.tb02635.x
出版商:Blackwell Publishing Ltd
年代:1985
数据来源: WILEY
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6. |
INCREASED SENSITIVITY OF RABBIT EAR ARTERY TO NORADRENALINE FOLLOWING PERIVASCULAR NERVE STIMULATION MAY BE A RESPONSE TO NEUROPEPTIDE Y RELEASED AS COTRANSMITTER |
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Clinical and Experimental Pharmacology and Physiology,
Volume 12,
Issue 3,
1985,
Page 227-230
W. E. Glover,
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摘要:
SUMMARY1. Neuropeptide Y (NPY 10‐10‐10‐7mol/l) had little or no effect on the perfusion pressure of rabbit isolated ear arteries but potentiated the brief contractile responses to injections of noradrenaline, histamine or brief periods of electrical stimulation (2–20 Hz for 5 s). This effect was slowly reversible.2. Similar potentiation was seen following long periods of electrical stimulation (2–40 Hz for 1–5 min) which produced well sustained increases in perfusion pressure.3. Following even longer periods of electrical stimulation (10–30 min) during which the perfusion pressure was not maintained, responses to noradrenaline and histamine were potentiated but the responses to electrical stimulation for 5 s were greatly reduced.4. The increase in sensitivity following prolonged electrical stimulation may be due to NPY released as a
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1985.tb02636.x
出版商:Blackwell Publishing Ltd
年代:1985
数据来源: WILEY
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7. |
INVESTIGATIONS INTO THE NATURE OF α2‐ADRENOCEPTORS IN RAT TAIL ARTERIES |
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Clinical and Experimental Pharmacology and Physiology,
Volume 12,
Issue 3,
1985,
Page 231-234
J. F. Marwood,
K. L. Chapman,
S. J. Armsworth,
G. S. Stokes,
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摘要:
SUMMARY1. In rat isolated perfused tail arteries, dose‐response curves were established for the vasopressor effects of phenylephrine (α1‐adrenoceptor agonist), clonidine (α1‐ and α2‐adrenoceptor agonist), clonidine in the presence of 10‐7mol/l prazosin (α2‐agonist), and BHT‐920 (α2‐agonist).2. The ED50values were: phenylephrine 1.85 × 10‐10mol; clonidine 6.3 × 10‐10mol; clonidine + prazosin 3.2 × 10‐6mol; BHT‐920 6.1 × 10‐6mol.3. The arterial reactivity to BHT‐920 was stable only after 4–5 h of perfusion.4. Responses to BHT‐920 were not antagonized by yohimbine (α2‐adrenoceptor antagonist) but were antagonized by low concentrations of prazosin (α1‐adrenoceptor antagonist).5. These data constitute conflicting evidence regarding the existence of α2‐adrenoceptors in rat tail arteries.6. The data are consistent with the proposal that there are two recognition sites on α1‐adrenoceptors; phenylephrine and BHT
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1985.tb02637.x
出版商:Blackwell Publishing Ltd
年代:1985
数据来源: WILEY
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8. |
MECHANISM OF ACTION OF NATRIURETIC FRACTION OF URINE |
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Clinical and Experimental Pharmacology and Physiology,
Volume 12,
Issue 3,
1985,
Page 235-238
Bhaskar J. Chakravarty,
Alastair H. B. Gillies,
Shane L. Carney,
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摘要:
SUMMARY1. The nature of calcium dependence of natriuretic fraction (NF)‐induced contractions in the rat smooth muscle anococcygeus and a possible correlation between the effect of NF on sodium transport and its natriuretic potency was investigated.2. NF and noradrenaline‐induced contractions were partially dependent on external calcium concentration. Ouabain and potassium (K) free solution (KoPSS)‐induced contractions were totally dependent on external calcium and were more effectively inhibited by calcium antagonists than those of NF and noradrenaline suggesting pharmacomechanical coupling as the mode of calcium dependence of NF.3. Like other agonists which contract by pharmacomechanical coupling, NF stimulted sodium transport (86rubidium uptake) in dog saphenous vein. Such stimulation correlated positively (r= 0.495,n= 17,P<0.05) with the natriuretic potency of NF.4. NF, like noradrenaline, contracts smooth muscle by pharmacomechanical coupling and NF‐induced natriuresis is associated with stimulation of the sodi
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1985.tb02638.x
出版商:Blackwell Publishing Ltd
年代:1985
数据来源: WILEY
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9. |
POTENTIATION OF ACTH HYPERTENSION IN MAN WITH SALT LOADING |
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Clinical and Experimental Pharmacology and Physiology,
Volume 12,
Issue 3,
1985,
Page 239-243
Judith A. Whitworth,
Dianne Saines,
Bruce A. Scoggins,
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摘要:
SUMMARY1. ACTH 1 mg/day for 5 days raises systolic blood pressure (SBP) in normotensive and hypertensive subjects on a fixed electrolyte intake of 100 mmol/day sodium (Na) and potassium (K) (Whitworthet al.1983).2. The present study examined the effect of Na intake in the high normal range on the haemodynamic and metabolic responses to ACTH.3. ACTH administration on a 200–300 mmol Na intake increased SBP by 35 mmHg (s.e.m. = 11,n= 5) compared with the 22 mmHg (s.e.m. = 4,n= 12) rise seen on a 100 mmol Na intake in our previous study.4. These studies suggest that the effects of adrenocortical steroids on blood pressure in man may be magnified by increasing dietary Na intak
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1985.tb02639.x
出版商:Blackwell Publishing Ltd
年代:1985
数据来源: WILEY
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10. |
HYPERTENSION CORRECTED AND ALDOSTERONE RESPONSIVENESS TO RENIN‐ANGIOTENSIN RESTORED BY LONG‐TERM DEXAMETHASONE IN GLUCOCORTICOID‐SUPPRESSIBLE HYPERALDOSTERONISM |
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Clinical and Experimental Pharmacology and Physiology,
Volume 12,
Issue 3,
1985,
Page 245-248
E. Woodland,
T. J. Tunny,
S. M. Hamlet,
R. D. Gordon,
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摘要:
SUMMARY1. Two males with glucocorticoid‐suppressible hyperaldosteronism had hyperaldosteronism, hypertension and hypokalaemia corrected by continuous administration of physiological doses of dexamethasone for more than a year.2. During long‐term dexamethasone treatment:(a) Plasma renin activity increased from subnormal to high normal levels, with normal posture‐mediated increases;(b) Plasma aldosterone became responsive to angiotensin infusion, a new observation;(c) A fall in plasma aldosterone between 0800 h (recumbent) and 1000 h (upright) was replaced by a rise;(d) Plasma aldosterone became suppressible with salt loading.3. These findings are consistent with a shift to more normal control of aldosterone by renin‐angiotensin, once abnormal responsiveness to ACTH has been nu
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1985.tb02640.x
出版商:Blackwell Publishing Ltd
年代:1985
数据来源: WILEY
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