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  • 1
    Electronic Resource
    Electronic Resource
    ACUTE HAEMODYNAMIC RESPONSES TO UNILATERAL RENAL ARTERY STENOSIS IN CONSCIOUS DOGS (1985)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 12 (1985), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The acute responses to renal artery stenosis were studied in chronically instrumented, unanaesthetized dogs.2. Stenosis of one renal artery produced a rise in arterial pressure and a fall in total peripheral conductance, but no change in cardiac output.3. The resistance to blood flow of the stenotic kidney 1 h after stenosis was 25% greater than before stenosis. This rise in resistance was due to the resistance of the renal artery stenosis itself.4. Blood flow to the contralateral kidney fell by 13% (s.e.m. =3) at 1 h and resistance rose by 39% (s.e.m. = 5).5. Plasma renin activity was elevated approximately 10 fold.6. Calculations of changes in peripheral conductances following stenosis showed that the stenotic kidney was responsible for 14% of the fall in total peripheral conductance at 1 h, and the contralateral kidney for 18%.7. Thus acute renal artery stenosis produced a prompt rise in arterial pressure due to reduced peripheral conductance, of which the two kidneys (stenotic and contralateral) were responsible for one-third.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1985.tb02650.x
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  • 2
    Electronic Resource
    Electronic Resource
    Proceedings of the Symposium ‘Angiotensin AT1 Receptors: From Molecular Physiology to Therapeutics’: STRUCTURAL CHANGES IN THE RENAL VASCULATURE IN THE SPONTANEOUSLY HYPERTENSIVE RAT: NO EFFECT OF ANGIOTENSIN II BLOCKADE (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 23 (1996), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 〈list xml:id="l1" style="custom"〉1There is strong evidence for a renal basis to the development of hypertension in the spontaneously hypertensive rat (SHR). Alterations of the SHR renal vasculature, including the glomerulus, may be involved in the initiation and maintenance of hypertension in this animal model.2The arterial walls of pre-glomerular vessels of the SHR are hypertrophied compared with WKY vessels. Unlike other vascular beds in the SHR, this hypertrophy is independent of angiotensin II (AngII).3Glomerular number and volume are similar between SHR and the normotensive Wistar-Kyoto (WKY) rats. These results provide no support for the theory that a reduced filtration surface area within the kidneys of the SHR contributes to the elevated blood pressure in these animals.4Intrarenal hypertrophy may have similar haemodynamic consequences to clipping of the main renal artery, as in Goldblatt hypertension. Further analysis of the role of pre-glomerular arterial hypertrophy is warranted to determine its involvement in the initiation and maintenance of hypertension in the SHR.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1996.tb03074.x
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  • 3
    Electronic Resource
    Electronic Resource
    RENAL VENOUS WEDGE PRESSURE IN RENAL WRAP HYPERTENSION IN RABBITS (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 16 (1989), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Renal cellophane wrapping to produce hypertension causes thickening of the capsule of the kidney. To determine whether this compresses the kidney, deep renal vein wedge pressure was measured as an estimate of tissue pressure in anaesthetized rabbits 1 month after cellophane wrapping (n= 5) or a sham operation (n= 3).2. Renal vein wedge pressure was 18.3 ± 2.0 mmHg in hypertensive rabbits and 8.4 ± 1.1 mmHg in the sham-operated rabbits.3. Arterial pressure was raised or lowered with angiotensin II or glyceryl trinitrate, respectively. Arterial and wedge pressures were approximately linearly related and, at any given arterial pressure, wedge pressure was approximately 8 mmHg higher in the cellophane-wrapped kidney than in the kidney of the sham-operated group.4. These results, showing that renal wedge pressure is elevated in renal wrap rabbits, indicate that the kidneys are compressed, probably by the thickened renal capsule. This may explain the increased renal vascular resistance seen in this form of hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1989.tb01621.x
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  • 4
    Electronic Resource
    Electronic Resource
    CHRONIC INTRARENAL INFUSION OF LOW-DOSE ANGIOTENSIN II IN DOGS INCREASES ARTERIAL PRESSURE WITHOUT IMPAIRMENT OF RENAL FUNCTION (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 24 (1997), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. To determine whether chronic angiotensin II (AngII) infusion into the renal artery, at a dose which increases systemic arterial pressure, reduces glomerular filtration rate (GFR) and renal blood flow, AngII was infused at 0.5 ng/kg per min into the renal artery or intravenously in chronically instrumented dogs for 1 month.2. Mean arterial pressure (MAP) rose significantly (P 〈 0.05) during the infusion of AngII into the renal artery (+7 ± 2 nunHg on days 26-30). There were no significant changes in GFR or renal blood flow. When the same dose of AngII was infused intravenously, MAP did not change significantly (−2 ± 2mmHg) and there were no significant changes in GFR or in renal blood flow.3. We conclude that AngII infused into the renal artery for 1 month, at a dose which was initially subpressor, causes a rise in arterial pressure that is not associated with impairment of renal function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1997.tb01219.x
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  • 5
    Electronic Resource
    Electronic Resource
    AUTORADIOGRAPHIC LOCALIZATION OF ACTIVE RENIN IN THE JUXTAGLOMERULAR APPARATUS OF THE DOG KIDNEY: EFFECTS OF SODIUM INTAKE (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 23 (1996), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The effects of dietary sodium intake on active renin binding in the juxtaglomerular apparatus (JGA) of superficial and juxtamedullary cortex of the dog kidney were examined by quantitative in vitro autoradiography using a radiolabelled renin inhibitor [125I]-H77, which has high affinity for dog renin.2. Changes in sodium intake resulted in marked alterations of active renin binding in the radiolabelled JGA. In comparison with the control kidney (190.8 ± 7.7 Bq/mm3), a higher density of binding occurred in the labelled JGA of sodiumdepleted kidney (277.7 ± 6.2 Bq/mm3), while a lower density of binding was found in the labelled JGA of sodium-loaded kidney (99.3 ± 7.4 Bq/mm3).3. Active renin binding in the labelled JGA was significantly higher in superficial JGA than in their juxtamedullary counterparts, irrespective of sodium intake.4. Pre-incubation with trypsin (0.5mg/mL), a procedure known to activate prorenin, markedly increased active renin binding in the labelled JGA of control (+∼ 35%; P 〈 0.01), and sodium-loaded kidneys (+∼ 75%; P 〈 0.01), but had little effect on binding in the labelled JGA of the sodium-depleted kidney (± 5–10%; NS). The proportions of active renin as a percentage of total renin were 60, 75 and 95% in the labelled JGA of sodium-loaded, control, and sodium-depleted kidneys, respectively.5. Emulsion microscopic autoradiography revealed that the binding was exclusively localized in the JGA, including the afferent and efferent arterioles, macula densa and extraglomerular mesangium. Labelling extended to the interlobular arteries in sodium depleted kidney.6. These results indicate that autoradiography combined with the in vitro binding of radiolabelled renin inhibitors may provide a useful tool to measure active and prorenin renin and thereby study the physiological regulation of renin in the kidney.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1996.tb02826.x
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  • 6
    Electronic Resource
    Electronic Resource
    Molecular biology in the service of physiology, pharmacology and endocrinology (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 22 (1995), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1995.tb02329.x
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  • 7
    Electronic Resource
    Electronic Resource
    RENAL EFFECTS OF RILMENIDINE IN VOLUME-LOADED ANAESTHETIZED DOGS (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 24 (1997), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. In anaesthetized, fluid expanded rats rilmenidine has diuretic and natriuretic effects. There is strong evidence that the natriuresis is mediated by putative imidazoline receptors. In contrast, in conscious euvolaemic dogs rilmenidine has a diuretic effect that is entirely attributable to activation of a2-adrenoceptors, but no natriuretic effect. To determine whether the effects of rilmenidine are truly species dependent, or merely dependent upon the influences of anaesthesia and volume status, we tested the effects of rilmenidine in pentobarbitone anaesthetized, volume-loaded dogs.2. The effects of rilmenidine in anaesthetized, volume-loaded dogs were similar to those found in conscious euvolaemic dogs. Compared with vehicle treatment, levels of glomerular filtration rate, urine flow and haematocrit were increased following rilmenidine treatment. No effect of rilmenidine on sodium excretion was observed.3. We conclude that the renal responses to rilmenidine in dogs are largely unaffected by anaesthesia and plasma volume status. In particular, the natriuretic effect seen in rats was not observed. We conclude that putative imidazoline receptors do not have a major influence on sodium excretion in dogs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1997.tb01784.x
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  • 8
    Electronic Resource
    Electronic Resource
    EVIDENCE FOR A RENOMEDULLARY VASODEPRESSOR HORMONE (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 23 (1996), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Recent physiological experiments have established that increasing the perfusion pressure of the kidney causes the release of a vasodepressor substance from the renal medulla.2. The substance is not a platelet activating factor, a prostaglandin or nitric oxide and the vasodepressor response to increased renal perfusion pressure is not due simply to inhibition of renin release.3. The mechanisms by which the renomedullary vasodepressor substance lowers arterial pressure remain to be determined. Sympathoinhibition may account for part of the response, but the hypotension still occurs in autonomic ganglion blocked animals.4. The source of the substance appears to be the renomedullary interstitial cells, though the control of the production and release of the substance remain to be determined.5. The substance may be a lipid but it is yet to be fully isolated and identified.6. The threshold for release of the substance appears to be close to normal resting arterial blood pressure.7. Despite strong evidence that the renal medulla releases a vasodepressor hormone in response to increased renal perfusion pressure, much is still to be determined regarding the physiology of this hormone and its involvement in the aetiology of hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1996.tb01179.x
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  • 9
    Electronic Resource
    Electronic Resource
    EFFECTS OF NG-NITRO-l-ARGININE ON PRESSURE NATRIURESIS IN ANAESTHETIZED RABBITS (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 22 (1995), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. We tested the effects of blockade of nitric oxide synthesis on renal function under conditions of controlled renal artery pressure. Our hypothesis was that endogenous nitric oxide plays a role in the natriuresis that accompanies increased renal perfusion pressure. We used a novel technique which employed an extracorporeal circuit to produce step changes over a wide range of renal artery pressures in pentobarbitone-anaesthetized rabbits.2. Rabbits were treated with either NG-itro-l-arginine (NOLA, 20 mg/kg, i.v.; n = 8) or its vehicle (n= 8). Renal artery pressure was set (by adjusting the extracorporeal circuit) at 65, 80, 95, 110 and then 130mmHg respectively, at the beginning of each of five 30 min experimental periods.3. NOLA treatment caused profound renal vasoconstriction that was largely independent of the level of renal artery pressure, renal blood flow being 35–43% lower in NOLA-treated than in vehicle-treated rabbits across the range of renal artery pressures tested (P= 0.002). NOLA treatment increased filtration fraction (P = 0.02), and tended to reduce glomerular filtration rate (P= 0.09).4. NOLA-treatment affected sodium excretion in a manner dependent on the level of renal artery pressure, with the slope of the relationship between sodium excretion and renal artery pressure being lower in NOLA-treated than in vehicle-treated rabbits (P= 0.006).5. These data provide direct evidence that in anaesthetized rabbits endogenous nitric oxide (i) tonically dilates the renal vasculature across a wide range of renal perfusion pressures, and (ii) enhances sodium excretion to a progressively greater degree as renal artery pressure is increased. It may therefore play a role in pressure-induced natriuresis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1995.tb01962.x
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  • 10
    Electronic Resource
    Electronic Resource
    Foreword (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 21 (1994), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: AUSTRALIAN PHYSIOLOGICAL AND PHARMACOLOGICAL SOCIETY ANNUAL GENERAL MEETING FEBRUARY 1994
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1994.tb02446.x
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