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  • 1
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    Role of pressure natriuresis in long-term control of renal electrolyte excretion.
    Ovid Technologies (Wolters Kluwer Health) ; 1993
    In:  Hypertension Vol. 22, No. 1 ( 1993-07), p. 102-110
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 22, No. 1 ( 1993-07), p. 102-110
    Abstract: If pressure natriuresis is to play an important role in arterial pressure control, renal perfusion pressure must have a long-term effect on urinary sodium excretion. The aim of this study was to quantitate the importance of renal perfusion pressure per se in controlling renal hemodynamics and electrolyte excretion chronically. Female mongrel dogs (n = 6) were instrumented with bilateral renal artery catheters for measurement of renal perfusion pressure and occluders on both renal arteries for servo-control of renal perfusion pressure at different levels; the urinary bladder was split for determination of renal clearances and electrolyte excretion from each kidney separately. Because both kidneys were exposed to the same neurohumoral influences, any changes in renal function could be attributed to differences in renal perfusion pressure between the two kidneys. After 5 days of control, renal perfusion pressure to one kidney was reduced from 86.7 +/- 0.2 to 74.2 +/- 0.6 mm Hg for 12 days, and pressure in the contralateral kidney increased to 91.5 +/- 0.4 mm Hg. Sodium excretion decreased from 41 +/- 2 to 25 +/- 1 mmol/d in the servo-controlled kidney and increased from 41 +/- 1 to 55 +/- 1 mmol/d in the contralateral kidney during 12 days of servo-control. Urine volume, chloride excretion, and potassium excretion exhibited similar patterns during servo-control. In addition, autoregulation of effective renal plasma flow and glomerular filtration rate was relatively well maintained; however, in the low-pressure kidney, glomerular filtration rate was slightly but significantly lower (approximately 8%) than in the contralateral kidney.(ABSTRACT TRUNCATED AT 250 WORDS)
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.22.1.102
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1993
    detail.hit.zdb_id: 2094210-2
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  • 2
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    Role of the liver in renal hemodynamic response to amino acid infusion
    American Physiological Society ; 1987
    In:  American Journal of Physiology-Renal Physiology Vol. 252, No. 6 ( 1987-06-01), p. F981-F985
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 252, No. 6 ( 1987-06-01), p. F981-F985
    Abstract: The purpose of this study is to determine the quantitative importance of the liver in mediating the increases in renal blood flow and glomerular filtration rate (GFR) that occur after elevation of plasma amino acids. A mixture of four amine acids (Gly, Ser, Ala, Pro at 0.075 mmol X kg-1 X min-1 total) was infused intravenously into normal anesthetized dogs and into a second group of dogs after ligating all blood vessels supplying the liver and inserting a hepatic portal-femoral venous shunt. In normal dogs, renal blood flow and GFR rose by an average of 20 +/- 3 and 15 +/- 4%, respectively, after 30 min of amino acid infusion, while renal vascular resistance fell 16% from 0.51 +/- 0.16 to 0.43 +/- 0.16 mmHg X ml-1 X min. The responses of dogs in which the hepatic circulation was ligated were not significantly different from those in normal animals; renal blood flow and GFR increased by 20 +/- 3 and 31 +/- 7%, respectively, and renal vascular resistance fell 26% from 0.80 +/- 0.13 to 0.59 +/- 0.08 mmHg X ml-1 X min after 30 min of amino acid infusion. Because ligation of the blood supply to the liver did not prevent the renal hemodynamic response to amino acid infusion, it appears that the liver does not play a major role in mediating renal vasodilation during elevation of plasma amino acids.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.1987.252.6.F981
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1987
    detail.hit.zdb_id: 1477287-5
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  • 3
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    Mechanisms controlling renal hemodynamics and electrolyte excretion during amino acids
    American Physiological Society ; 1986
    In:  American Journal of Physiology-Renal Physiology Vol. 251, No. 2 ( 1986-08-01), p. F303-F312
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 251, No. 2 ( 1986-08-01), p. F303-F312
    Abstract: Our purpose was to investigate the mechanisms by which increased plasma amino acids elevate renal blood flow (RBF) and glomerular filtration rate (GFR). Since transport of amino acids and Na+ is linked in the proximal tubule, we hypothesized that increased amino acids might stimulate proximal tubular Na+ reabsorption (PRNa) and thus increase RBF and GFR by a macula densa feedback mechanism. A solution of four amino acids (Ala, Ser, Gly, Pro) was infused intravenously (0.075 mmol X kg-1 X min-1 total) into anesthetized dogs with normal kidneys (NK) and with kidneys in which the tubuloglomerular feedback mechanism was blunted by lowering renal artery pressure (LPK) or blocked by making the kidneys nonfiltering (NFK). In NK, RBF and GFR increased by 35 +/- 4% and 30 +/- 7% after 90 min of amino acid infusion, while PRNa (estimated from lithium clearance) and O2 consumption increased by 31 +/- 5% and 29 +/- 5% and distal Na+ delivery remained relatively constant. Autoregulation of RBF and GFR in response to step decreases in renal artery pressure was impaired during amino acids in NK. The hemodynamic responses to amino acids were abolished in LPK and NFK. Infusion of the nonmetabolized alpha-aminoisobutyric acid (0.075 mmol X kg-1 X min-1) into NK produced changes in renal hemodynamics that were similar to the responses observed with the four metabolizable amino acids. These data are consistent with the hypothesis that elevation of plasma amino acids increases RBF and GFR by a mechanism that requires an intact macula densa feedback. Metabolism of the amino acids does not appear to be necessary for these changes to occur.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.1986.251.2.F303
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1986
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  • 4
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    Atrial natriuretic peptide and sodium homeostasis in compensated heart failure
    American Physiological Society ; 1996
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 271, No. 5 ( 1996-11-01), p. R1353-R1363
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 271, No. 5 ( 1996-11-01), p. R1353-R1363
    Abstract: The purpose of this study was to determine whether high plasma levels of atrial natriuretic peptide (ANP) in compensated heart failure are important in the maintenance of sodium balance. This was achieved by subjecting eight dogs to bilateral atrial appendectomy (APX) to blunt the ANP response to pacing-induced heart failure. Five intact dogs served as controls. In controls, 14 days of left ventricular pacing at 240 beats/min produced a sustained fall in cardiac output and mean arterial pressure of approximately 40 and 20%, respectively; compared with cardiac output, reductions in renal blood flow (up to approximately 25%) were less pronounced and even smaller decrements in GFR occurred (up to 9%). Despite these changes and a threefold elevation in plasma norepinephrine concentration, plasma renin activity (PRA) did not increase and sodium balance was achieved during the second week of pacing in association with a six- to eightfold rise in plasma levels of ANP. Similar responses occurred in four dogs in which APX was relatively ineffective in blunting the ANP response to pacing. In marked contrast, there were substantial increments in PRA and in plasma norepinephrine concentration, and marked sodium and water retention during the last week of pacing in four dogs with APX and severely deficient ANP. These results indicate that ANP plays a critical role in promoting sodium excretion in the early stages of cardiac dysfunction.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.1996.271.5.R1353
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1996
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 5
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    Role of nitric oxide in long-term angiotensin II-induced renal vasoconstriction.
    Ovid Technologies (Wolters Kluwer Health) ; 1993
    In:  Hypertension Vol. 21, No. 6_pt_2 ( 1993-06), p. 949-955
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 21, No. 6_pt_2 ( 1993-06), p. 949-955
    Abstract: In vitro studies have indicated that nitric oxide may play an important role in modulating the renal vascular actions of angiotensin II (Ang II). However, the physiological importance of this interaction in the long-term regulation of renal hemodynamics is unknown. Therefore, the goal of this study was to determine if long-term Ang II-induced renal vasoconstriction was potentiated by nitric oxide synthesis inhibition. The intrarenal effects of Ang II were examined in eight unilaterally nephrectomized, conscious dogs before and after systemic inhibition of nitric oxide synthesis. Ang II infusion into the renal artery at 0.5 ng/kg per minute resulted in decreases in renal plasma flow of 15% and 9% after 3 and 5 days, respectively. During this time, glomerular filtration rate decreased 12% after 3 days of angiotensin but was not significantly changed after 5 days. After 4 days of recovery from Ang II, nitric oxide synthesis was inhibited with intravenous NG-nitro-L-arginine-methyl ester (L-NAME) at 10 micrograms/kg per minute for 5 days, and this caused a significant decrease in renal plasma flow but no change in glomerular filtration rate. Infusion of Ang II into L-NAME-pretreated dogs for an additional 5 days further decreased renal plasma flow and glomerular filtration 14% and 11%, respectively. However, the effects of Ang II and L-NAME on renal plasma flow were only additive on days 3 and 5 of this period, and the effects on glomerular filtration were additive on day 3 but were potentiated on day 5.(ABSTRACT TRUNCATED AT 250 WORDS)
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.21.6.949
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1993
    detail.hit.zdb_id: 2094210-2
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  • 6
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    Control of sodium excretion in NE-ACTH hypertension: role of pressure natriuresis
    American Physiological Society ; 1988
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 255, No. 6 ( 1988-12-01), p. R894-R900
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 255, No. 6 ( 1988-12-01), p. R894-R900
    Abstract: The purpose of this study was to test the hypothesis that, in the presence of high circulating catecholamines, ACTH decreases renal excretory capability and that its natriuretic effects are caused by increased renal arterial pressure (RAP). In six conscious dogs, norepinephrine (NE, 0.4 micrograms.kg-1.min-1) alone for 5 days caused a small but significant rise in arterial pressure (AP) from 102 +/- 6 to 115 +/- 8 mmHg. An infusion of ACTH (600 micrograms/day) for 7 days, superimposed upon the NE, caused a further rise in AP to a plateau of 143 +/- 9 mmHg after 5 days while cumulative sodium balance fell to -149 +/- 41 meq by the 7th day. Cumulative water balance fell to -660 +/- 232 ml by the 3rd day and then increased slightly. In contrast, when ACTH infusion was repeated during NE infusion while RAP was prevented from increasing using a servo-controlled aortic occluder, cumulative sodium balance increased to 197 +/- 35 meq and AP rose from 108 +/- 5 to 168 +/- 5 mmHg after 7 days and did not plateau. Cumulative water balance rose to 2,325 +/- 445 ml. Thus, in dogs receiving a background infusion of NE, ACTH causes moderate hypertension and natriuresis. However, when RAP is not allowed to rise, ACTH is associated with sodium retention and severe systemic hypertension, suggesting that the natriuretic effects of ACTH are caused by increased RAP and that the natriuresis blunts the chronic hypertensive effects of ACTH.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.1988.255.6.R894
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1988
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 7
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    Renal escape from vasopressin: role of pressure diuresis
    American Physiological Society ; 1986
    In:  American Journal of Physiology-Renal Physiology Vol. 250, No. 5 ( 1986-05-01), p. F907-F916
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 250, No. 5 ( 1986-05-01), p. F907-F916
    Abstract: This study was designed to examine the role of increased renal artery pressure (RAP) in mediating escape from the antidiuretic action of vasopressin (AVP). In six conscious dogs in which RAP was permitted to increase, AVP infusion, at a rate (0.2 mU X kg-1 X mm-1 iv) that was acutely subpressor, gradually raised mean arterial pressure (MAP) from 97 +/- 2 to 126 +/- 4 mmHg after 5 days while decreasing urine volume and increasing urine osmolality. However, after 4-5 days of AVP infusion, urine volume and osmolality returned to control, and the hypertensive effect of AVP waned so that after 9 days of AVP, MAP averaged only 113 +/- 5 mmHg. In contrast, when RAP was prevented from increasing in seven dogs with a servo-controlled aortic occluder, AVP caused sustained decreases in urine volume and elevated urine osmolality from 609 +/- 27 to 1,160-1,711 mosmol/kg H2O throughout 8 days of infusion. The hypertensive effect of AVP did not wane when RAP was servo-controlled, and after 8 days of AVP infusion, MAP averaged 152 +/- 7 mmHg, compared with a control of 96 +/- 2 mmHg. Servo-controlling RAP also prevented the marked sodium and chloride losses seen with chronic AVP infusion in normal dogs. These findings indicate that escape from the antidiuretic action of AVP is mediated by increased RAP, which causes diuresis and natriuresis, thereby diminishing the hypertensive effect of AVP. However, when pressure diuresis and natriuresis are prevented, AVP causes severe chronic hypertensive, suggesting that AVP could be an important hypertensive mechanism when renal function is impaired.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.1986.250.5.F907
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1986
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  • 8
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    Role of renal nerves in compensatory adaptation to chronic reductions in sodium intake
    American Physiological Society ; 1987
    In:  American Journal of Physiology-Renal Physiology Vol. 252, No. 2 ( 1987-02-01), p. F291-F298
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 252, No. 2 ( 1987-02-01), p. F291-F298
    Abstract: The aim of this study was to investigate the importance of the renal nerves in adaptation to chronic reductions in sodium intake. Conscious dogs with unilateral (n = 7) or bilateral (n = 4) renal denervation were studied. In dogs studied before and after bilateral denervation, there were no differences in urine volume (UO), Na excretion (UNaV), or fractional reabsorption of Li (FR Li, an index of proximal tubular Na reabsorption) between innervated and denervated kidneys on either normal (80 meq/day) or low Na intake (5 meq/day, 15 days). Plasma renin activity (PRA) was attenuated following denervation on both normal (0.39 +/- 0.06 vs. 0.18 +/- 0.01 ng angiotensin I X ml-1 X h-1) and low Na intake (1.00 +/- 0.06 vs. 0.59 +/- 0.01). In unilaterally denervated dogs the left kidney was denervated and the bladder was split, allowing continuous urine collection from separate innervated and denervated kidneys in the same dog. There was no difference in UO between innervated and denervated kidneys on normal (80 meq/day) or low (7 meq/day, 9 days) Na intake. UNaV averaged 33.6 +/- 1.3 and 37.6 +/- 2.1 meq/day in innervated and denervated kidneys, respectively, on normal Na intake and 3.5 +/- 0.5 and 4.0 +/- 0.4 meq/day in innervated and denervated kidneys on low Na intake. FR Li was not different in denervated compared with innervated kidneys during normal or low sodium intake. Norepinephrine content was reduced by 99 +/- 1% in denervated kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.1987.252.2.F291
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1987
    detail.hit.zdb_id: 1477287-5
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  • 9
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    Interactions between angiotensin II and renal nerves during chronic sodium deprivation
    American Physiological Society ; 1988
    In:  American Journal of Physiology-Renal Physiology Vol. 255, No. 5 ( 1988-11-01), p. F823-F827
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 255, No. 5 ( 1988-11-01), p. F823-F827
    Abstract: The aim of this study was to examine the importance of the renal nerves in mediating the sodium-retaining actions of angiotensin II (ANG II) during chronic sodium deprivation. In seven female dogs the left kidney was denervated and the urinary bladder was split, allowing continuous urine collection from separate innervated and denervated kidneys in the same dog. The dogs were maintained on a low-sodium diet (7 meq/day) for 9 days and then infused with the converting-enzyme inhibitor captopril (CAP, 14 micrograms.kg-1.min-1, 7 days) followed by CAP plus ANG II (10 ng.kg-1.min-1, 7 days). Mean arterial pressure (MAP) fell from a control of 88 +/- 4 (average for 5 days preceding CAP) to 65 +/- 3 mmHg during CAP. Infusion of ANG II along with CAP restored MAP to 97 +/- 5 mmHg. There were no significant differences in urine volume or sodium, potassium, chloride, or osmolar excretions between innervated and denervated kidneys during the control period, CAP infusion, or CAP plus ANG II infusion. Norepinephrine content was reduced by 99 +/- 1% in denervated kidneys. Because a differential response was not observed between innervated and denervated kidneys during ANG II blockade or infusion of ANG II, we conclude that the renal nerves do not play a major role in mediating the sodium-retaining effects of ANG II during chronic sodium restriction.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.1988.255.5.F823
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1988
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  • 10
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    Control of renal hemodynamics in hyperglycemia: possible role of tubuloglomerular feedback
    American Physiological Society ; 1987
    In:  American Journal of Physiology-Renal Physiology Vol. 252, No. 1 ( 1987-01-01), p. F65-F73
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 252, No. 1 ( 1987-01-01), p. F65-F73
    Abstract: The purpose of this study was to test the hypothesis that hyperglycemia, comparable with that found in uncontrolled diabetes mellitus, increases renal blood flow (RBF) and glomerular filtration rate (GFR) through a tubuloglomerular feedback (TGF) mechanism. We infused glucose intrarenally (0.1-0.3 g/min) into anesthetized dogs with normal kidneys (NK), with nonfiltering kidneys (NFK) in which changes in TGF were blocked, and with normal kidneys in which renal perfusion pressure (RAP) was lowered to the limits of renal autoregulation (LPK). Calculated intrarenal plasma glucose levels rose to 250-400 mg/dl. In NK (n = 6) RBF and GFR increased by 18 +/- 3 and 19 +/- 5%, respectively, and renal vascular resistance fell by 17 +/- 2% after 90 min. The renal hemodynamic responses to glucose were abolished in NFK (n = 8); RBF averaged 96 +/- 4% of control after 60 min of hyperglycemia. RBF and GFR did not change during hyperglycemia in LPK (n = 5), averaging 96 +/- 1 and 100 +/- 8% of control, respectively, after 60 min. Autoregulation of RBF and GFR during reductions in RAP was impaired during hyperglycemia in NK; RBF and GFR were effectively autoregulated between RAP of 126 and 70-85 mmHg during the control period, whereas during glucose infusion RBF and GFR fell by 31 +/- 9 and 47 +/- 10%, respectively, when RAP was reduced in steps to 70 mmHg. These data suggest that hyperglycemia impairs renal autoregulation and may increase renal blood flow and GFR through a tubuloglomerular feedback mechanism.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.1987.252.1.F65
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1987
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