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  • Ovid Technologies (Wolters Kluwer Health)  (3)
  • Franco-Saenz, R  (3)
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  • Ovid Technologies (Wolters Kluwer Health)  (3)
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  • 1
    Online Resource
    Online Resource
    Effect of changes in sodium or potassium balance, and nephrectomy, on adrenal renin and aldosterone concentrations.
    Ovid Technologies (Wolters Kluwer Health) ; 1984
    In:  Hypertension Vol. 6, No. 2_pt_2 ( 1984-03)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 6, No. 2_pt_2 ( 1984-03)
    Abstract: An active form of renin was confirmed in the adrenal gland of rats. It had a molecular weight of 40,000, generated angiotensin I (AI) from natural renin substrate at pH 7.4, and was found at concentrations 30 to 60 times higher than plasma renin in rats on a normal diet. Changes in sodium diet induced changes in adrenal capsular renin concentration (high Na 2.21 +/- 0.34, normal Na 4.34 +/- 0.53, low Na 13.19 +/- 1.67 ng AI/mg protein/hr). A high potassium diet also increased adrenal capsular renin from 5.27 +/- 0.53 to 39.78 +/- 5.68 ng AI/mg protein/hr, while plasma renin concentration decreased from 7.28 +/- 0.63 in the normal diet to 5.05 +/- 0.60 on the high potassium diet. Neither diet altered the concentration of renin in the fasciculata-medullary portion of the adrenal gland. Nephrectomy markedly increased the renin concentration in the adrenal capsules without any effect on the decapsular cells (20 hours after nephrectomy, 71.5 +/- 10.6 ng AI/mg protein/hr). Sodium loading or dexamethasone treatment prior to nephrectomy blunted the rise in adrenal renin (nephrectomy + dexamethasone = 27.64 +/- 4.33 ng AI/mg protein/hr; nephrectomy + NaCl = 38.70 +/- 5.82 ng AI/mg protein/hr). In all experiments, there was a positive correlation between adrenal renin and adrenal aldosterone concentrations, but the experiments did not rule out the possibility that this positive correlation was due to two independent variables changing in the same direction and not causally related. In conclusion, adrenal renin may be a local hormone, involved in the regulation of aldosterone production.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.6.2_Pt_2.I124
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1984
    detail.hit.zdb_id: 2094210-2
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  • 2
    Online Resource
    Online Resource
    Mechanisms by which nephrectomy stimulates adrenal renin.
    Ovid Technologies (Wolters Kluwer Health) ; 1986
    In:  Hypertension Vol. 8, No. 11 ( 1986-11), p. 997-1002
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 8, No. 11 ( 1986-11), p. 997-1002
    Abstract: Renin has been identified in the adrenal gland by several investigators. Nephrectomy is the most potent stimulator of adrenal renin, and in the present study we investigated the mechanism by which nephrectomy stimulates adrenal renin. The pituitary plays a permissive role since hypophysectomy abolished the response of adrenal renin to nephrectomy (from 117.3 +/- 14.55 to 10.37 +/- 1.63 ng angiotensin I/mg protein/hr) and adrenocorticotropic hormone (ACTH) treatment restored the response to nephrectomy in hypophysectomized rats to 120 +/- 20.62 ng angiotensin I/mg protein/hr. However, large doses of ACTH given to intact rats did not increase adrenal renin to the high level observed after nephrectomy. Potassium also plays an important role, since prevention of hyperkalemia after nephrectomy by treatment with a cation exchange resin, sodium polystyrene sulfonate (Kayexalate), significantly reduced the adrenal renin response to nephrectomy. A third factor involved is the lack of negative feedback by plasma angiotensin II. Infusion of angiotensin II intraperitoneally prevented the rise in adrenal renin after nephrectomy (from 65.25 +/- 7.60 to 9.27 +/- 0.99 ng angiotensin I/mg protein/hr) despite an increase in plasma potassium and corticosterone. In conclusion, three factors influence the response of adrenal renin to nephrectomy: 1) the pituitary through the release of ACTH, 2) a direct stimulation by high plasma potassium levels, 3) the lack of angiotensin II feedback inhibition. Whether the high adrenal renin contributes to the high aldosterone observed in rats after nephrectomy remains to be established.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.8.11.997
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1986
    detail.hit.zdb_id: 2094210-2
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  • 3
    Online Resource
    Online Resource
    Evidence for an extrarenal source of inactive renin in rats.
    Ovid Technologies (Wolters Kluwer Health) ; 1984
    In:  Hypertension Vol. 6, No. 5 ( 1984-09), p. 627-632
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 6, No. 5 ( 1984-09), p. 627-632
    Abstract: We studied the source of inactive renin in plasma by investigating the changes of active and inactive renin after bilateral nephrectomy in the rat. Active renin rapidly decreased after bilateral nephrectomy, with a half-life of approximately 15 minutes. Inactive renin, on the other hand, was 20.96 +/- 1.63 ng/ml/hr before nephrectomy and gradually increased to reach a peak at 20 hours after nephrectomy (193 +/- 62 ng/ml/hr). The molecular weight of active renin was approximately 40,000 and that of inactive renin was approximately 60,000 on a Sephacryl S-200 column. Inactive renin was separated from active renin by a Cibacron blue column, and the 0 time inactive renin eluted in the same fractions as the inactive renin from 20 hours after nephrectomy. The pH optimum of inactive renin in rat renin substrate was between 5.5 and 7.5, which differs from the optimal value of pepsin or cathepsin D. The increase of inactive renin in nephrectomized rats was not prevented by removal of the salivary glands, uterus, spleen, pancreas, stomach, intestines, adrenal glands, or pituitary. In summary, inactive renin is present in the anephric rat and does not appear to be converted to active renin in the peripheral blood. The source and control of this extrarenal inactive renin are still unclear, but this renin is secreted in the rat within hours after nephrectomy.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.6.5.627
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1984
    detail.hit.zdb_id: 2094210-2
    Location Call Number Limitation Availability
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