First Advisor

Stanley S. Hillman

Term of Graduation

Summer 1997

Date of Publication

11-21-1997

Document Type

Thesis

Degree Name

Master of Science (M.S.) in Biology

Department

Biology

Language

English

Subjects

Renin, Angiotensins, Kidneys -- Aging Rats, -- Physiology

DOI

10.15760/etd.7281

Physical Description

1 online resource (iii, 56 pages)

Abstract

Progressive deterioration of renal function is one consequence of aging. Glomerular maladaptation is one aspect of this and includes increased glomerular capillary hypertension and a reduced ultrafiltration coefficient, which can lead to glomerular sclerosis and proteinuria. In the aging rat, angiotensin converting enzyme inhibitors (CEI) lower proteinuria (UprotV) and decrease glomerular sclerosis (2, 18, 24, 45). Accordingly, alterations in the circulating and renal renin-angiotensin system (RAS) are hypothesized to play a role in the pathogenesis of renal disease in the aging rat. Previous studies using rat models have demonstrated a lower responsiveness to converting enzyme inhibitor treatment in the older rat compared to the young and diabetic models (2, 12). However, these results are not found consistently (7). We treated young (3 month old) and older (15 month old) Sprague-Dawley rats with the converting enzyme inhibitor, enalapril, to investigate the responsiveness to this treatment, of the older rat compared to the young rat. Blood pressure, proteinuria, renal function, and blood and renal reninangiotensin component concentrations were compared in young and older male Sprague-Dawley rats treated for 4 weeks with two dose levels of enalapril. Young and older untreated controls received no enalapril treatment. All rats were normotensive at baseline and the older rats were proteinuric. Enalapril reduced systolic blood pressure in both age groups; however, this treatment failed to significantly reduce proteinuria in the older rats. Renal function decreased in the older rats. Enalapril treatment did not improve the renal function of either the young or the older rat. Mean arterial pressure was reduced, with enalapril treatment, in the young, but not the older rats. Biochemical RAS measurements were not altered with age. Plasma renin concentration, kidney angiotensin II (Ang II) and blood Ang II responded appropriately with the converting enzyme inhibitor enalapril, and showed no age-related responses to this treatment. We conclude that the 15 month old rat does not exhibit an age-related alteration in response to converting enzyme inhibition when compared to the young rat. At this transition age, the decline in renal function does not appear to be a consequence of an altered reninangiotensin system.

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Comments

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Persistent Identifier

https://archives.pdx.edu/ds/psu/32547

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