Abnormal pressure-diuresis-natriuresis response in spontaneously hypertensive rats. Am J Physiol 1985 Feb;248(2 Pt 2):F199-205
Date
02/11/1985Pubmed ID
3970210DOI
10.1152/ajprenal.1985.248.2.F199Scopus ID
2-s2.0-0021965652 (requires institutional sign-in at Scopus site) 161 CitationsAbstract
The renal responses to changes in perfusion pressure (RPP) were studied in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) to determine whether an abnormality in the pressure-diuresis phenomenon could be involved in the resetting of kidney function in hypertension. Differences in the neural and endocrine background to the kidneys were minimized by denervating the kidney and by holding plasma vasopressin, aldosterone, corticosterone, and norepinephrine levels constant by intravenous infusion. In WKY, increasing renal perfusion pressure 54 mmHg, from 103 to 157 mmHg, produced a ninefold increase in urine flow and sodium excretion with no measurable change in renal blood flow (RBF) or glomerular filtration rate (GFR). In SHR, increasing renal perfusion pressure 54 mmHg, from 133 to 187 mmHg, produced only a fourfold increase in urine flow and sodium excretion. GFR, RBF, and peritubular capillary pressures were well autoregulated and were similar in the SHR and WKY at pressures above 110 mmHg. These results indicate the presence of intrinsic changes in the kidney of SHR that enhance fractional tubular reabsorption and impair the pressure-diuresis response. This blunting of the renal pressure-diuresis phenomenon in SHR may represent the functional resetting of the kidney that is necessary for sustained hypertension.
Author List
Roman RJ, Cowley AW JrAuthor
Allen W. Cowley Jr PhD Professor in the Physiology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsBlood Pressure
Diuresis
Glomerular Filtration Rate
Homeostasis
Hypertension
Kidney
Male
Natriuresis
Perfusion
Rats
Rats, Inbred SHR
Rats, Inbred Strains
Renal Circulation