Premium
Renin release and autoregulation of blood flow in a new model of non‐filtering non‐transporting kidney.
Author(s) -
Sanowski J,
Wocial B
Publication year - 1977
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1977.sp011765
Subject(s) - autoregulation , renal blood flow , kidney , chemistry , perfusion , plasma renin activity , renin–angiotensin system , medicine , blood pressure , endocrinology , blood flow , renal circulation , mannitol , biochemistry
1. A recently developed model of a non‐filtering, non‐transporting dog kidney, obtained by an in situ filling of tubules with low‐viscosity oil, was applied for studies of renin release and autoregulation of renal blood flow (RBF). 2. Renal blood flow was partially autoregulated after oil blockade of tubules, as indicated by a mean autoregulation index (Semple‐de Wardener (1959) of 0‐5. This was comparable to autoregulation of the stop‐flow kidney (index 0‐6) and contrasted with abolition of autoregulation after hypertonic mannitol loading at stop‐flow conditions (index 1‐1). 3. The aortic construction at a suprarenal level, which decreased renal perfusion pressure of the oil‐blocked kidney 35 +/‐ (S.E. of mean) 6 mmHg, produced an increase in arterial plasma renin activity of 1‐8 +/‐ 0‐1 ng. ml.‐1 (P less than 0‐02). Renin secretion rate decreased 33 to 70 ng.min‐1 in three dogs in which renal perfusion pressure was reduced to 60‐‐66 mmHg, but increased 110 +/‐ 41 ng.min‐1 when pressure reductions were kept within the renal blood flow autoregulation range (n=8, P less than 0‐025). 4. These results suggest that signals from the tubular receptor (macula densa) are not necessary for stimulation of renin release or autoregulation of renal blood flow.