Key result
Various factors including arterial pressure, vasomotor activity, noradrenaline, potassium, angiotensin II, and sodium load influence the intrarenal secretion of renin into the bloodstream.
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May guide renin level interpretation in hypertension; leaves open prospective validation in modern cohorts.
True renin is known to be secreted into the blood stream from the juxtaglomerular apparatus (J.G.A.) of the kidney (Hartroft & Hartroft, 1955; Hartroft, 1957 & 1963; Cook & Pickering, 1959; Chandra et al, 1964; Robertson et al, 1965), and many of the factors influencing the rate of this secretion have been established. A small fall in systemic mean arterial pressure (To-bian, 1960; Skinner et al, 1963 & 1964), reflex vasomotor activity (Hodge et al, 1966) and infusions of noradrenaline (Vander, 1965) increase plasma renin. Increase either in the concentrations of plasma potassium (Vander, 1970) or of angiotensin II (Vander & Geelhoed, 1965) inhibits the secretion of renin into the blood stream. Sodium deprivation results in hypertrophy of the J.G.A. and an increase in the concentration of plasma renin (Pitcock et al, 1959; Brown et al, 1964). Conversely, sodium-loading decreases the granularity of the J. G. cells and causes a fall in the concentration of plasma renin (Hartroft & Hartroft, 1953; Brown et al, 1964). Finally, the secretion of renin into the blood stream is thought to be influenced either by the load or concentration of sodium passing the luminal surface of the macula densa, or traversing the cells (Thurau, 1964; Vander & Miller, 1964; Gross et al, 1965; Vander, 1967; Vander & Carlson, 1969).
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Gan et al. (1973) conducted a review in Factors affecting intrarenal secretion of renin. Various factors including arterial pressure, vasomotor activity, noradrenaline, potassium, angiotensin II, and sodium load influence the intrarenal secretion of renin into the bloodstream.
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