THE STIMULUS TO HYPERTROPHIC GROWTH
ill
E. Summary
It is clear from the experimental evidence that the stimulus to hypertrophic growth in the liver following partial hepatectomy does not come
from the pituitary, thyroid, or adrenal glands and that the increased blood
flow may contribute to but does not itself cause the hypertrophy. There is
no evidence that increased functional activity is the stimulus to hypertrophy, and the rapidity of the response would seem to preclude this
possibility. The evidence concerning the involvement of humoral factors is
contradictory, but the best, most carefully controlled experiments have
yielded generally negative results.
However, we are still faced with the fact that liver does hypertrophy,
that somehow the information that the liver mass has been reduced is
conveyed to the remaining liver tissue. We also have strong evidence of a
systemic if not necessarily a humoral effect (Leong et al., 1964; Sigel et al.,
1963; Virolainen, 1964). We shall return to a consideration of this problem
below.
V. Compensatory Renal Hypertrophy
A. Description of the Process
The process of kidney hypertrophy has been known for a long time (see
review of early literature by Sacerdotti, 1896), but it has been studied much
less extensively than liver restoration. When one kidney is removed, the
remaining kidney gets bigger. There is usually an increase in cell size, as
well as in the number of cells, but no new nephrons or glomeruli are formed
(Arataki, 1926; Rollason, 1949). Fajers (1957) reports that 2 hr after
unilateral nephrectomy the remaining kidney has decreased somewhat in
weight and does not regain its initial weight until 1 day later. After 1 day
rapid growth begins. The mitotic activity of kidney has a diurnal cycle
like that of liver (Blumenfeld, 1938; Rollason, 1949), and the peak mitotic
activity in the kidney remaining after unilateral nephrectomy occurs 2 or
3 days after the operation (Ogawa and Sinclair, 1958; Sulkin, 1949; G. E. G.
Williams, 1961). There is an increased incidence of binucleate cells in the
hypertrophying kidney (Sulkin, 1949) and an increase in the polyploidy
of the kidney nuclei (Ogawa, 1961). The rate and degree of hypertrophy
decline with age (E. M. MacKay et al., 1932). The proliferative response to
unilateral nephrectomy is confined to the kidney (Simpson, 1961b).
Rosenthal et al. (1962) reported that there is a transient increase in
succinodehydrogenase activity in the kidney remaining after unilateral
nephrectomy, but that the activities of cytochrome oxidase and cytochrome
c reductase are unchanged. Immediately after unilateral nephrectomy the
ill
E. Summary
It is clear from the experimental evidence that the stimulus to hypertrophic growth in the liver following partial hepatectomy does not come
from the pituitary, thyroid, or adrenal glands and that the increased blood
flow may contribute to but does not itself cause the hypertrophy. There is
no evidence that increased functional activity is the stimulus to hypertrophy, and the rapidity of the response would seem to preclude this
possibility. The evidence concerning the involvement of humoral factors is
contradictory, but the best, most carefully controlled experiments have
yielded generally negative results.
However, we are still faced with the fact that liver does hypertrophy,
that somehow the information that the liver mass has been reduced is
conveyed to the remaining liver tissue. We also have strong evidence of a
systemic if not necessarily a humoral effect (Leong et al., 1964; Sigel et al.,
1963; Virolainen, 1964). We shall return to a consideration of this problem
below.
V. Compensatory Renal Hypertrophy
A. Description of the Process
The process of kidney hypertrophy has been known for a long time (see
review of early literature by Sacerdotti, 1896), but it has been studied much
less extensively than liver restoration. When one kidney is removed, the
remaining kidney gets bigger. There is usually an increase in cell size, as
well as in the number of cells, but no new nephrons or glomeruli are formed
(Arataki, 1926; Rollason, 1949). Fajers (1957) reports that 2 hr after
unilateral nephrectomy the remaining kidney has decreased somewhat in
weight and does not regain its initial weight until 1 day later. After 1 day
rapid growth begins. The mitotic activity of kidney has a diurnal cycle
like that of liver (Blumenfeld, 1938; Rollason, 1949), and the peak mitotic
activity in the kidney remaining after unilateral nephrectomy occurs 2 or
3 days after the operation (Ogawa and Sinclair, 1958; Sulkin, 1949; G. E. G.
Williams, 1961). There is an increased incidence of binucleate cells in the
hypertrophying kidney (Sulkin, 1949) and an increase in the polyploidy
of the kidney nuclei (Ogawa, 1961). The rate and degree of hypertrophy
decline with age (E. M. MacKay et al., 1932). The proliferative response to
unilateral nephrectomy is confined to the kidney (Simpson, 1961b).
Rosenthal et al. (1962) reported that there is a transient increase in
succinodehydrogenase activity in the kidney remaining after unilateral
nephrectomy, but that the activities of cytochrome oxidase and cytochrome
c reductase are unchanged. Immediately after unilateral nephrectomy the