Hypertension, Vol 1, 598-604, Copyright © 1979 by American Heart Association
WV Judy, AM Watanabe, WR Murphy, BS Aprison and PL Yu
The genetic basis of hyperactivity of the sympathetic nervous system (SNA)
in spontaneously hypertensive rats (SHR) was assessed by measuring SNA in
animals derived from a backcross (BC) breeding program designed to isolate
single gene differences causing changes in blood pressure. Selective
breeding of the male hypertensive rats with inbred normotensive female
Wistar/Lewis rats yielded progeny with a range of blood pressures, but
whose group mean pressures were lower than the group mean pressures of the
original SHR. Progressive generations had progressively lower group mean
pressures. There was a positive correlation between SNA and mean arterial
pressure in BC rats. These results indicate that the genetic defect in SHR
may be abnormality in SNA, and the hypertension in these animals is a
secondary result of this primary defect. Baroreceptor function was also
assessed in SHR and in BC rats. In young (8 to 24 weeks old) SHR,
baroreceptor function was similar to that in BC rats, whereas SNA was
markedly increased. Only in older (24 to 40 weeks old) SHR was there an
abnormality in the gain of baroreceptors. The development of hypertension
in SHR therefore appears to be due to increased SNA resulting from a defect
in the central nervous system. Changes in baroreceptor function are
secondary to the hypertension and occur after the hypertension is
established.
ARTICLES
Sympathetic nerve activity and blood pressure in normotensive backcross rats genetically related to the spontaneously hypertensive rat
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