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.

Aging↗

PubMedDate not supplied

Effects of graded renal artery constriction on blood pressure, renal artery pressure, and plasma renin activity in Goldblatt hypertension.

One-kidney, one clip (1K1C) and two-kidney, one clip (2K1C) Goldblatt hypertension was produced in rats by placing 0.30, 0.25, or 0.20 mm silver clips on the left renal artery. Mean arterial pressure (MAP) and plasma renin activity (PRA) were measured in conscious rats 24 to 28 days after clipping. The MAP in control rats (n = 38) was 116 +/- 1 mm Hg (mean +/- SEM). The 0.30, 0.25, and 0.20 mm clips produced MAPs of 133 +/- 2, 161 +/- 5, and 189 +/- 5 mm Hg, respectively, in 1K1C rats, and 123 +/- 2, 129 +/- 3, and 172 +/- 5 mm Hg in 2K1C rats (n = 17-20). When 1K1C and 2K1C groups were compared, MAP was significantly greater in 1K1C rats at all clip sizes. No treatment group's PRA was different than control (4.8 +/- 0.4 ng AI/ml/hr), except for the 0.20 mm 2K1C rats (16.2 +/- 3.1 ng AI/ml/hr). Renal artery pressure (RAP) was measured in another series of experiments and was not different from control in all but the 0.20 mm 1K1C rats. With identical clip sizes, 2K1C rats showed smaller pressure gradients than 1K1C across the clips: 0.30 mm, 8.5 +/- 1.7 vs 10.7 +/- 1.9 mm Hg; 0.25 mm, 16.5 +/- 1.2 vs 42.1 +/- 7.5 mm Hg; 0.20 mm, 51 +/- 5.3 vs 79.1 +/- 5.7 mm Hg (n = 8-12). Therefore, both the increase in MAP and the pressure gradient across the clip were greater in the 1K1C rats at every clip size.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Role of the renal nerves in one-kidney, one clip hypertension in rats.

The effects of renal denervation on the onset and maintenance of one-kidney, one clip Goldblatt (1K1C) hypertension were determined. Renal denervation was performed at the time of 1K1C surgery, and was repeated at 3-week intervals to prevent renal nerve regeneration. Denervation delayed the onset of 1K1C hypertension by about 5 weeks, but the final hypertensive state was unaltered. Mean arterial pressure (MAP) averaged 196 +/- 11.4 mm Hg in six rats at 9 weeks after 1K1C surgery and 194 +/- 11.3 mm Hg in eight renal-denervated rats at this time. The delay in the development of 1K1C hypertension following renal denervation could not be explained by interference with renin release. This delay in the development of hypertension could be prevented, however, in renal-denervated 1K1C rats by substituting saline for the drinking water. Two weeks after 1K1C surgery and a high sodium diet, MAP averaged 164 +/- 6.4 mm Hg in eight rats rats with intact renal nerves and 173 +/- 4.8 mm Hg in nine renal-denervated rats. Intact renal nerves are not necessary for the development or maintenance of 1K1C hypertension. Renal denervation delays development of 1K1C hypertension, possibly by delaying the ability of these rats to retain sodium.

Animals↗