Biomedical subjects
Publications and source records attributed to E C Wallace.
During a six-month period five patients presented to The Royal Belfast Hospital for Sick Children between the ages of three weeks and three years with recurrent vomiting and failure to thrive. All were diagnosed as having organoaxial malrotation of the stomach by barium meal examination. Symptoms were refractory to conservative management but combined gastropexy and fundoplication was successful in all cases.
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1. Chronic two-kidney, one-clip hypertensive rats were infused with captopril for 5 days and the daily variability of blood pressure compared with that for both hypertensive rats infused with glucose and normotensive animals. 2. Blood pressure was measured continuously using a computer data collecting system. 3. Normotensive animals showed a stable level of arterial pressure throughout each 24 h period with troughs occurring when they slept during the daytime. 4. Hypertensive animals given glucose had an enhanced diurnal rhythm of blood pressure compared with normotensive rats, with peaks occurring during periods of activity at night as well as troughs when they slept during the day. 5. Hypertensive rats given captopril retained this enhanced pressure variability, in spite of the fact that blood pressure was significantly lower and angiotensin II was suppressed. 6. These results suggest that angiotensin II is not involved in the increased blood pressure variability of renal hypertension and that some other irreversible mechanism is responsible.
The effect of changes in dietary sodium intake and of DOC hypertension on plasma atrial natriuretic peptide (PANP), and affinity (Kd) and number (Bmax) of vascular atrial natriuretic peptide binding sites was studied in the rat. There was no difference in PANP between rats on a high or low sodium intake [33.2 +/- 13.9 versus 30.7 +/- 17.3 (s.d.) fmol/ml], Kd [21.1 +/- 2.7 versus 19.7 +/- 4.5 (s.d.) pmol/l] or Bmax [14.8 +/- 1.6 versus 12.6 +/- 1.8 (s.d.) fmol/mg], respectively. In DOC hypertensive rats, PANP was increased compared with control animals [66.1 +/- 32.4 versus 26.4 +/- 9.9 (s.d.) fmol/ml, P less than 0.05] and there was apparent receptor down-regulation [Bmax 7.7 +/- 1.6 versus 19.7 +/- 3.5 (s.d.) fmol/mg, P less than 0.05] with no change in affinity [Kd 15.6 +/- 3.9 versus 18.3 +/- 3.2 (s.d.) pmol/l]. Down-regulation was confirmed when the membrane-bound enzyme 5'-nucleotidase, rather than protein, was used as an index of receptor number. These results suggest that in the rat, atrial natriuretic peptide (ANP) may be important in regulating cardiovascular homeostasis only following non-physiological alterations in sodium and volume status.
The effect on blood pressure (BP) of acute and chronic suppression of angiotensin (ANG) II was studied in the two-kidney, one clip hypertensive rat. Conscious, chronically catheterized rats were given a bolus injection of captopril (2.5 mg/kg) followed by a chronic infusion of either dextrose or captopril (1 mg/kg per h) lasting 5 days. Blood pressure was measured continuously by a computer technique. Following the acute injection of captopril, arterial BP fell from 165.1 +/- 19.4 mmHg (mean +/- s.d.) to a minimum of 137.6 +/- 23.3 mmHg after 15 min. Twelve hours after starting the chronic infusion of captopril, BP fell to a minimum of 112.5 +/- 19.4 mmHg. This was significantly lower than that after the acute injection of captopril. Blood pressure remained lower throughout the 5-day infusion ranging, on the 5th day, from 122.1 +/- 23.4 to 136.0 +/- 30.2 mmHg. In contrast, BP continued to rise in rats given dextrose chronically ranging, on the 5th day, from 163.6 +/- 23.8 to 180.4 +/- 22.5 mmHg. Both the fall in pressure after acute captopril and that after chronic captopril were related to pre-treatment levels of plasma renin concentration. These results suggest that in the two-kidney, one clip hypertensive rat ANG II, in addition to its acute vasoconstrictor property, contribute to the hypertension through a secondary effect, the mechanism of which is as yet uncertain.
A sensitive and specific radioimmunoassay for arginine vasopressin was used to compare the relative importance of changes in plasma osmolality, angiotensin II and dopamine in the regulation of vasopressin secretion in man. One hour after water loading plasma vasopressin fell from 0.40 to 0.06 pmol/l, while 8 h and 24 h fluid restriction resulted in a rise of vasopressin from 0.29 to 0.54 and 1.37 pmol/l respectively. In contrast neither dietary sodium deprivation, when plasma angiotensin II increased 5-fold, nor dopamine infusion, at a rate which increased circulating dopamine levels up to 244-fold, had any effect on basal plasma vasopressin values. These results confirm that, under physiological conditions, osmoregulation is the major mechanism controlling vasopressin release and suggests that circulating angiotensin II and dopamine have no significant part to play.
Immediately after clipping, plasma renin and angiotensin II concentrations are raised in the two-kidney, one clip rat. Plasma renin and angiotensin II fall to relatively low levels between two and five weeks after operation, while blood pressure continues to rise. An experiment was carried out to determine whether complete suppression of angiotensin II during this two- to five-week period would have any effect on the development of hypertension. Captopril infused chronically (2 mg/kg/h) for up to 20 days completely prevented the rise in mean blood pressure [110.8 +/- 17.9 at day 0 compared to 88.3 +/- 8.4 (s.d.) mmHg at day 20] seen in an equivalent control group infused with dextrose (109.2 +/- 11.6 at day 0 compared to 131.7 +/- 23.6 mmHg at day 20). Preinfusion values for plasma renin and angiotensin II concentration were within the upper half of the range found for sham-operated normal rats. These findings would suggest that while the plasma levels of angiotensin II are low in relation to those seen immediately after clipping, they are still raised in comparison with normal sham-operated rats; this may contribute to the development of hypertension by a slow chronic, rather than an acute, effect.
1. Blood pressure, renin concentration and angiotensin II were measured in unanaesthetized two-kidney one-clip hypertensive rats at 1 and 2 days, at weekly intervals up to 10 weeks and at 15 and 20 weeks after clipping. 2. Compared with values in sham-operated rats, renin and angiotensin II were initially increased at 1-2 days but were then suppressed between 2 and 4 weeks to levels similar to that found in sham-operated rats. Between 5 and 20 weeks renin and angiotensin II increased again to high levels. 3. There was a significant correlation between angiotensin II and blood pressure in acute rats 1-2 days after clipping (P less than 0.05) and in chronic rats 8-20 weeks after clipping (P less than 0.001). There was no difference in the slope of the regression lines but the regression line for the chronic rats was shifted upwards in a parallel manner. 4. The acute hypotensive response (-20.3 +/- SD 24.9 mmHg) in 26 chronic rats given converting enzyme inhibitor was related to the basal renin and angiotensin II levels and followed the slope of the angiotensin II/blood pressure regression line for all chronic rats. Only one out of 26 rats reduced its blood pressure to normal levels. 5. In 12 rats at 4 weeks after clipping, when blood pressure was elevated but angiotensin II was suppressed, there was only a small fall in blood pressure (-7.1 +/- SD 7.2 mmHg). This also followed the angiotensin II/blood pressure regression line for chronic rats but at the lower end. Blood pressure again was not reduced to normal. 6. These results suggest that renin and angiotensin II are increased up to 20 weeks after clipping, that there is no change in the net vascular responsiveness to endogenous angiotensin II at any stage in this experimental model and that the acute effect of angiotensin II is determined solely by its position in the same dose-response curve. Also with the exception of 1-2 days immediately after clipping the acute effect of angiotensin II plays only a minor, though variable, role in the hypertension and that some other mechanism, as yet undetermined, is of greater importance and begins to have an effect as early as 2 weeks after clipping.
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