The form of sodium-calcium competition at the frog myoneural junction.

The times required for a steady rate of miniature end-plate potential discharge to be reached in response to changes in extracellular [K(+)], [Na(+)], and [Ca(++)] have been measured. In the presence of 15 mM KCl, Ca(++) raises and Na(+) lowers the steady-state mepp frequency; but the depressive effect on Na(+) is not specific: Li(+) can replace Na(+) to a large extent. Mepp frequency has been found to depend on the ratio of [Ca(o) (++)]/[Na(o) (+)]. It is assumed that in the steady state, intracellular sodium will change when extracellular sodium is changed. Because both intracellular and extracellular sodium at motor nerve endings affect acetylcholine release, it is proposed that mepp frequency depends on the ratio [Ca(o)] [Na(i)](2)./[Na(o)](2) Two models are proposed. Firstly, to account for the action of sodium and calcium a carrier is postulated for which Ca(++) and Na(+) compete. The carrier determines a maximum level of intracellular Ca(++) far lower than predicted by the Nernst equation for Ca. Secondly, to account for activation of acetylcholine release by a small influx of Ca(++), the ions are presumed to enter the nerve ending in a two stage process through a small intermediate compartment and to act on the acetylcholine release site in this region rather than after entering directly into the cell.

Fat induced hypertension in rabbits. Effects of dietary fibre on blood pressure and blood lipid concentration.

Rabbits were fed diets containing 200 g.kg-1 coconut oil, palm oil, or safflower oil. Some of the diets also contained 200 g.kg-1 cellulose. The blood pressure was measured daily by a non-invasive technique for the 2 month duration of the experiment. Blood samples were drawn after an overnight fast at intervals during the experiment and analysed for lipids. Blood pressure was always increased by a fat-enriched diet. This effect was diminished and delayed by adding cellulose to the diets, though cellulose itself had no effect on the blood pressure in the absence of fat. There was a modest negative correlation between fasting serum triglyceride concentration and the blood pressure in animals fed fat enriched diets without added cellulose, but not in animals fed diets containing both fat and cellulose. These results coupled with those of Wright, Burstyn and Gibney may serve partly to explain the observation that vegetarians have lower blood pressures than omnivores, the latter consuming diets which are relatively richer in fats and poorer in fibre than the former.

Effects of three fat-enriched diets on the arterial pressure of rabbits.

Rabbits were fed diets enriched with proprietary edible fats for 5 weeks, raising the fat content of their diet from 4% to 23%. The diet enriched with animal fat caused a 13.5% rise in arterial pressure. The diet enriched with vegetable oil caused an 8.5% rise in arterial pressure. The diet enriched with butter caused an initial rise of 10% decreasing to 6% by the fifth week. Histological examination of the carotid and renal arteries, and aorta revealed no changes in connective tissue or lipid content as compared with those of control animals. It is concluded that changes in arterial pressure can occur after ingestion of excess dietary lipid, and that these changes are not confined to any class of lipid, or related to its properties as an atherosclerotic agent.

Milk, serum cholesterol, and the Maasai. A hypothesis.

The Maasai of East Africa have been found to have low serum concentrations of cholesterol and a low incidence of cardiovascular disease in spite of apparently very high milk intakes. On that basis it has been frequently suggested that milk contains a "hypocholesterolaemic factor". The hypocholesterolaemia of the Maasai had also been attributed to a genetic adaptation. We feel that the milk intakes reported for the Maasai are excessively high and that the low incidence of cardiovascular diseases and low levels of serum cholesterol may be adequately explained by their variable and generally low energy intakes.

Sodium and water metabolism under the influence of prolactin, aldosterone, and antidiuretic hormone.

1. Rabbits were placed in metabolism cages in order to measure their intakes of food, water, and sodium chloride (as 1% saline solution), and to measure urinary and faecal excretion of sodium, potassium, and water. 2. Antidiuretic hormone (0.2 i.u./day) caused a reduction in urine volume and no change in sodium excretion. There was full compensatory reduction in water intake so that no accumulation of water occurred. 3. Aldosterone (4 mg/da) caused a reduction in renal sodium excretion for 1--2 days. The saline intake was reduced, though this was insufficient to prevent some sodium accumulation. 4. Renal mineralocorticoid 'escape' resulted in a large increase in sodium excretion at the end of the aldosterone treatment period. This was fully compensated through increased saline intake, and balance was maintained. 5. Prolactin (200 i.u./day) caused a reduction in urine volume and in renal sodium excretion and since there were no compensatory changes in water and sodium intake, this led to substantial accumulation of both water and sodium. 6. The effects of smaller doses of both aldosterone and prolactin were investigated and found to be similar but smaller. 7. It is suggested that whereas prolactin may have little or no role to play in the sodium homoeostasis of the normal animal, the hormone may well be responsible for the substantial increase in body fluids in pregnancy.

Dietary fibre and blood pressure.

Ninety-four volunteers participated in a three-day weighed dietary survey and had their blood pressures measured once. They were classified according to their fibre intake. Subjects with a high-fibre intake were found to have lower mean blood pressures than those with a low-fibre intake. Forty-two of the volunteers further participated in a group of experiments. Those eating a high-fibre diet decreased their dietary fibre, and those eating a low-fibre diet increased their dietary fibre. The first group (11 subjects) showed increased mean blood pressures after four weeks of eating the experimental diet. The last group (31 subjects) showed decreased mean blood pressures after four weeks of eating the experimental diet. The 11 subjects consuming the low-fibre experimental diet showed a decrease in mean blood pressure when some of the saturated fat in their diet was replaced by polyunsaturated fat. A similar substitution carried out by 14 of the subjects consuming the high-fibre experimental diet also resulted in decreased mean blood pressure, but this was not statistically significant. Twelve more volunteers, with hypertension, were all found to have low-fibre diets. They consumed a high-fibre diet for a six-week experimental period, but their mean blood pressures did not decrease significantly; individual recordings varied substantially during this period.It is suggested that differences in the type and quantity of dietary fibre and fat may be responsible for the lower mean blood pressures of groups of vegetarians compared with similar groups of non-vegetarians.