Lorraine Tassinari

Differential Development of Salt-Induced and Renal Hypertension in Dahl Hypertension-Sensitive Rats After Neonatal Sympathectomy

Rats with a genetic susceptibility to salt hypertension were given repeated neonatal injections of guanethidine. Vascular reactivity and tissue catecholamine concentrations indicated that a peripheral sympathectomy had been produced. Chemically sympathectomized rats had lower blood pressure than controls while fed a diet containing 0.4% NaCl. Furthermore, the dramatic rise in blood pressure exhibited by control rats fed a diet containing 8.0% NaCl was completely absent in sympathectomized rats similarly fed. The absence of salt-induced hypertension was observed regardless of whether the animals were anesthetized with ether or pentobarbital or had the blood pressures determined in an unanesthetized state. Finally, two-kidney Goldblatt hypertension did develop in sympathectomized rats, but to a level below intact rats similarly treated.

Hypertension and Death from Consumption of Processed Baby Foods by Rats

Summary Some processed baby foods were lethal to hypertension-prone rats. Among 25 rats from a genetically hypertension-prone strain fed solely on such baby foods, all developed significant hypertension (averaging 180–190 mm Hg in the last 3 months of observation), 12 died, and 2 others became seriously ill during the 8 months of study. In contrast, the IS control rats maintained on a low sodium chow were all alive and their average pressure at 8 months was 141.4 mm Hg. Considerable evidence suggests that the difference in response of test and control groups was due to the high NaCl content added to the processed baby foods. This added NaCl is unnecessary for the health of infants. It may contribute to the later development of hypertension in genetically predisposed individuals.

Blood lactic acid in rats and men: comparison of normo- and hypertensive individuals.

Summary Among rats from two strains with opposite genetic predisposition to experimental hypertension, lactic acid concentrations in the blood were equivalent. Lactic acid concentration could not be correlated with the presence or absence of overt hypertension. Blood lactic acid values in these rats were comparable to those in man. In confimation of reports by others, among humans the average blood lactic acid value of a small group of hypertensive patients was increased as compared with the average value of an appropriate control group. Lactic acid concentration in all samples increased when the blood was allowed to stand at room temperature. This increase was larger in rat blood than in human samples and, in man, it increased faster in hypertensive patients than in controls. It is proposed that these differences may reflect ion transport activity by the red cell, and that the difference between man and rat is related to the dissimilar surface-to-volume ratio of the cells.