SUMMARY In a study of the effects of K + in stroke prone spontaneously hypertensive rats, adding K + to normal chow was found to reduce the mortality from 83% to 2%, a 98% reduction. An 86% reduction in mortality occurred even when blood pressure was virtually equal in the two stroke prone spontaneously hypertensive groups being compared. Dietary K + supplements also reduced mortality in hypertensive Dahl salt-sensitive rats from 55% to 4%, a 93% reduction. There was an 87% reduction in mortality even when blood pressure was equal in the Dahl salt-sensitive groups being compared. The added dietary K + decreased blood pressure moderately in stroke prone spontaneously hypertensive rats and modestly in Dahl salt-sensitive rats, which probably contributed to the reduced death rate. More importantly, however, the added K + seemed to prevent severe lesions in cerebral arteries and deaths even when blood pressure lowering was eliminated as a protective factor. In another group of stroke prone spontaneously hypertensive rats, there was a 40% incidence of cerebral hemorrhage in surviving rats not receiving K + supplements and no incidence of cerebral hemorrhage in similar surviving rats receiving K + supplements, which suggests that K + supplements confer protection against brain hemorrhage. ( other mammals living in the wild and presumably eating the large amount of K + in natural foods. In a recent study we explored the possibility that adding K + supplements to the diet would reduce the renal lesions in hypertensive, salt-fed Dahl salt-sensitive rats (DS).5 -6 They were fed a standard Punna chow with 4% added NaCl for 24 weeks. This diet produced the expected hypertension 5 and the expected lesions in the tubules and arterioles of the kidney. Several rats also had 1.36% K + added to the diet over the entire 24 weeks of the study. The addition of K + did not lower the blood pressure; however, renal tubular lesions in the renal cortex were reduced by 50%, in the outer medulla by 30%, and in the inner medulla by 44%.6 Thus, the addition of K + provided a protective effect of major proportions against renal tubular lesions without lowering the blood pressure. Furthermore, the hypertension had produced the expected 38% thickening of the walls of the renal arterioles, but when K + supplements were added to the diet (1.36% added K), the thickness of the arteriolar walls was reduced by 20 to 30% even though the blood pressure was not lowered.
A high NaCI diet can raise blood pressure in both susceptible people and in susceptible animals, and the mechanisms are probably quite similar for both humans and animals. The possibly harmful effects of a high NaCI diet are not unexpected since both prehistoric man and mammals evolved in a low NaCI world. Evolutionary forces molded mammals to adapt well to a low sodium intake; the modern high NaCI intake goes "against the grain" of this adaptation. The high NaCI diet can cause premature mortality by raising blood pressure in susceptible people. We have new evidence that in a hypertensive setting, a high NaCI diet can increase mortality even though it does not cause a further rise of blood pressure. Multiple small cerebral infarcts are a partial cause of this excess mortality. Recent evidence also indicates that a high potassium diet reduces the rise of blood pressure caused by a high NaCI diet, whereas a low normal potassium intake encourages an NaCI-induced rise of blood pressure. It is the combination of kidneys that tends to retain NaCI together with a high NaCI intake that produces a rise in blood pressure. This combination tends to cause NaCI retention, which can trigger a rise in blood pressure in susceptible humans and animals. Such a rise in blood pressure can augment renal NaCI excretion and regain the previous NaCI balance. In the Dahl salt-sensitive (DS) rat, there are several renal abnormalities that would tend to encourage sodium retention. By analogy, renal "abnormalities" are probably present in people susceptible to hypertension. When renal dysfunction plus a high NaCI diet tend to cause NaCI retention, how is this NaCI signal perceived? Evidence indicates that one signal is probably an excess of extracellular fluid volume registering in the brain. Ablation of central nervous system structures around the third brain ventricle influences NaCI hypertension. A hydrocephalus of the third and lateral brain ventricles prevents 60% of an NaCI-induced rise in blood pressure in DS rats and reduces mortality by 90%. Such observations suggest that structures near the third brain ventricle are important for receiving the excess NaCI signal. (Hypertension 1991;17[suppl I]:I-52-I-58) H uman essential hypertension appears to be a salt-related disease. Low salt societies have no hypertension at all. Yet if such people migrate to a high salt society, about 30% will show a significant rise in blood pressure. Similarly, there are certain strains of rat that also develop a significant rise in blood pressure when placed on a high salt diet. Dogs with reduced renal mass are also susceptible to salt-induced hypertension. It is very likely that the mechanisms that cause a high NaCI intake to raise blood pressure in animals would be the same mechanisms that cause a high NaCI diet to raise blood
High NaCI diets often increase blood pressure and thereby accelerate lesions in arterial walls. Could high NaCI diets increase arterial lesions without raising blood pressure? To test this, 100 uninephrectomized Dahl salt-resistant (DR) rats (highly resistant to NaCI hypertension) were administered deoxycorticosterone acetate (DOCA) (250 mg/kg) in silicone implants and drinking water containing 1% NaCI for 6 weeks. Then the DOCA and saline were removed, and the rats were allowed to recover for 4 weeks. Intra-arterial mean blood pressures on all rats allowed division of the rats into two matched groups, each group with an average blood pressure of 160 mm Hg. One group continued on a 03% NaCI diet, whereas the other group began an 8% NaCI diet for 8 weeks. After 5 weeks on these two diets, the intra-arterial blood pressure averaged 158 mm Hg in both groups. Thus, the 8% NaCI diet produced no further increase in blood pressure in the DR rats. Nevertheless, after 8 weeks on the 8% NaCI diet, 53% of the rats (26 of 49) had died; whereas in the group on the 03% NaCI diet, not one rat (0 of 51) had died (p<0.000001). After 7 more weeks on the 8% NaCI diet, all the rats in this group had died. The chief cause of death in the group of rats on the 8% NaCI diet was likely cerebral infarction because small cerebral infarcts were observed in rats that died on this diet Uremia, congestive failure, cerebral hemorrhage, and arrhythmia were not likely causes of death. Thus, it appears that a high NaCI diet in mildly hypertensive DR rats can greatly accelerate cerebral arterial disease with brain infarction and very high mortality, even when the high NaCI diet causes no increase in blood pressure whatsoever. Seemingly, salt's infamy goes beyond blood pressure. It is even possible that "salt-resistant" hypertensive humans could reduce vascular complications by adhering to a low NaCI diet (Hypertension 1990;15:900-903) A mbard and Beaujard 1 showed in 1904 that / \ some hypertensive patients will have a large J. \ . decrease in blood pressure when they reduce the amount of NaCI in their diets. With dietary intakes as low as 10 meq/day, investigators such as Kempner 2 and Watkin et al 3 found that a sizable percentage of hypertensive patients would show a decrease in blood pressure. Even modest reductions in NaCI intake of approximately 60-100 meq/day can lower blood pressure in many hypertensive patients. -5 For this reason, most hypertensive patients are advised to limit their NaCI intake to lower blood pressure, which then reduces hypertensive complications. Recent well-controlled studies have confirmed that reducing the level of NaCI intake to 50 meq/day is accompanied by a decrease in blood pressure, 6 and resuming the higher NaCI intake is associated with a return of blood pressure to the previous higher levels.Several very short-term studies, however, have shown that when hypertensive patients are placed on a low NaCI diet for 5 days and are then switched for a second 5 days to a high NaCI diet, not all of the hypertensive pa...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.