X-Message-Number: 9402 Date: Fri, 3 Apr 1998 11:28:41 -0800 (PST) From: Doug Skrecky <> Subject: Could need for cryonics be delayed by taking NoSalt? (KCL) Citations: 1-9 *************************** <1> Unique Identifier 97174895 Authors Tobian L. Institution Department of Internal Medicine, University of Minnesota Hospital, Minneapolis 55455, USA. tobia001:maroon.tc.umn.edu Title Dietary sodium chloride and potassium have effects on the pathophysiology of hypertension in humans and animals. [Review] [21 refs] Source American Journal of Clinical Nutrition. 65(2 Suppl):606S-611S, 1997 Feb. Abstract A diet high in NaCl can raise blood pressure in susceptible people and animals, probably by similar mechanisms. The possibly harmful effects of a high-NaCl diet are not unexpected because both prehistoric humans and mammals evolved in a low-NaCl environment. Evolutionary forces molded mammals to adapt well to a low sodium intake; modern high NaCl intakes go against this adaptation. A high-NaCl diet can cause premature mortality by raising blood pressure in susceptible people. We have new evidence that in hypertension, a high-NaCl diet can cause a great increase in mortality even though it does not cause a further blood pressure rise, partially because of multiple small cerebral infarcts. Recent evidence also indicates that a high-potassium diet reduces the rise of blood pressure caused by a high-NaCl diet, whereas a low-normal potassium intake encourages an NaCl-induced blood pressure rise. The combination of a tendency by the kidneys to retain NaCl together with a high NaCl intake can produce a blood pressure rise. This combination tends to cause NaCl retention, which can trigger blood pressure rises in susceptible humans and animals. Such blood pressure rises can augment renal NaCl excretion and regain the previous NaCl balance. In Dahl salt-sensitive rats several renal abnormalities encourage sodium retention. By analogy, renal "abnormalities" are probably present in people susceptible to hypertension. [References: 21] <2> Unique Identifier 96160850 Authors Ishimitsu T. Tobian L. Sugimoto K. Lange JM. Institution Department of Medicine, University of Minnesota, USA. Title High potassium diets reduce macrophage adherence to the vascular wall in stroke-prone spontaneously hypertensive rats. Source Journal of Vascular Research. 32(6):406-12, 1995 Nov-Dec. Abstract Our previous study demonstrated that high potassium (K) diets reduce stroke mortality in stroke-prone spontaneously hypertensive rats (SHRsp) even when the blood pressure is not lowered. On the other hand, macrophage infiltration into the vascular wall is known to play an important role in the development of arterial lesions. In this study, in vivo and in vitro experiments were performed to examine the effect of high K diets on macrophage adherence to the vascular wall in SHRsp rats. In the in vivo study, 51Cr-labelled macrophages, collected from the peritoneal cavity, were injected intravenously to SHRsp rats fed 6% high NaCl diets containing either normal 0.5% K or high 2.1% K, and, 45 min later, the rats were perfused with buffered saline to remove blood. Radioactivity from macrophages in the aorta was 40% lower in the high K SHRsp than in the normal K SHRsp (p < 0.002), and the brain of high K SHRsp also showed a 52% lower macrophage radioactivity than that of normal K SHRsp (p < 0.007). Although the mean blood pressure was slightly lower in the high K diet group than in the normal K diet group (167 vs. 184 mm Hg), these differences remained still prominent even when we compared groups with matching blood pressures; -33% for the aorta (p < 0.02) and -55% for the brain (p < 0.02). In the in vitro study, the aortas of SHRsp rats similarly fed on normal or high K diet were excised and mounted in a perfusion chamber. They were perfused with labelled macrophages at normotensive or hypertensive pressure. In normal K SHRsp, macrophage radioactivity remained in the washed aorta was 158% higher in high perfusion pressure group than in normal pressure (p < 0.002). However, they did not significantly differ between two perfusion pressures in high K SHRsp. These results indicate that high K diets reduce endothelial injuries which allow adherence and infiltration of macrophages into the vascular wall of hypertensive animals, and thereby contribute to the reduction of vascular lesions and stroke mortality. <3> Unique Identifier 92096351 Authors Ganguli M. Tobian L. Sugimoto T. Institution Renal and Hypertension Section, University of Minnesota Hospital and School of Medicine, Minneapolis 55455. Title Deleterious effects of high magnesium diets and beneficial effects of high potassium diets in hypertensive stroke-prone rats. Source Magnesium Research. 3(4):255-61, 1990 Dec. Abstract The effect of varying amounts of dietary magnesium (Mg) in conjunction with potassium (K) on hypertension and stroke mortality in hypertensive stroke-prone (SHRsp) rats was studied. These results show that high K (2.1%) diets strongly protect against stroke mortality and rises of blood pressure, while high Mg (0.26%) diets appeared to increase stroke mortality and accelerate the rise of blood pressure in SHRsp rats. Similarly, medium high (1.3%) levels of K in the diet significantly reduced blood pressure and stroke mortality but not nearly as much as the 2.1% K in the high K diet. <4> Unique Identifier 90152840 Authors Volpe M. Camargo MJ. Mueller FB. Campbell WG Jr. Sealey JE. Pecker MS. Sosa RE. Laragh JH. Institution Department of Medicine, Cornell University Medical College, New York, New York. Title Relation of plasma renin to end organ damage and to protection of K+ feeding in stroke-prone hypertensive rats. Source Hypertension. 15(3):318-26, 1990 Mar. Abstract We studied the effects of regular diet (0.35% NaCl/1.1% potassium), high sodium diet (4% NaCl/0.75% potassium), or high sodium and high potassium diet (4% NaCl/2.11% potassium) on blood pressure, plasma renin activity, renal and cerebrovascular lesions, and incidence of stroke and mortality in male stroke-prone spontaneously hypertensive rats (SHRSP). In the first 4 weeks, the rise in blood pressure was higher in high NaCl than in high NaCl/high potassium or regular diet groups. However, by 8 and 12 weeks, the blood pressure in all three groups was similar. After 4 weeks of diet, plasma renin activity was similar in the three groups (3.4 +/- 0.8, 4.1 +/- 0.9, and 5.2 +/- 1.6 ng/ml/hr, in high NaCl, high NaCl/high potassium, and regular diet groups, respectively) and were not related to sodium excretion. After 8 weeks, plasma renin activity was significantly increased only in the high NaCl group (13.7 +/- 3.7 ng/ml/hr), and by 12 weeks plasma renin activity was significantly higher in the high NaCl group (25.3 +/- 3.6 ng/ml/hr) than in the high NaCl/high potassium (11.1 +/- 2.9 ng/ml/hr) or in the regular diet (7.8 +/- 4.6 ng/ml/hr) groups. Moderate to severe renal vascular lesions were first detected in the high NaCl group by 8 weeks of diet. At 12 weeks, renal vascular damage index (RVDI), estimated histologically, was significantly higher in the high NaCl group (RVDI = 79 +/- 14) than in the high NaCl/high potassium (RVDI = 40 +/- 11) and regular diet (RVDI = 7.8 +/- 4.6) groups.(ABSTRACT TRUNCATED AT 250 WORDS) <5> Unique Identifier 90027590 Authors Ganguli M. Tobian L. Sugimoto T. Institution Department of Medicine, University of Minnesota Hospital and School of Medicine, Minneapolis 55455. Title High magnesium diets increase blood pressure and enhance stroke mortality in hypertensive SHRsp rats. Source American Journal of Hypertension. 2(10):780-3, 1989 Oct. Abstract The effect of varying amounts of dietary magnesium in conjunction with potassium (K) on hypertension and stroke mortality in hypertensive stroke prone (SHRsp) rats was studied. These results show that high K (2.1%) diets strongly protect against stroke mortality and rises of blood pressure, while high magnesium (Mg) (0.26%) diets appeared to increase stroke mortality and accelerate the rise of blood pressure in SHRsp rats. Similarly, medium-high (1.3%) levels of K in the diet significantly reduced blood pressure and stroke mortality but not nearly as much as the 2.1% K in the high K diet. <6> Unique Identifier 87090202 Authors Khaw KT. Barrett-Connor E. Title Dietary potassium and stroke-associated mortality. A 12-year prospective population study. Source New England Journal of Medicine. 316(5):235-40, 1987 Jan 29. Abstract Hypertension is the most important known risk factor for stroke. Clinical, experimental, and epidemiologic evidence suggests that a high dietary intake of potassium is associated with lower blood pressure. In hypertensive rats, a high intake of potassium is reported to protect against stroke, even though blood pressure is not affected. We examined the relation between the 24-hour dietary potassium intake at base line and subsequent stroke-associated mortality in a population-based cohort of 859 men and women (aged 50 to 79 years) in Southern California. After 12 years, 24 stroke-associated deaths had occurred. The relative risks of stroke-associated mortality in the lowest tertile of potassium intake, as compared with that in the top two tertiles combined, were 2.6 (P = 0.16) in men and 4.8 (P = 0.01) in women. In multivariate analyses, a 10-mmol increase in daily potassium intake was associated with a 40 percent reduction in the risk of stroke-associated mortality (P less than 0.001). This effect was independent of other dietary variables, including the intake of calories, fat, protein, fiber, calcium, magnesium, and alcohol. The effect was also apparently independent of known cardiovascular risk factors, including age, sex, blood pressure, blood cholesterol level, obesity, fasting blood glucose level, and cigarette smoking. These findings support the hypothesis that a high intake of potassium from food sources may protect against stroke-associated death. <7> Unique Identifier 87001705 Authors Tobian L. Title High potassium diets markedly protect against stroke deaths and kidney disease in hypertensive rats, a possible legacy from prehistoric times. Source Canadian Journal of Physiology & Pharmacology. 64(6):840-8, 1986 Jun. Abstract Male spontaneously hypertensive stroke-prone (SHRsp) rats were fed 4% NaCl diets containing either 0.75% (normal) K or 2.11% (high) K, starting at 6 weeks of age. After 8 months on these diets, 40 out of 58 SHRsp rats on the 0.75% K diet had died (69% mortality) versus 2 dead out of 95 on the 2.11% K diet (2% mortality), a 97% reduction in mortality, p less than 0.00001. After 20 weeks on the diets, the daytime and nighttime blood pressures of each rat were measured intraarterially under light ether anesthesia. Using these accurate blood pressures, we selected two groups precisely matched for blood pressure. One matched SHRsp group (BP 182) ate the 0.75% K diet and 30 out of 47 rats died (64% mortality). The other matched SHRsp group (BP 182) ate the 2.11% K diet and 2 out of 35 died (6% mortality), a 91% reduction of mortality, p less than 0.0001. Seemingly, this striking reduction in mortality rate with the 2.11% high K diet does not depend on a lowering of blood pressure. High K diets do not change body Na or K. Dry weight of mesenteric arterioles was reduced 29% on the 2.11% K diet versus the 0.75% K diet (5.43 vs. 7.66 mg) (p less than 0.0001), indicating a greatly reduced hypertensive hypertrophy. In nine surviving SHRsp rats on the 0.75% K diet, 13 of 36 brain hemisphere slides (4 slides per rat) showed infarcts (36%). In 11 surviving SHRsp rats on the 2.11% K diet, 1 of 44 brain slides showed infarcts (2%), a 94.5% reduction, p less than 0.0001.(ABSTRACT TRUNCATED AT 250 WORDS) <8> Unique Identifier 85206200 Authors Tobian L. Lange J. Ulm K. Wold L. Iwai J. Title Potassium reduces cerebral hemorrhage and death rate in hypertensive rats, even when blood pressure is not lowered. Source Hypertension. 7(3 Pt 2):I110-4, 1985 May-Jun. Abstract 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. <9> Unique Identifier 85113389 Authors Messiha FS. Stocco DM. Title Effect of cesium and potassium salts on survival of rats bearing Novikoff hepatoma. Source Pharmacology, Biochemistry & Behavior. 21 Suppl 1:31-4, 1984. Abstract The effect of CsCl on the life span of female Sprague-Dawley rats innoculated with Novikoff's hepatoma was studied as a function of both pre- and post-treatment with CsCl and as a function of the inoculant dose. The effect of KCl on the CsCl treatment was also studied. Rats treated with CsCl for 12 consecutive days prior to or immediately after inoculation with 1.0 ml of viable hepatoma cell suspension showed an increase in mortality score from corresponding controls. Conversely, increases in the dose of the inoculant resulted in delaying the onset of toxicity in rats receiving the Cs-treatment after inoculation as evidenced by a decrease in mortality. Availability of KCl in drinking water ad lib further decreased total mortality when given alone but not when combined with CsCl. The results indicate a dose-dependent paradoxical effect of CsCl on Novikoff hepatoma cell toxicity and suggest a critical intercellular balance requirement between Cs+ and K+ on the effect studied. Rate This Message: http://www.cryonet.org/cgi-bin/rate.cgi?msg=9402