Knud D. Knudsen

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Thyroid function was evaluated in the Marshallese who were accidentally exposed to fallout-containing radioiodine isotopes in 1954. Measurements of thyrotrophin (TSH, thyroid-stimulating hormone) levels and free thyroxine (T4) index (FT4I) have revealed that, among 86 persons exposed on Rongelap and Ailingnae atolls, 14 have shown evidence of thyroid(More)
Parabiosis has been found to modify the expected blood pressure response of rats from two strains with opposite genetic propensities for experimental hypertension. When a member from one strain was united in parabiosis with a member from the other and both were maintained on high NaCl diet, the rat from the strain ordinarily resistant to it rapidly(More)
Two strains of rats with opposite, genetically determined predispositions to hypertension were compared. Rats from the hypertension-prone strain had significantly lower plasma and kidney renin activities than did rats from the hypertension-resistant strain. Although renin activities were modified by NaCl intake and blood pressure, significant differences(More)
A strain of rats that will predictably develop experimental hypertension by means of different techniques was used to study NaCl-induced hypertension. Observations were continued for 1 year after weaning unless death intervened. Among groups of rats on 0.4, 1, 2, 4, and 8% NaCl chow, respectively, blood pressures generally rose as dietary NaCl increased.(More)
TWO STRAINS OF RAT HAVE BEEN DEVELOPED BY SELECTIVE BREEDING: one strain (R rats) is resistant to salt hypertension, the other strain (S rats) is highly susceptible. The inheritance of these traits has been explored in the first (F(1)) and second (F(2)) generation of crossbred rats and in backcrosses between parent and first filial (F(1) x R, F(1) x S)(More)
I n experimental hypertension due either to high salt in take or to renal manipulat ions, we repor ted previously tha t rats from a s train with a genetic predisposit ion to hyper tension produced a humoral factor which was t ransmit table in parabiosis and induced hypertension in rats genetically resistant to this condition. We surmised tha t the factor is(More)
There is considerable evidence which can be interpreted to indicate a familial trend in human essential hypertension (1-5). A familial disease could be due exclusively to common environmental factors, exclusively to common genetic patterns, or to an interaction of the two. For some years we have been exploring the effects of chronic excess salt ingestion in(More)
In a genetically hypertension-prone (S) strain of rats it was observed previously that males generally developed hypertension more rapidly on a high salt diet than did females although final pressure ultimately were similar in both sexes. A genetic study had shown that there was no sex-linkage involved in setting blood pressure levels, so it was thought(More)