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Biomedical subjects

J Iwai

Publications and source records attributed to J Iwai.

At least 109 records · Page 6Linked to original sources
PubMed1977

Influence of thiazide on salt hypertension.

This study was undertaken to evaluate the effect of chronic diuretic therapy with chlorothiazide on the course of salt hypertension in hypertension-resistant (R) and hypertension-sensitive (S) strains of rats. Investigation of the effects of chlorothiazide on blood pressure, 24-hour urinary 24Na and aldosterone excretion, and plasma renin activity (PRA) produced the following observations: (1) Chlorothiazide failed to prevent the development of salt hypertension in S rats. (2) After 12 weeks, S rats on high salt puls chlorothiazide exhibited a rapid fall in blood pressure to levels indistinguishable from those of S rats on low salt. (3) Chlorothiazide significantly increased urinary 24Na excretion only in S rats on high salt (P less than 0.01). (4) Chlorothiazide significantly increased PRA and urinary aldosterone excretion in both strains on low or high salt diets (P less than 0.001). (5) Morbidity and mortality of salt hypertension were alleviated by chlorothiazide treatment. The unique aspect of this study is the finding that chlorothiazide did not abolish the hypertensiogenic action of salt in S rats.

Aldosterone↗
PubMed1976

Genetic predisposition and stress-induced hypertension.

When chronically exposed to an approach-avoidance conflict, rats with a genetic susceptibility to hypertension showed persisten elevations in systolic blood pressure, but rats with a genetic resistance to hypertension did not. Hence, psychic stress is selectively efficacious in producing hypertensive effects depending on genetic predisposition of the animal.

Animals↗
PubMed1970

Genetic influence on the renin-angiotensin system. Evidence for a renin inhibitor in hypertension-prone rats.

TWO STRAINS OF RATS WITH OPPOSITE GENETIC PROPENSITY FOR HYPERTENSION WERE TESTED FOR: (a) the sensitivity to injections of angiotensin and renin, and (b) the influence of their plasma on the reaction velocity of renin and its substrate in vitro. Intact hypertension-prone (S) rats on low salt had higher sensitivity to angiotensin and a lower sensitivity to renin than hypertension-resistant (R) rats. High NaCl diet did not change the response of the R rats to these injections, but increased the response to renin and angiotensin in intact S rats. Bilateral nephrectomy caused increased response to renin and a decreased response to angiotensin in the S rats, so that both strains were equivalent after bilateral nephrectomy. In vitro, plasma from intact S rats inhibited the activity of hog renin. Plasma from R rats showed no inhibition. The inhibitor disappeared after bilateral nephrectomy. It was speculated that renin inhibitor may be involved in the development of hypertension by increasing sensitivity to angiotensin and other hypertensinogenic stimuli.

Angiotensin II↗
PubMed1970

Effects of chronic excess salt ingestion. Inheritance of hypertension in the rat.

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) generations. Male F(1) rats had an average blood pressure close to the mid-parental (R and S) values, and the average of F(2) males was equivalent to that of F(1). Male offspring of F(1) with R, or F(1) with S also showed averages close to the respective mid-parental values. Female offspring showed deviations from this linear relationship, indicating a significant dominance in the female for the genes of normal blood pressure. A model of two autosomal, nonlinked diallelic loci, with a dominance deviation at one locus in the female, gave predictions with a reasonable agreement to the observed values. The same model also appeared compatible with human data if we assume a gene frequency of 0.13 for the hypertensinogenic allele on both loci. Random fluctuations in blood pressure, and incomplete homogeneity of parental strains permit several alternative models. The major conclusions are: that more than one locus is needed to explain the findings though as few as two loci may possibly suffice; the allelic effect seems additive in males, but there is a sex-determined influence on the expression in females; there is no consistent evidence for sex-linked inheritance. Furthermore, this model developed from the study of rats may provide a framework for analysis of human data.

Analysis of Variance↗
PubMed1969

Genetic influence on the development of renoprival hypertension in parabiotic rats. Evidence that a humoral hypertensinogenic factor is produced in kidney tissue of hypertension-prone rats.

Rats from two strains with opposite constitutional predisposition to hypertension were joined in parabiosis and one partner was nephrectomized. The influence of genetic factors and of diet on the blood pressures of the two classes of parabionts, operated and intact, indicated that renoprival hypertension occurred with equal frequency in rats from both strains; that the development of renoprival hypertension depended on the influence from an intact S partner, or on a high salt intake, or on both. A nephrectomized S rat developing renoprival hypertension did not induce high blood pressure in its intact R partner. In this respect renoprival hypertension differs from salt and renal hypertension. The findings are interpreted to mean that the hypertensinogenic agent specific for S rats is produced by S kidneys.

Analysis of Variance↗
PubMed1969

Effects of adrenalectomy on blood pressure in salt-fed, hypertension-prone rats. Failure of hypertension to develop in absence of evidence of adrenal cortical tissue.

In adrenalectomized, genetically hypertension-prone rats, a high degree of correlation was found between evidence of functioning adrenal tissue and the development of salt hypertension. There is considerable evidence that some rats have the capacity to regenerate functioning adrenal cortical tissue from accessory glands and microscopic rests, sometimes in remote locations. Therefore, the criteria for continued absence of adrenal function after surgical adrenalectomy are critical. In this study we used three tests to validate the presence, or absence, of adrenal function: (a) a biochemical test, the quantitative, serial measurement of plasma glucocorticoids in individual rats; (b) a physiological test, the ability to survive a virtually sodium-free diet; and (c) the anatomical search for histological evidence of adrenal cortical tissue. Among those animals that developed hypertension after adrenalectomy, the correlation between plasma steroid concentration and blood pressure was statistically significant. We suspect that this correlation exists only during the period when cortical tissue is regenerating; it does not exist among intact animals with and without hypertension induced by salt. It was concluded that some adrenocortical function is necessary for salt hypertension to develop. The evidence was insufficient to settle the question whether the action of corticosteroids is causative, or whether they play a supporting, although necessary, role for an extraadrenal hypertensinogenic factor to become manifest.

Adrenal Glands↗
PubMed1969

Genetic influence on the development of renal hypertension in parabiotic rats. Evidence for a humoral factor.

The effects of several renal manipulations including uninephrectomy, unilateral renal artery constriction, and a combination of these two (Goldblatt procedure) were studied in two strains of rats with opposite constitutional predispositions to experimental hypertension. The protective value of intact renal tissue to protect against hypertension was shown to be genetically determined. The Goldblatt procedure carried out on only one member of a parabiotic pair induced hypertension in this operated rat but significant hypertension developed in the intact partner only when the operated animal belonged to the strain predisposed to hypertension. It was speculated that there were qualitative differences in the pressor signals of the two strains of rats. In the strain genetically predisposed to hypertension there are at least two pressor principles: (a) one which is common to both strains, not transmittable via the parabiosis junction and presumably related to the renin-angiotensin system; and (b) a second which is specific for the hypertension-prone strain and can be transmitted through the parabiosis junction. This transmittable agent is probably identical with the factor that produces salt hypertension and is associated with the salt-excreting mechanism.

Angiotensin II↗
PubMedDate not supplied

Effects of sulfur dioxide and ozone on hypertension sensitive and resistant rats.

Two lines of Dahl rats, one resistant to salt-induced hypertension (DR) and one susceptible to salt-induced hypertension (DS) were subchronically exposed to SO2 (50 ppm, 6 hr/d, 5 d/wk for 31 weeks) or ozone (2.0 ppm, 6 hr/d, 5 d/wk for 20 weeks). Subgroups of rats were maintained on either high or low salt diets. In rats not expected to develop hypertension, exposure to SO2 caused a slight but consistent decrease in blood pressure. In DS rats on a high salt diet exposure to SO2 resulted in an increase in blood pressure over that of their air exposed counterparts. All exposure-related differences in blood pressure disappeared after the last exposure to SO2. Exposure to ozone was fatal to all DS rats, regardless of the amount of salt in the diet. The DR rats were more resistant to ozone, with most animals surviving the 20-week exposure. Ozone-exposed rats exhibited a decrease in both growth rate and blood pressure in all groups when compared to their air-exposed counterparts. It is not known if exposure-related blood pressure differences would persist after ending ozone exposures. After brief exposures, ozone caused increased lung weights in both groups, but there were no consistent changes in pulmonary nonprotein sulfhydryl groups. Hepatic nonprotein sulfhydryl levels were consistently, but not significantly, lower in ozone-exposed rats.

Animals↗