Search PubMed⌕ Search

Biomedical subjects

J Iwai

Publications and source records attributed to J Iwai.

At least 91 records · Page 5Linked to original sources
PubMed1981

Paraventricular--suprachiasmatic lesions prevent salt-induced hypertension in Dahl rats.

1. We studied the effects that lesions produced in the paraventricular and suprachiasmatic nuclei and intervening periventricular area had on 24 h mean circadian blood pressures in Dahl salt-sensitive and -resistant rats and their sham-operated controls. We measured blood pressures while the animals were on a low salt diet and after 1, 5 and 13 weeks of 8% NaCl diet. 2. Salt-sensitive rats with lesions had lower blood pressures than salt-sensitive sham-operated controls at all points of the study. In contrast, identical lesions in salt-resistant rats produced a transient pressor response to the diet. Twenty-four hour mean heart rate, determined after 13 weeks of 8% NaCl intake, was low only in salt-sensitive rats with lesions. Sodium intake and excretion per kg of body weight, as well as plasma sodium concentrations, were similar in all groups. 3. We conclude that the anteromedial hypothalamic area, which includes the paraventricular nucleus, the suprachiasmatic nucleus and the intervening periventricular area, participates in the development of Dahl hypertension. We suggest that a multifactorial mechanism is involved: (a) the facilitatory role of this region in ACTH release, (b) this region's participation in the baroreceptor reflex via vasopressinergic efferents to the nucleus of the tractus solitarius, and (c) the roles of the paraventricular and suprachiasmatic nuclei in the regulation of salt and water balance.

Animals↗
PubMed1981

Brain lesions in the paraventricular nuclei and catecholaminergic neurons minimize salt hypertension in Dahl salt-sensitive rats.

1. The rise in blood pressure in Dahl salt-sensitive rats that received intracerebroventricular 6-hydroxydopamine was almost half that of the control rats throughout 20 weeks of high (8%) NaCl feeding. 2. The rise in blood pressure in Dahl salt-sensitive rats with bilateral complete electrolytic lesions of the paraventricular nuclei was almost half that of the control rats during 12 weeks of high (8%) NaCl feeding. 3. The bilateral complete electrolytic lesions of the suprachiasmatic nuclei enhanced the development of NaCl hypertension in Dahl salt-sensitive rats. 4. These results show that NaCl-induced hypertension in Dahl salt-sensitive rats requires the integrity of the central nervous system catecholaminergic neurones and the paraventricular nuclei for its full expression.

Animals↗
PubMed1980

Pressure natriuresis in isolated kidneys from hypertension-prone and hypertension-resistant rats (Dahl rats).

Dahl described a strain of rats with genetically controlled propensities for hypertension. Chronic excess salt feeding increased blood pressure in sensitive (s) rats, whereas resistant rats (R) remain normotensive. We tested the pressure natriuretic function (urinary sodium excretion versus perfusion pressure) in isolated kidneys perfused with a cellular medium: in sodium-restricted normotensive sensitive (S0) and resistant (R0) animals; in sensitive rats receiving a high-salt diet for 3 weeks (S3): and in both S and R animals exposed to excess sodium for 7 weeks (R7 and S7). The aim of these studies was to determine if a preset alteration of the pressure natriuretic function might be present in S animals prior to the development of hypertension. Systolic blood pressure in S0, S3, and S7 animals were 123 +/- 4, 136 +/- 2, and 162 +/- 4 mm Hg, respectively, whereas that of R0 and R7 were 121 +/- 5 and 126 +/- 5 mm Hg. An increase of the perfusion pressure of isolated kidneys from 105 to 185 mm Hg in stepwise fashion resulted in a pressure natriuresis whose slope was similar in R0 and S0 animals. Of interest was that the pressure natriuretic function slope of kidneys from R0 (low sodium) and R7 (high sodium) rats was as predicted by the Guyton system analysis of normal blood pressure control Micropuncture of the proximal nephrons demonstrated that the origin of the natriuresis resulted from a site beyond the accessible proximal tubule. Results from S7 kidneys contrasted with all others in that the natriuretic response was depressed (P less than 0.01), which resulted from significantly lower filtration rates at higher perfusion pressures. We concluded (1) in normal R rats, the pressure natriuretic function is that predicted by the Guyton hypothesis, (2) Dahl S animals have no preset abnormality of this function until hypertension is present for some time, and (3) a depression of the pressure natriuretic function may aggravate hypertension in S rats once high blood pressure has persisted.

Animals↗
PubMed1980

Genetic influence on brain catecholamines: high brain noradrenaline in salt-sensitive rats.

1. Rats genetically sensitive to salt-induced hypertension showed higher levels of plasma noradrenaline and adrenaline than rats genetically resistant to hypertension. 2. The hypertension-sensitive rats had higher hypothalamic noradrenaline and lower adrenaline than resistant rats. 3. In response to a high salt diet brain-stem noradrenaline increased in sensitive rats and resistant rats exhibited a decrease on the same diet.

Animals↗
PubMed1980

Etiological role of cadmium in hypertension in an animal model.

Dahl hypertension-resistant (R) and hypertension-sensitive (S) lines of rats were used to determine whether cadmium plays an etiological role in hypertension. In Study I, weanling (3-week-old) R and S rats of both sexes were given a low-salt (0.4% NaCl) diet and were divided into two groups. Rats in the cadmium group were injected with cadmium (2 mg/kg body weight, ip), whereas the controls received identical volumes of saline. Three weeks after the first injection, no elevations of systolic blood pressure were detected. A second dose of cadmium (1 mg/kg) produced hypertension in S females but not in S males or in R rats of either sex. Also, female S cadmium rats manifested significant (p less than 0.01) mild to moderate renal vascular changes. The concentrations of cadmium in hepatic and renal tissues of S cadmium rats were significantly higher (p less than 0.001) than in R rats. In Study II, weanling (3-week-old) female S rats on a high-salt (4% NaCl) diet were given cadmium (2 mg/kg body weight, ip) at week 3 followed by second and third injections of cadmium (1 mg/kg) at weeks 6 and 23. S controls received the same volumes of saline. Cadmium enhanced the rate and the degree of salt-induced hypertension development. Pathological lesions of periarteritis nodosa in the mesenteric arteries and renal vascular lesions occurred to the same extent in the cadmium and control groups. These data indicate that differences in genetic background influence the development of cadmium-induced hypertension in weanling rats, and that cadmium exacerbates the severity of salt-induced hypertension.

Animals↗
PubMed1979

A circulating humoral pressor agent in Dahl S rats with salt hypertension.

1. In Dahl S rats becoming hypertensive while on a diet of high NaCl content there appears to be a blood-borne humoral agent which produces vasoconstriction in a bioassay using the isolated hindquarters of rats. 2. This vasoconstrictor effect strongly suggests the presence of a humoral pressor agent or the lack of a vasodilator agent in the blood of hypertensive S rats. 3. The vasoconstrictor effect is not due to high renin concentrations. 4. This humoral vasoconstrictor action could partly account for the high vascular resistance in the hypertensive S rat.

Animals↗
PubMed1979

Effects of cadmium ingestion in rats with opposite genetic predisposition to hypertension.

This study was undertaken to explore the effects of chronic low-level cadmium ingestion in Dahl hypertension-resistant (R) and hypertension-sensitive (S) lines of rats. Groups of weanling female R and S rats were given 0 or 1 mg cadmium/1. in drinking water and fed either a low salt (0.4% NaCl) or a high salt (4% NaCl) diet for 28 weeks. Cadmium produced hypertension associated with gross cardiac hypertrophy and mild to moderate renal vascular changes in S, but not in R, rats on a low salt diet. Cadmium enhanced the rate and degree of development of salt-induced hypertension without exacerbating the hypercholesterolemia or renal vascular lesions normally observed in S rats on a high salt diet. Cadmium lowered circulating cholesterol levels in both lines on a low salt diet. Cadmium had no influence on growth, blood urea nitrogen concentration, plasma renin activity, tumor formation, or survivorship in R and S rats on either salt diet. This study indicates that the genetic composition is a critical determinant of the adverse effects of chronic low-level cadmium ingestion in rats. In addition to the experimental implications, these findings may have relevance to the problem of human "essential" hypertension.

Animals↗
PubMed1979

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.

Angiotensin II↗
PubMed1978

Central nervous system pressor responses in rats susceptible and resistant to sodium chloride hypertension.

1. The pressor responses to hypertonic saline and angiotensin II introduced into the left lateral ventricle were both significantly greater in salt-sensitive (S) rats compared with salt-resistant (R) rats, with all rats on a low Na diet. 2. When S rats were given thiazide to nullify the pressor effect of dietary NaCl, their blood pressure averaged only 5 mmHg higher than that of the R rats; nevertheless, these S rats had significantly higher central nervous system pressor responses to angiotensin II and hypertonic saline. 3. Thus, if excessive dietary Na increases blood pressure by way of action on the central nervous system, these heightened pressor responses could partially account for the NaCl hypertension in S rats. Alternatively, depressed central nervous system pressor responses in R rats could partially explain the resistance of R rats to NaCl hypertension.

Angiotensin II↗
PubMed1978

Genetic influence on cadmium-induced hypertension.

Dahl hypertension-resistant (R) and hypertension-sensitive (S) rats were used to determine whether cadmium-induced hypertension is dependent on genetic predisposition. In experiment I, 16 wk-old R and S rats of both sexes were injected with two doses of cadmium (1 and 2 mg/kg body wt, ip), whereas the controls received the same volumes of saline. Hypertension and renal vascular changes were observed in cadmium-injected S rats but not in R rats. The S females appeared more sensitive than S males to the hypertensinogenic effect of cadmium. In experiment II, groups of weanling female R and S rats were given 0, 1, 2.5, 5, or 10 mg cadmium/liter drinking water and fed either a low-salt (0.4% NaCl) or a high-salt (4% NaCl) diet for 28 wk. Cadmium produced cardiac hypertrophy (1 mg cadmium/liter) and hypertension associated with renal vascular changes (1--5 mg cadmium/ liter), and it enhanced proteinuria (1-10 mg cadmium/liter) in S rats on a low-salt diet. Also, the development of salt-induced hypertension was accelerated in cadmium-fed (1 and 2.5 mg/liter) S rats. These adverse effects of cadmium were not detected in R rats on either salt diet. In experiments I and II, cadmium concentrations in the kidneys and liver of S rats were higher (P less than 0.001) than in those of R rats. These data indicate that genetic differences influence the pathogenesis of cadmium-induced hypertension.

Analysis of Variance↗