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Biomedical subjects

J Iwai

Publications and source records attributed to J Iwai.

At least 73 records · Page 4Linked to original sources
PubMed1986

Comparison of various genetic hypertensive rat strains.

Comparative studies on nine genetic hypertensive rat strains [two stroke-prone spontaneously hypertensive rats (SHRSP) and Dahl salt-sensitive (DS) strains, and one strain each of spontaneously hypertensive rats (SHR), Lyon hypertensive rats (LH), Milan hypertensive strain (MHS), genetically hypertensive rats (GH) and Sabra hypertensive rats (SBH)] and their respective controls [two Dahl salt-resistent (DR) strains and one strain each of Wistar-Kyoto rats (WKY), Lyon normotensive rats (LN); Lyon low blood pressure rats (LL), Milan normotensive strain (MNS), genetically normotensive rats (GN) and Sabra normotensive rats (SBN) and their original strain, Sabra rats (SB)], in groups consisting of 6-10 males from each strain, were carried out at 10-12 weeks of age under the same experimental conditions. After checking the developmental course of blood pressure and changes in body weight, they were killed at 12 weeks of age for blood analysis and organ-weight examinations. The SHRSP and SHR showed markedly higher blood pressure levels and earlier blood pressure rises in comparison with other hypertensive strains, although they had higher blood pressure than their respective controls. Among various organ weights examined, all hypertensive strains commonly showed increases in left ventricular weight in proportion to blood pressure rises. Kidney weights were significantly decreased only in MHS compared with MNS, while they were either unchanged or significantly greater in other hypertensive strains. Weights of adrenal glands were greater in the two strains of DS and in LH than in their respective control strains. These comparative data indicate possible differences in the pathogenic mechanism involved in these genetic hypertensive rat strains.

Animals↗
PubMed1986

Dahl salt-sensitive rats and human essential hypertension.

At Brookhaven we have two new strains of rats with opposing genetic predispositions to hypertension: one strain [inbred Dahl salt-sensitive (Dahl-S)] develops severe hypertension on a high-salt diet, while the other [inbred Dahl salt-resistant (Dahl-R)] responds only mildly, if at all. The striking observation is that, unlike other salt-sensitive hypertension-prone rats, inbred Dahl-S rats remain normotensive on a low-salt diet. The observation that hypertension in the inbred Dahl-S, but not the inbred Dahl-R, rat develops only after exposure to a high-salt diet indicates that the development of hypertension in the inbred Dahl-S strain is not spontaneous and that the genetic substrate is a critical determinant of the hazard of excess salt in the diet.

Animals↗
PubMed1986

Reduction of blood pressure in salt-fed Dahl salt-sensitive rats with diets rich in olive oil, safflower oil or calcium biphosphate but not with calcium carbonate.

Increased dietary calcium as CaCO3 had no effect in NaCl-induced hypertension in Dahl salt-sensitive (Dahl-S) rats, while the calcium supplementation as CaHPO4 did lower the blood pressure (BP). A diet rich in either monounsaturated or polyunsaturated fatty acids produced a significant lowering of blood pressure compared with the relatively saturated palm-oil diet in NaCl-induced hypertension in Dahl-S rats. The lower BP found with olive oil is probably not related to increased amounts of PGE2 and PGI2.

Animals↗
PubMed1986

Dual tracer autoradiographic study of beta-methyl-(1-14C) heptadecanoic acid and 15-p-(131I)-iodophenyl-beta-methylpentadecanoic acid in normotensive and hypertensive rats.

The myocardial distribution of 15-p-[131I]iodophenyl-3-(R,S)-methylpentadecanoic acid (BMPDA) and 1[14C]-3-(R,S)-methylheptadecanoic acid (BMHDA) was compared in normotensive and hypertensive rats using quantitative dual tracer autoradiographic techniques. The myocardial distribution of carbon-14 [14C] BMHDA and iodine-131 [131I] BMPDA was nearly homogeneous in the normotensive rats, while both tracers showed similar, though very heterogeneous, distribution in hypertensive hearts with decreased uptake in the endocardial region. Our data demonstrate that myocardial distribution of [131I]BMPDA was essentially the same as [14C]BMHDA, and thus single photon emission computed tomographic imaging with 123I-labeled BMPDA could be useful for the detection of regional changes of myocardial fatty acid uptake in patients with prolonged and severe hypertension.

Animals↗
PubMed1985

Regional myocardial substrate uptake in hypertensive rats: a quantitative autoradiographic measurement.

Severe hypertension causes global and regional changes in myocardial perfusion and substrate utilization. Regional perfusion and fatty acid utilization were evaluated by dual-tracer autoradiography in normotensive and hypertensive rats of the Dahl strain. The regional distributions of perfusion and fatty acid utilization were homogeneous in normotensive rats. Severe hypertension was associated with a homogeneous pattern of regional perfusion, but fatty acid utilization was focally decreased in the free wall of the left ventricle. The decrease in fatty acid uptake was associated with a concomitant increase in glucose utilization. These findings suggest that severe hypertension is associated with uniform myocardial perfusion and focal alterations in the substrates used for the performance of myocardial work.

Animals↗
PubMed1985

Prostaglandin alterations in barely hypertensive Dahl S rats.

In summary, prostacyclin, PGE2, and PGD2 are vasodilators and had significantly lower renal cortical and outer medullary concentrations in the borderline hypertensive S rats compared to normotensive R rats. Conversely, thromboxane is a vasoconstrictor which had significantly higher renal cortical and outer medullary concentrations in borderline hypertensive S rats compared to normotensive R rats. Thus, in borderline hypertensive S rats, both renal cortex and outer medulla have a prostaglandin pattern which favors vasoconstriction in cortical vessels and in descending vasa recta. This could partially account for the increased renal vascular resistance and low papillary plasma flows which are integral components of Dahl hypertension. The low PGE2 in S kidneys would also enhance Na reabsorption in collecting tubules and ascending limbs, thereby encouraging Na retention and hypertension.

Animals↗
PubMed1984

Potassium prevents death from strokes in hypertensive rats without lowering blood pressure.

Adding potassium to normal chow reduces death rate in hypertensive stroke-prone (SHRSP) rats from 83 to 2%, a 98% reduction. An 86% reduction in deaths occurred even when blood pressure (BP) was virtually equal in the two SHRSP groups being compared. Potassium supplements in the diet also reduced stroke deaths in hypertensive Dahl S rats from 55 to 4%, a 93% reduction. There was an 87% reduction in deaths even when BP was actually equal in the two Dahl S groups being compared. The added potassium in the diets decreased BP moderately in SHRSP rats and modestly in Dahl S rats, which contributed somewhat to the reduction in strokes. However, more importantly, the added potassium seems to reduce the intrinsic susceptibility to cerebral artery lesions for a given level of hypertension, even when BP is not lowered.

Animals↗
PubMed1983

Open-field behavior in two models of genetic hypertension and the behavioral effects of salt excess.

In order to assess the relationship of behavior to blood pressure and salt intake, open-field behavior was studied in 123 rats of the spontaneously hypertensive (SHR), Wistar-Kyoto (WKY), Sprague-Dawley (SD), and Dahl resistant (DR) and sensitive (DS) strains. DS rats become hypertensive upon exposure to either high dietary salt or psychogenic stress, while DR rats remain normotensive. A circular photobeam open field was used under full room illumination. Three 5-min trials were given on consecutive days. Rats were tested with or without 5 days of an 8% NaCl diet. We found that DS rats were less active than DR rats, regardless of diet. In contrast, SHR rats were more active than WKY rats. However, DS and SHR rats were equally active. Thus, behavioral differences between these two models of hypertension are expressed by the normotensive control strains. The relative ranking of activity levels between strains was DR = SD greater than SHR = DS greater than WKY. High-salt-enhanced intertrial habituation, defined as the decrease in activity across trials (DS, 100%; SD, 82%; SHR, 90%; WKY, 1350%; but DR, -50%) as well as intratrial habituation, defined as the decrease from the first to the second half of the trial (14%, all subjects). Defecation was increased with high salt (DS, 975%; SD, 59%; SHR, 267%; WKY, 89%; but DR, 40%). These effects of high salt may reflect an increase in an emotionality factor. DR rats were largely resistant to the behavioral effects of salt. Total activity was positively correlated with blood pressure in hypertensive rats, r(42) = 0.33, p less than .01, but negatively correlated in normotensive rats, r(81) = -0.34, p less than .01. The proportion of total activity occurring in the first half of the trial for the initial test day was correlated with blood pressure in normotensive rats r(81) = 0.44, p less than .01. Dietary salt excess has behavioral as well as cardiovascular consequences.

Animals↗
PubMed1983

Increased adrenal catecholamines in salt-sensitive genetically hypertensive Dahl rats.

Catecholamine levels and activity of catecholamine-forming enzymes have been quantitated in adrenal glands of Dahl sodium-resistant (R) and sodium-sensitive (S), genetically hypertensive rats maintained on low- or high-salt diets. A high-salt diet results in markedly different changes in the catecholamine metabolism in R and S rats. In R rats, a high-salt diet reduces the activities of tyrosine 3-hydroxylase (TH;-5%) and dopamine beta-hydroxylase (DBH; -18%) as well as the levels of all catecholamines (dopamine -28%, norepinephrine -11%, and epinephrine -28%). In contrast, S rats fed a high-salt diet showed increased TH (+7%) and phenylethanolamine N-methyltransferase (+16%) activities as well as an increased content of adrenal norepinephrine (+13%) and epinephrine (+21%). These findings demonstrate a genetic difference in the effects of a high-salt diet on the synthesis of catecholamines in the adrenal gland of Dahl R and S rats. Hypertension only occurs in S rats on a high-salt diet, concomitant with large increases in the formation of adrenal catecholamines.

Adrenal Cortex↗
PubMed1983

[Influence of the catheter diameter on the manometric measurements of the lower esophageal sphincter (LES); with special reference to the application for children].

In order to study the influence of the catheter diameter for measurement of the LES pressure, the LES pressure of rats was measured by using 6 kinds of catheters of different diameters. The results showed that the pressure of LES was 13.8 +/- 3.7 cmH2O, 15.2 +/- 3.2 cmH2O, 18.1 +/- 4.4 cmH2O, 22.3 +/- 6.7 cmH2O, 30.3 +/- 10.0 cmH2O and 42.0 +/- 11.9 cmH2O, respectively with the catheter diameter of 3, 4, 5, 6, 8 and 10 Fr. The larger the diameter of the esophageal tube, the higher the pressure of LES, in the range of more than a 5 Fr. tube. (P less than 0.05) Even in the LES model made of the isolated esophagus of rat, the diameter-pressure curve was similar with the LES measurement of the anesthetized rats. The increased pressure of LES was caused by an increase in tension from the esophageal wall to its proper pressure. For measurement of LES pressure of rats, the catheter of 3 Fr. or 4 Fr. in the outer diameter was more suitable since there was no tension from the esophageal wall. In order to search an appropriate catheter diameter for children, the LES pressure of 11 neonates and 12 infants were either measured with various kinds of tubes. The pressure of LES of neonates was 34.4 +/- 8.4 cmH2O, 36.4 +/- 10.7 cmH2O, 39.6 +/- 10 cmH2O, 46.0 +/- 8.7 cmH2O and 61.8 +/- 22.9 cmH2O, respectively with the catheter diameter of 4, 6, 8, 10 and 12 Fr.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1982

Effect of an anteroventral third ventricle lesion on NaCl hypertension in Dahl salt-sensitive rats.

An anteroventral third ventricle (AV3V) lesion in the brain prevents several forms of experimental hypertension. The present experiment was designed to determine whether the AV3V lesion prevents NaCl-induced hypertension in Dahl salt-sensitive (S) rats and whether attenuation of vasopressin release reported in lesioned rats contributes to the protective effect of the AV3V lesion against hypertension. After the AV3V lesion Dahl S rats received daily injections of either vasopressin (pitressin tannate, 500 mU/kg) or vehicle during 10 wk of 8% high-NaCl diet. Sham-lesioned rats served as controls. The blood pressure in sham-lesioned rats receiving vehicle was 189 mmHg after 10 wk of high-NaCl diet. Lesioned rats given vehicle showed a significantly smaller increase in blood pressure than sham-lesioned rats (P less than 0.001), the blood pressure averaging 161 mmHg at 10 wk. Lesioned rats given vasopressin also showed a smaller increase in blood pressure than sham-lesioned rats (P less than 0.05), but the final blood pressure averaged 176 mmHg and was significantly higher than that of lesioned rats given vehicle (P less than 0.025). Vasopressin injections corrected the hypernatremia in lesioned rats. In another experiment the effect of the AV3V lesion on the renal papillary plasma flow (RPPF) in Dahl S rats was studied. Dahl S rats have a lower RPPF than Dahl salt-resistant (R) rats even on a low-NaCl intake. The AV3V lesion increased the RPPF by 14% in S rats (P less than 0.025). These findings suggest that NaCl-induced hypertension in Dahl S rats requires the integrity of the AV3V region for its full expression, and the ability of the AV3V lesion to attenuate the NaCl-induced hypertension in Dahl S rats is partly related to the attenuation of vasopressin release. Moreover, the AV3V lesion partly corrected one of the characteristic features of Dahl S rats, the reduction in RPPF, when compared with Dahl R rats, with both strains on a low-NaCl intake.

Animals↗
PubMed1982

Prevention of malignant hypertension in salt loaded "S" Dahl rats with the calcium antagonist nifedipine.

Female "S" Dahl rats, fed an 8% NaCl diet from the 6th week of age developed malignant hypertension and heart hypertrophy in the course of 6 weeks on the salt regimen. Simultaneous treatment with nifedipine (300 ppm in diet additional to 8% NaCl) prevented the increase in blood pressure, reduced heart hypertrophy and mortality and improved the impaired renal function in "S" rats. The decrease in hematocrit in salt loaded "S" rats was prevented by nifedipine. The prophylactic effect of the calcium antagonist nifedipine is only partly due to the prevention of increase in systemic vascular resistance. In addition an improvement of failed intrarenal hemodynamics by nifedipine can be postulated. This enables the kidney of "S" rats to excrete the salt load without increasing blood pressure and plasma volume.

Animals↗
PubMed1982

Aortic morphology in salt-dependent genetic hypertension.

Excessive salt intake is an important determinant of human essential hypertension. Hypertension resulting from genetically determined salt sensitivity can be studied by the used of the salt-sensitive (S) and -resistant (R) rat strains developed by Dahl. A longitudinal morphometric and ultrastructural study of S and R Dahl rats fed different amounts of salt (0.6%, 4.0%, and 8.0% NaCl) for 2-14 weeks was undertaken. Only S rats responded to high-salt (4.0% and 8.0%) diets with an increase in blood pressure, and the rate of hypertension development was proportional to the daily amount of salt consumed. Likewise, S but not R rats fed high-salt diets showed thickening of the aortic media which paralleled the rise of blood pressure. Intimal lesions were characterized by the accumulation of an amorphous, electron-dense substance in the subendothelial space (SES), adherence or penetration of lymphoid cells, and subendothelial fibrin deposition. The extent and severity of SES expansion correlated more closely with the duration of salt feeding than with the level of blood pressure. Fibrin deposition was noted only in severely hypertensive animals and was not related to the salt concentration in the diet. Morphologic abnormalities in endothelial cells were noted in hypertensive animals by transmission and scanning electron microscopy as well as by en face preparation, but endothelial denudation and junctional disruptions were notably absent. In contrast to the large numbers of lymphoid cells, neither platelets nor fibrin were seen adherent on the endothelium. These results, in conjunction with previous studies in other hypertensive models, indicate that the nature and extent of vascular lesions depend not only on the severity of hypertension but also on its rate of development, duration, and pathophysiologic characteristics.

Age Factors↗
PubMed1982

[Etiological studies of manometric asymmetry in the lower esophageal sphincter (LES)].

In order to study the reason for manometric asymmetry of LES, the manometric profile of LES was measured at 3 different points (at the same level) of 20 normal infants and children by using 5 kinds of 3-lumen tubes with different rigidities. The results were; (1) the pressure was highest at 8 degrees (posterolateral wall) in LES by using all of the 5 esophageal tubes (p less than 0.001), and the length was shortest at 8 degrees in LES with 4 esophageal tubes, except for one 8 Fr. silicone tube. With this tube, LES had no asymmetry in the length. (2) The lower the rigidity of the esophageal tube, the less the asymmetry of the LES. In exact terms, the average coefficient of variations of LES pressure and length were; (in order of rigidity) 28.9% and 24.2% with a 12 Fr. vinyl-chloride tube, 25.7% and 23.4% with a 10 Fr. vinyl-chloride tube, 27.2% and 23.6% with a 8 Fr. evatate tube, 24.5% and 22.0% with a 8 Fr. vinyl-chloride tube, and 12.0% and 7.0% with a 8 Fr. silicone tube respectively. The variation in asymmetry of LES pressure and length were smollest by using the latter tube with the lowest rigidity. Therefore, the results suggest that the asymmetrical profile of LES was caused mainly by the rigidity of the esophageal tube rather than by the anatomical specialty of the esophago-cardiac junction.

Child, Preschool↗