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Biomedical subjects

D Ben-Ishay

Publications and source records attributed to D Ben-Ishay.

At least 55 records · Page 3Linked to original sources
PubMed1985

Nifedipine in the treatment of hypertension in the elderly.

The effect of nifedipine monotherapy, retard tablets, 20 mg bid, was evaluated in 23 hypertensive patients, mean age, 79 +/- 2 years. Twenty-one patients completed an eight-week study. Blood pressure (BP) decreased to 160/90 mm Hg in 15 patients; in four additional patients diastolic BP dropped by 15% to 28%. In a subset of five patients with isolated systolic hypertension, a significant reduction in systolic BP was noted. Side effects were relatively mild and only two patients discontinued the study. The results suggest that nifedipine monotherapy offers an alternative, logic, therapeutic approach to hypertension in the elderly.

Age Factors↗
PubMed1985

Water handling by the sabra hypertension prone (SBH) and resistant (SBN) rats.

The renal handling of water by SBH and SBN rats was evaluated under basal conditions and following various intervention procedures. During 17 weeks of unrestricted water intake, SBH rats drank less water and excreted less urine with a higher osmolality than SBN. The differences in urine volume and osmolality persisted during 2 weeks of paired water intake. Acute water loading elicited comparable dilution of the urine in the two strains. Water deprivation for 48 h resulted in a marked rise in urine osmolality, which tended to be higher in SBN. Administration of exogenous vasopressin in water loaded animals caused a similar rise in urine osmolality. Papillary solute and urea content was higher in SBH than in SBN, but comparable in water loaded animals. The results show that although SBH differ from SBN rats in the handling of water under basal conditions, their renal diluting and concentrating capacity is comparable at extreme conditions. GFR and RBF were equal in both strains. The data suggest that SBH rats have increased renal water reabsorption as compared to SBN, which may be mediated by ADH, PG or other mechanisms. This characteristic may be related to their propensity to develop hypertension.

Animals↗
PubMed1985

Salt-induced hypertension in the 'Sabra' rat strain: influence of nifedipine treatment.

The effects of chronic dietary salt-loading and nifedipine therapy on hypertension-prone (SBH), -resistant (SBN) and parental (SB) Sabra rats were investigated. Salt diet for 12 weeks resulted in a sustained hypertension and heart hypertrophy only in SBH. Nifedipine therapy (300 p.p.m. = 300 mg/kg of food) introduced after week 7 on a salt diet, achieved small changes in salt-loaded SBN and SB rats, but resulted in a marked decrease in blood pressure in SBH rats within 1 week and in a regression of cardiac hypertrophy. Plasma renin activity rose slightly in nifedipine treated SB and SBN rats, but decreased significantly in treated SBH rats. Histopathological investigations revealed hypertensive vasculopathy in three out of nine untreated SBH rats, whereas there were no morphological changes in the treated rats.

Aldosterone↗
PubMed1985

Phosphoinositide turnover in erythrocyte membranes in human and experimental hypertension.

The metabolism of phosphoinositides, a class of membrane lipids involved in Ca2+ -transport and/or mobilization systems was investigated in patients with moderate essential hypertension and in Sabra rats. Experiments were performed in vitro on isolated erythrocyte membranes by measuring the 32P-labelling of phosphatidylinositol 4,5-bisphosphate (PI-P2) and of phosphatidylinositol 4-phosphate (PI-P) following the incubation of membranes with [gamma-32P] ATP. In untreated essential hypertensives (n = 31) or in hypertensive patients whose blood pressure was controlled by beta-blocker therapy (n = 20), 32P-PI-P2 was significantly higher than in normotensive controls (n = 30); no significant difference was observed between the two groups of hypertensive patients. In Sabra rats fed on a low Na diet, 32P-PI-P2 levels were significantly higher in hypertensive-prone animals (SBH) than in hypertensive-resistant animals (SBN). When the animals were fed a high Na diet or were DOCA/salt treated, 32P-PI-P2 did not change in either substrain, although such conditions differentially affected the blood pressure of SBH and SBN. Our data indicate that the modification of phosphoinositide metabolism is not a consequence of the blood pressure elevation, but can be considered as an intrinsic membrane defect which may be associated with functional alterations of Ca2+ fluxes which in hypertensives result in an enhanced intracellular Ca2+ level.

Adrenergic beta-Antagonists↗
PubMed1985

Reduced sympathetic neuronal uptake (uptake1) in a genetic model of desoxycorticosterone-NaCl hypertension.

The effect of desoxycorticosterone (DOC)-NaCl treatment upon sympathetic neuronal uptake of norepinephrine (uptake1) was evaluated in strains of hypertension-resistant (SBN) and -prone (SBH) rats. Uninephrectomized animals were given either a placebo pellet sc and tapwater (untreated) or a 25-mg DOC pellet and 1% NaCl. Four weeks later, tail systolic pressure was significantly higher in DOC-NaCl SBH, 183 +/- 3 mm Hg, than SBN, 141 +/- 2 (P less than 0.01). [3H]Norepinephrine (NE) uptake was determined in heart slices of all four groups by incubation in Krebs buffer at 37 degrees C for 20 min at several concentrations. Preliminary studies confirmed that this is a measure of uptake1. Heart slices of DOC-NaCl-treated SBN and SBH rats had significantly reduced NE uptake at concentrations of 10-80 nM (P less than 0.01); there was no significant difference between SBN and SBH in this regard. Untreated SBH rats have been shown to have a defect in baroreflex regulation when normotensive. The results raise the possibility that the greater increase in arterial pressure caused by DOC-NaCl in SBH compared to SBN may be related to both the inborn difference in reflex function and an acquired reduction in inactivation of norepinephrine by sympathetic neuronal uptake.

Animals↗
PubMed1985

[Phosphoinositide metabolism in essential and experimental hypertension].

The metabolism of phosphoinositides, a class of membrane lipids that appears to be intimately involved in the regulation by the membrane of the intracellular Ca2+ level, has been reported to be modified in the erythrocyte of the spontaneously hypertensive rat (SHR and SHR/SP). In order to elucidate the link between the phosphoinositide alteration and hypertension, the metabolism of phosphoinositides was studied in human essential hypertension and in Sabra rats under various patho-physiological conditions. Experiments were performed in vitro on isolated ghost membranes by measuring the radioactivity incorporated into triphosphoinositides (PI-P2) and diphosphoinositides (PI-P) following the incubation of membranes with [gamma 32P]-ATP. 32P-PI-P2, in moderate untreated essential hypertensive controls (n = 31) was higher than in normotensives (n = 30) (1.18 +/- 0.06 vs 0.92 +/- 0.04, 32P nmol/15 min/mg prot, p less than 0.005); 32P-PI-P2 and 32P-PI-P in hypertensive patients treated with beta-blocking agents (n = 20) did not differ from the values observed in untreated hypertensives. In Sabra rats, 32P-PI-P2 values were 0.79 +/- 0.03 and 1.32 +/- 0.08 for SbN and SbH, respectively (8-11 animals per group); difference was significant. 32P-PI-P values varied similarly. Both 32P-PI-P2 and 32P-PI-P did not change significantly when animals were fed a high sodium diet or were injected with DOCA, though such treatments rose the blood pressure. Our data indicate that the modification of phosphoinositide metabolism that we observed both in rat and human hypertension is not a consequence of the blood pressure elevation, but may be considered as an intrinsic membrane defect. Changes in the phosphoinositide metabolism may therefore be associated with the functional and structural alterations concerning the transmembrane Na+ and Ca2+ fluxes which may be of pathogenic importance.

Adult↗
PubMed1985

Erythrocyte Na+-K+ cotransport in elderly hypertensive subjects.

Na+-K+ cotransport was measured in 21 hospitalized geriatric patients, all recovering from hip surgery. Twelve of these had hypertension, and the other 9 were the control group. Although both groups were comparable for age, blood pressure was significantly different. Mean cotransport values in red blood cells showed no significant difference between the two groups. While Na+-K+ cotransport activity may be hereditary, the authors do not feel the test may be used as a genetic marker for hypertension.

Aged↗
PubMed1984

Cerebral and renal alpha-adrenoceptors in Sabra hypertensive (SBH) and normotensive (SBN) rats: effects of high-sodium diet.

The aim of the present study was to investigate the effect of high (8%) versus normal (0.2%) sodium diet on cerebral and renal alpha-adrenoceptors of Sabra hypertensive (SBH) and normotensive (SBN) rats. Cerebral alpha 2-adrenoceptor densities were higher in SBN than in SBH rats. In contrast, renal alpha 2-adrenoceptor density was higher in SBH than in SBN rats. No difference in alpha 1-adrenoceptor densities was observed between the two strains. After 2 and 5 weeks of high-sodium diet, alpha 2-adrenoceptor densities were increased in renal cortex of SBH and SBN rats. In contrast, cerebral alpha 2-adrenoceptor densities were markedly decreased in SBN but not in SBH rats. alpha 1-Adrenoceptor densities were unchanged by high salt intake. Blood pressure increased only after 5 weeks of high-sodium diet, markedly in SBH and to a lesser extent in SBN rats. The variation in alpha 2-adrenoceptor densities thus preceded the blood pressure elevation. The dietary sodium-induced increase in renal alpha 2-adrenoceptor densities observed both in SBH and SBN rats does not appear to be a genetic marker of hypertension. In contrast, the marked decrease in cerebral alpha 2-adrenoceptors in SBN rats may represent an adaptative change in sympathetic activity responsible for the resistance to the development of salt-induced hypertension.

Animals↗
PubMed1984

Baroreflex sensitivity and susceptibility to systolic hypertension induced by DOCA-salt in the Sabra rat.

Rats of the salt-resistant Sabra strain (SBN) have a more sensitive baroreflex control of heart rate than do normotensive hypertension-prone salt-sensitive (SBH) rats. To test the hypothesis that increased baroreflex sensitivity confers resistance to hypertension, aortic baroreceptor deafferentation (ABD) was performed in 7- to 10-wk-old SBN rats. This treatment reduced the slope of the mean arterial pressure-heart period (MAP-HP) relationship in response to infusions of increasing doses of phenylephrine in conscious rats, from 1.92 +/- 0.21 to 0.66 +/- 0.11 ms X mmHg-1 (P less than 0.01). The latter value did not differ significantly from that of untreated SBH rats (0.56 +/- 0.07 ms X mmHg-1). Treatment of uniphrectomized SBH, SBN-ABD, and sham-operated SBN rats for 3 wk with deoxycorticosterone acetate (DOCA; 25-mg pellet) and 0.9% NaCl + 0.4% KCl (to maintain normal serum K+ values) as drinking fluid caused increases in systolic blood pressure from 126 +/- 3 to 147 +/- 5 mmHg and 104 +/- 6 to 130 +/- 8 mmHg in the former two groups, respectively, but no significant change (105 +/- 3 to 110 +/- 4 mmHg) in SBN rats when measured by an indwelling arterial catheter in the tail artery. The slopes of the MAP-HP relationships of each of the above three groups of rats were not significantly altered by DOCA-salt treatment. It is concluded that a decrease in baroreflex control of the heart by ABD can render SBN rats sensitive to DOCA-salt-induced systolic hypertension.

Animals↗
PubMed1984

Erythrocyte 22Na+ influx in hypertension.

We assessed 22Na+ uptake by erythrocytes (RBC) from 38 individuals with essential hypertension and 37 healthy controls. All subjects were male, white, non-obese and with normal renal function, obviating sex, race, hormonal, ponderal and renal factors known to influence RBC Na+ handling. The mean +/- sem 22Na+ uptake of the patients was 284 +/- 16 mumole/liter RBC/hour while that of normal controls was 249 +/- 11 mumole/liter RBC/hour; although the difference reached borderline significance, individual values showed considerable overlap. Consequently, in our population, RBC 22Na+ uptake is not a reliable marker for essential hypertension. We believe that previous studies should be reassessed with regard to patients' characteristics and future studies employ rigorous criteria in selection of subjects.

Adult↗
PubMed1984

Dietary sodium regulation of alpha 2-adrenoceptors in Sabra hypertensive (SHB) and normotensive (SBN) rats.

Cerebral and renal alpha 2-adrenoceptors, modulated in vitro by sodium ions, are implicated in the control of sympathetic activity and of sodium reabsorption, respectively. The aim of the present study was to investigate the effect of high (8%) versus normal (0.2%) sodium diet on cerebral and renal alpha-adrenoceptors of Sabra hypertensive (SBH) and normotensive (SBN) rats. After two or five weeks of high sodium diet alpha 2-adrenoceptor density was increased in the renal cortex of SHB and SBN rats. In contrast, cerebral alpha 2-adrenoceptor densities were markedly decreased in SBN but unchanged in SBH rats. Blood pressure increased only after five weeks of high sodium diet, in SBH and to a lesser extent in SBN rats. The change in alpha 2-adrenoceptor densities thus preceded the blood pressure elevation. The dietary sodium-induced increase in renal alpha 2-adrenoceptor densities which precedes the blood pressure elevation does not appear to be a genetic marker of hypertension. Conversely, the marked decrease of cerebral alpha 2-adrenoceptors in SBN rats may represent an adaptative change in sympathetic activity responsible for the resistance to the development of salt-induced hypertension.

Animals↗
PubMed1984

Sympathetic component of baroreflex control of heart rate is impaired in hypertension-prone (SBH) Sabra rats.

Baroreflex control of heart rate in response to phenylephrine was studied in conscious Sabra hypertension-prone (SBH) rats, at a prehypertensive stage, and hypertension-resistant (SBN) rats. Baroreflex sensitivity as determined from the slope of the relationship of mean arterial blood pressure and heart period was significantly lower in SBH rats (0.58 +/- 0.06 versus 1.71 +/- 0.11 ms/mmHg in SBN rats, P less than 0.01) before the development of hypertension. Sympathetic nerve blockade with guanethidine (15 mg/kg) significantly reduced the slope of the mean arterial blood pressure-heart period relationship in SBN rats to 0.45 +/- 0.05 ms/mmHg (P less than 0.01) and increased the pressor response to phenylephrine, without having any effect on these parameters in SBH rats. Atropine methyl nitrate (1 mg/kg) abolished reflex vagal bradycardia in response to phenylephrine in both groups of rats. This suggests that SBH rats are unable to withdraw the sympathetic cardiac component of the baroreflex in response to a pressor stimulus and appear to rely only on increased vagal activity to effect bradycardia.

Animals↗
PubMed1983

Stress-induced secretion of adrenocorticotropin, corticosterone, and prolactin in experimentally and genetically hypertensive rats.

Plasma levels of immunoreactive ACTH, corticosterone (CS), and PRL in two-kidney, one clip (2K1C) hypertensive SABRA, hypertension-prone (SBH), hypertension-resistant (SBN), and normotensive SABRA rats were compared under both quiescent conditions and after acute (2 min) cold water stress. Serum levels of CS were higher in 2K1C hypertensive compared with normotensive SABRA rats under both quiescent and stressful conditions. Circulating levels of ACTH and PRL were similar in both groups under quiescent conditions. Resting circulating levels of CS were higher in the SBH rats compared with SABRA or SBN rats. Serum PRL levels were similar in SBH and SABRA rats under both quiescent and stressful conditions. Resting PRL levels in the SBN rats were lower compared with the SABRA rats. Resting serum levels of ACTH and CS in the SBN rats were similar to those found in the SABRA rats. After stress exposure serum ACTH and CS levels were elevated in all groups. Serum PRL levels in SBN rats were not affected by stress, unlike the marked elevation seen in the other groups. Our study demonstrates increased secretion of CS in both 2K1C hypertensive and SBH rats under quiescent conditions. Both 2K1C hypertensive and SBH rats have normal hormonal capacity to respond to stress. SBN rats exhibited reduced PRL secretion under both quiescent and stressful conditions. It is suggested that abnormal activity of the hypothalamic-pituitary-adrenal system may play a role in the pathogenesis of 2K1C and genetic hypertension as well as in resistance to hypertension.

Adrenocorticotropic Hormone↗
PubMed1983

Erythrocyte Na+, K+ cotransport and blood pressure in identical twins.

The erythrocyte Na+, K+ cotransport system was studied in ten pairs of identical twins. Cation fluxes were remarkably similar in each pair of twins, which supports the concept of a genetic determinant for the cotransport system. There was, however, no apparent correlation between cotransport values and the family history of hypertension.

Adolescent↗
PubMed1983

Na-K-ATPase in single nephron segments of hypertension-prone rats.

The activity of renal Na-K-ATPase was compared in hypertension-prone (SBH) and hypertension-resistant (SBN) Sabra rats on regular sodium intake and 2-3 weeks after a high sodium diet. ATPase activity was determined in single nephron segments by a micromethod. The activity profile was found to be similar in the two substrains on both regimens. Following high sodium intake there was a significant increment of Na-K-ATPase activity which was limited to the medullary thick ascending limb in the two substrains. The results clearly indicate a lack of relationship between renal Na-K-ATPase activity and proneness or resistance to hypertension in this experimental model.

Animals↗