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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The renal handling of an oral isotonic saline load was studied in hypertension-prone (SBH), hypertension-resistant (SBN) and the parental Sabra (SB) rats. The diuretic and natriuretic response of SBH rats was unequivocally diminished, thus lending further support to the concept of impaired salt handling in hypertension.
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PMID:Renal response to acute saline loading in Sabra hypertension-prone and -resistant rats. 400 28

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.
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PMID:Water handling by the sabra hypertension prone (SBH) and resistant (SBN) rats. 401

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.
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PMID:Na-K-ATPase in single nephron segments of hypertension-prone rats. 609 80

Distinct differences in central and peripheral noradrenaline (NA) were observed in the hypertension prone (SBH) and resistant (SBN) strain, derived from the Hebrew University SABRA rats. In the medulla oblongata NA concentration was 90% higher and tyrosine hydroxylase activity 88% lower in SBN when compared to SBH, suggesting marked strain differences in NA turnover. In this area, NA-induced cAMP generation was higher in SBH than in SBN, while the hypothalamus, the reverse situation was present. The relevance of hypertension of the reciprocal cAMP changes is still uncertain. The concentration of NA in heart tissue was significantly higher in SBN than in SBH. Doca-salt treatment caused hypertension and depletion of atrial NA in SBH, but had no effect on either blood pressure or atrial NA in SBN rats. The results suggest that resistance to hypertension in SBN rats is associated with decreased NA turnover in medulla oblongata and reduced activity of cardiac neuronal sympathetic endings.
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PMID:Distinguishing traits in the Sabra hypertension-prone (SBH) and hypertension-resistant (SBN) rats. 611 32

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.
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PMID:Baroreflex sensitivity and susceptibility to systolic hypertension induced by DOCA-salt in the Sabra rat. 670 79

Fluorescence polarization of diphenylhexatriene embedded in membranes was used as an index of 'microviscosity' in platelets and erythrocyte ghosts of spontaneously hypertensive rats of the Okamoto-Aoki strain (SHR), Wistar-Kyoto strain (WKY) and of the hypertension-prone and -resistant Sabra strains (SBH and SBN ), and the original Sabra strain (SB). Microviscosity was increased both in erythrocyte ghosts and platelet membranes of male but not female SHR rats compared with WKY rats and in hypertension-prone Sabra rats compared with the original Sabra rats. Acute and chronic salt loading increased the microviscosity of platelet membranes in all strains of rats but had no effect on the erythrocyte membranes. Microviscosities of vesicles made of lipids extracted from SHR and WKY erythrocyte ghosts were similar. This supports the hypothesis that membrane proteins play a major role in the differences in microviscosity observed in SHR rats.
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PMID:Further analysis of cell membrane changes in genetic hypertension in rats by diphenylhexatriene fluorescence polarization. 672 8

This study was designed to investigate the effects of a hypertensive stimulus, high salt intake, in hypertension-prone (SBH) and -resistant (SBN) Sabra rats on erythrocyte Na+ content (Na+i), Ca2+ influx and cytosolic Ca2+ concentration ([Ca2+]i). The relationships of these parameters to plasma lipids, circulating digoxin-like immunoreactivity and membrane microviscosity, determined by the fluorescence anisotropy of trimethylamino-diphenylhexatriene (TMA-DPH) and diphenylhexatriene (DPH), were also evaluated. Erythrocytes of SBH rats were characterized by increased [Ca2+]i, unchanged Ca2+ influx and reduced Na+i. There were no significant differences in the plasma digoxin-like immunoreactivity between the two strains. High-salt intake decreased membrane microviscosity (DPH anisotropy) in SBH rats but did not alter the above parameters. Erythrocyte [Ca2+]i correlated positively with diastolic blood pressure and negatively with erythrocyte Na+i. Membrane dynamics evaluated by the two fluorescent probes did not correlate with [Ca2+]i, Ca2+ influx or Na+i whereas DPH anisotropy was inversely related to blood pressure. These relationships were independent of plasma cholesterol or triglycerides. It can be concluded that 1) similarly to earlier observations in essential hypertension and spontaneously hypertensive rats, erythrocyte [Ca2+]i correlates positively with blood pressure in salt-dependent hypertension, and 2) increased erythrocyte Na+ content need not be a hallmark of hypertension.
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PMID:Alterations of membrane properties in erythrocytes of salt hypertensive Sabra rats. 796 37

alpha 2-adrenoceptors are involved in various renal functions regulating blood pressure. They were classified in subtypes whom genes were identified in both humans and rats. In rat renal cortex it was evidenced that the alpha 2B isoform is predominant. This result was confirmed in Sabra rats. However, the renal cortex alpha 2B density is higher in salt-sensitive (SBH) than in salt-resistant (SBN) Sabra rats. alpha 2B-adrenoceptors were recently subclassified in two pharmacologically distinct subtypes exhibiting high and low affinity for guanoxabenz and respectively called alpha 2B1 and alpha 2B2. We studied sodium loading effect on alpha 2B1 and alpha 2B2 distribution in Sabra rat renal cortex using competition experiments between [3H]-yohimbine and guanoxabenz. The rats were submitted to normal (0.2%) or high sodium diet (8%) for six weeks. Under normal diet, proportion alpha 2B1 and alpha 2B2 was similar in SBH and SBN. Nevertheless, their respective densities were significantly higher in SBH as compared to SBN (alpha 2B1: 90.6 +/- 4.1 vs 57.4 +/- 2.5 fmoles/mg prot, p < 0.0001; n = 5; alpha 2B2: 102.7 +/- 4.0 vs 66.4 +/- 4.6 fmoles/mg prot; p < 0.0001; n = 5). Under high sodium diet the distribution of these two isoforms was altered. The densities of alpha 2B1 were decreased by 27.0 +/- 5.9% in SBH (68.0 +/- 4.0 fmoles/mg prot; p < 0.0001, n = 5) and by 47.3 +/- 7.4% for SBN (29.2 +/- 3.1 fmoles/mg prot; p < 0.0001; n = 5). Conversely, the densities of alpha 2B2 were increased by 28.3 +/- 5.4% in SBH (131.1 +/- 9.5 fmoles/mg prot; p < 0.001; n = 5) and by 75.0 +/- 17% in SBN (123.2 +/- 9.1 fmoles/mg prot; p < 0.0001; n = 5). In conclusion, alpha 2B1- and alpha 2B2-adrenoceptor subtypes are found in renal cortex of both SBH and SBN. Our data demonstrated an equal distribution of these two isoforms between SBH and SBN under normal salt diet. This distribution is largely altered, especially in SBN, by the high sodium diet. From these modifications might result differential renal responses to activation of alpha 2B-adrenoceptors between SBH and SBN, and consequently responsible for normal or high blood pressure after high sodium diet.
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PMID:[Evidence for two alpha 2B-adrenoreceptor isoforms in the renal cortex of salt-sensitive and salt resistant Sabra rats. Effect of salt loading]. 857 79

Increased platelet cytosolic free calcium concentration ([Ca2+]i) has been demonstrated in both human essential hypertension and spontaneous hypertension of the rat. The present study was designed to extend the investigation on platelet Ca2+ handling to two models of salt-dependent genetic hypertension (Sabra and Dahl rat strains). No major [Ca2+]i elevation was seen in salt hypertensive SBH Sabra or SS/Jr Dahl rats. This contrasts with the data obtained in Lyon hypertensive rats (a spontaneous form of genetic hypertension) in which basal platelet [Ca2+]i was clearly increased and correlated positively with diastolic blood pressure. In these two strains, basal platelet [Ca2+]i correlated with pulse pressure but not with diastolic pressure. The absence of a significant relationship between platelet [Ca2+]i and diastolic pressure in both Sabra and Dahl rats indicates that, at least in young rats with developing salt hypertension, platelet cytosolic calcium need not reflect calcium changes occurring in the vascular smooth muscle or resistance arterioles. In contrast to the high values seen in Lyon hypertensive rats, the [Ca2+]i rise induced by thrombin was unchanged in salt-sensitive SS/Jr Dahl rats and substantially reduced in hypertension-prone SBH rats (irrespective of salt intake). The initial rate of thrombin-induced Mn2+ entry through receptor-operated Ca2+ channels was similar in SBN and SBH as well as in SR/Jr and SS/Jr rats kept on a low-salt diet but was reduced by high salt intake in platelets of salt-resistant (SBN and SR/Jr) animals only. Since platelets of Lyon hypertensive rats are also characterized by greater initial rate of thrombin-induced Mn2+ entry, this parameter was always higher in rats with established hypertension compared to their respective normotensive controls. Our study demonstrated that alterations of platelet Ca2+ handling are different in salt-dependent than in spontaneous forms of genetic hypertension.
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PMID:Platelet calcium handling is different in rats with salt-dependent and spontaneous forms of genetic hypertension. 886 28

We recently re-inbred the original colony of SBH-SBN rats, a model of salt-induced hypertension. In the course of phenotyping the new colony, SBH/y were found to excrete a lower urine flow with a higher urine osmolality than SBN/y. Thus disparate water handling between the substrains, a phenotype characteristic of the original colony, was retained throughout the selection procedure and transmitted down the generations to the new colony. As water handling is directly linked to arginine vasopressin (AVP) and in view of potential linkage of this phenotype to salt sensitivity or resistance in terms of the development of hypertension, the AVP axis was further investigated in the new substrains. Basal plasma AVP levels were higher in SBH/y (2.86 +/- 0.22 pg/ml; n = 10) than in SBN/y (1.98 +/- 0.11 pg/ml; n = 10, P < 0.05). Water deprivation for 48 h increased plasma AVP levels severalfold in both substrains to similar levels. Niravoline, a kappa receptor agonist that inhibits central release of AVP, produced at 0.6 and 0.9 mg/kg a more profound diuretic effect in SBN/y than in SBH/y, suggesting greater pituitary release of AVP into the circulation of SBH/y. AVP mRNA contents were compared in SBH/y and SBN/y rats in whole hypothalamic extracts and in the supraoptic (SON) and paraventricular (PVN) nuclei by RNA protection assay. Under basal conditions, AVP mRNA content (in ng) in the hypothalamus of SBH/y was 4.48 +/- 0.52 (n = 29) and of SBN/y was 3.13 +/- 0.35 (n = 30), P < 0.05; in the SON of SBH/y, AVP mRNA content was 3.62 +/- 0.44 (n = 11) and of SBN/y was 2.21 +/- 0.54 (n = 10), P < 0.05; in the PVN of SBH/y, AVP mRNA content was 0.78 +/- 0.16 (n = 9) and of SBN/y was 0.77 +/- 0.13 (n = 11, not significant). Thus the differences in hypothalamic AVP mRNA were primarily in the SON. Water deprivation as well as salt loading (8% NaCl) induced a significant elevation in AVP mRNA content in SBN/y but a blunted response in SBH/y. These data suggest that there is genetically transmitted enhanced hypothalamic expression of the AVP gene in SBH/y compared with SBN/y which results, under basal conditions, in greater pituitary release of AVP, in higher plasma AVP levels, and in increased renal concentrating activity. As AVP has been implicated in various forms of hypertension, these findings render AVP a candidate gene for salt sensitivity or resistance in the Sabra rat model of hypertension.
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PMID:Disparate expression of the AVP gene in Sabra hypertension-prone and hypertension-resistant rats. 889 10


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