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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have used 23Na nuclear magnetic resonance spectroscopy to examine the relationship between intracellular sodium and cardiac muscle alterations in genetic hypertension. In the spontaneously hypertensive rat (SHR) compared with the normotensive Wistar-Kyoto rat (WKY) (aged 15 to 19 weeks), mean systolic blood pressures (measured using the tail-cuff method) were significantly (P < .05) different (WKY: 118 +/- 8 mm Hg, n = 5; SHR: 185 +/- 9 mm Hg, n = 5). Heart weights were also increased significantly (P < .05) in SHR (grams dry heart to kilograms body weight ratio was 0.73 +/- 0.04, n = 5, for SHR and 0.55 +/- 0.02, n = 5, for WKY). Intracellular sodium levels, measured using shift-reagent-aided and triple quantum filtered (TQF) nuclear magnetic resonance techniques, were significantly increased (P < .05) in the isolated Langendorff perfused hypertensive rat hearts (17.3 +/- 3.6 mmol/L, n = 5) compared with normotensive rat hearts (8.4 +/- 2.3 mmol/L, n = 5). These data demonstrate increased sodium in cardiac muscle in essential hypertension. We also investigated the effect of pacing on cardiac TQF 23Na nuclear magnetic resonance and found an increase in TQF Na+ content in both WKY and SHR hearts on stepped up pacing. These results support the existence of sodium pump lag in the rat heart perfused at physiologic Ca2+ concentration and suggest that the hypertensive rat heart has adapted to compensate for increased basal intracellular Na+ and maintain a normal response to increased heart rate. Our data appear to suggest an ionic contribution to the cardiac hypertrophy of genetic hypertension in the rat.
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PMID:Nuclear magnetic resonance measurement of intracellular sodium in the perfused normotensive and spontaneously hypertensive rat heart. 806 May 76

Recent evidence from both salt-sensitive humans and several rat models of hypertension indicates an association between metabolic acidosis and genetic hypertension. Preliminary findings of increased renal acid excretion suggest that the perturbation of acid-base status may be the result of increased metabolic acid production. This would be compatible with the previous findings of enhanced Na+/H(+)-antiporter activity, reduced intracellular pH levels, and abnormalities of carbohydrate and lipid metabolism present in both patients with essential hypertension and rat models of genetic hypertension. Further investigation of the factors controlling acid-base metabolism in animal models of hypertension and in salt-sensitive humans may disclose underlying metabolic abnormalities that could account for both the alterations in blood pressure and acid-base status associated with genetic hypertension.
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PMID:Acid-base abnormalities in hypertension. 814 Nov 48

The epidemiologic links among essential hypertension, obesity, and noninsulin-dependent diabetes mellitus (NIDDM) are well recognized, and it has been proposed that these links may reflect an underlying common pathophysiologic link of resistance to the action of insulin (insulin resistance). In essential hypertension, data suggest the insulin resistance pertains predominantly to nonoxidative glucose disposal, especially in skeletal muscle and adipose tissue, which contrasts with a more generalized deficit in obesity and NIDDM. A number of animal studies of genetic hypertension have confirmed the presence of insulin resistance, whereas acquired models of animal hypertension have not. The clinical significance of insulin resistance on long-term morbidity in hypertension remains unclear; there is limited evidence that insulin resistance may be an independent risk factor for subsequent vascular events, but it is more likely that it clusters with other better defined risk factors for the vascular complications of hypertension. The potential clinical sequelae of insulin resistance and hyperinsulinemia and the effect of antihypertensive medication on insulin resistance in general are addressed.
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PMID:Insulin resistance and essential hypertension: mechanisms and clinical implications. 814 Nov 65

To examine whether sympathetic nervous activation has an impact on renal circulation in subjects at risk for high blood pressure, we assessed renal hemodynamics and cardiovascular response to mental stress in 40 healthy young white males, 12 normotensive subjects without and 14 with familial hypertension, and 14 with borderline hypertension. The response of systolic and diastolic blood pressure to mental stress was assessed while each patient performed a mental arithmetic task; this was taken as the parameter for the activation of the sympathetic nervous system. Renal plasma flow was measured by para-aminohippuric acid clearance under steady-state conditions. In parallel, glomerular filtration rate as a parameter for functional impairment of the kidneys was determined by creatinine clearance, and filtration fraction was also calculated. Patients with borderline hypertension were characterized by a reduced renal blood flow and increased filtration fraction in comparison with both normotensive groups. The increase in systolic blood pressure during mental stress was more pronounced in borderline hypertensives. We observed no significant difference in renal hemodynamics and cardiovascular response to mental stress between normotensives with and without a family history of hypertension. In the total population, cardiovascular response to mental stress was correlated with renal hemodynamics: The greater the increase in systolic blood pressure during mental stress, the lower was the renal plasma flow and the greater the filtration fraction. Thus, renal plasma flow was found to be already reduced and filtration fraction increased before sustained hypertension developed. Because this pattern in renal hemodynamics was related to cardiovascular response to mental stress, our data suggest that sympathetic activation already appeared to affect renal hemodynamics at the onset of essential hypertension.
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PMID:Renal hemodynamics and cardiovascular reactivity in the prehypertensive stage. 821 30

Dopamine has been well recognized to be a precursor of norepinephrine, exhibiting cardiovascular effects through alpha-adrenoceptor stimulation by norepinephrine production and release in sympathetic nerve endings. It also has the specific and unique effects of natriuresis and vasodilation. Since dopamine is one of the important endogenous hypotensive and natriuretic substances, it is speculated that impaired dopamine generation and/or the disturbance of the effects of dopamine could cause hypertension with suppression of plasma renin activity and/or salt-sensitivity. A non-specific enzyme of aromatic L-amine acid decarboxylase (AAAD) converting from 3,4-dihydroxyphenylalanine (DOPA) to dopamine is widely distributed in the peripheral tissue, e.g. the sympatho-adrenomedullary system, the small intestine, the lung, the liver, the kidney, etc. Since tyrosine hydroxylase is a rate-limiting enzyme of catecholamine biosynthesis, DOPA generation in the neuronal tissues is accelerated with the sympathetic nerve activation by stress such as emotional and environmental changes, resulting in an increase of DOPA delivery to the non-neuronal tissues containing non-neuronal AAAD. More than five receptors for dopamine are cloned in the brain, and it is suggested that more than three different types of dopamine receptors are in the peripheral tissues. In spontaneously hypertensive rats, the post-receptor defect of renal dopamine D1-receptor has been proposed where peripheral dopamine generation compensatorily increased. In Dahl salt-sensitive rats, another model of genetic hypertension, the blunted response of urinary dopamine to sodium loading has been demonstrated. It is controversial whether abnormalities of the neuronal and/or non-neuronal (particularly renal) dopamine system play a contributory role on the pathogenesis of essential hypertension. However, it is plausible that the impairment of dopamine generation and/or the defective responses of a dopamine receptor might induce sodium retention and hypertension.
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PMID:[Dopamine and hypertension]. 826 73

Several animal models of genetic hypertension have been developed but not all of them possess a closely related control strain. Therefore, a new model based on Wistar rats is described in which both hypertensive and normotensive lines were bred from a single parental pair. Several basic data on the two lines (called the Prague Hypertensive Rat, PHR, and the Prague Normotensive Rat, PNR) are given. PNR had a longer survival compared with PHR. At the age of 7 weeks, systolic blood pressure was 161 +/- 14 mmHg in PHR males and 109 +/- 9 mmHg in PNR males. Its further increase with age was very slow in PNR but very steep in PHR. Typical left ventricular cardiac hypertrophy developed in PHR in which cardiac output was not significantly different from that of PNR but total peripheral resistance was higher. Kidney weight was also greater in PHR than in PNR. There was no difference in basic renal functions except of proteinuria which was higher in PHR than in PNR. No differences were observed in extracellular and interstitial fluid volumes whereas plasma and blood volumes were slightly but significantly greater in PHR than in PNR suggesting a shift of extracellular fluid towards the intravascular compartment. This hypertensive model the parameters of which resemble to those of human essential hypertension should be especially suitable for cross-transplantation studies.
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PMID:The Prague Hypertensive Rat: a new model of genetic hypertension. 840 16

Recent advances in molecular biology have allowed the study of the candidate genes for essential hypertension. To identify the genes responsible for basal blood pressure in the spontaneously hypertensive rat strain, the rat model of genetic hypertension, we performed a cosegregation analysis between the genotype and blood pressure in a set of male F2 progeny obtained from SHR and Wistar-Kyoto rats, a reference normotensive strain. Our investigation revealed that a locus on the chromosome 4 cosegregates with the blood pressure in SHR, especially at neuropeptide Y locus. The degree of cosegregation with all values of blood pressure without sodium loading was moderate but consistent. We propose that neuropeptide Y locus on chromosome 4 is a new candidate for the hypertensive effect in original SHR.
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PMID:A neuropeptide Y locus on chromosome 4 cosegregates with blood pressure in the spontaneously hypertensive rat. 847 28

In renal cross-transplantation studies between four different strains of genetically hypertensive rats including Dahl salt-sensitive hypertensive rats, Milan hypertensive rats, spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP) on the one hand and their respective normotensive control strains on the other hand, it was found that BP determinants were carried within the kidney. To determine whether post-transplantation hypertension in recipients of an SHRSP kidney was due to a primary or secondary defect in the renal graft, hypertension in SHRSP kidney donors was prevented by chronic antihypertensive drug treatment. Despite sustained BP normalisation in SHRSP kidney donors, the recipients developed post-transplantation hypertension. This finding indicates that SHRSP kidneys carry a primary defect which can elicit hypertension. F1 hybrids bred from SHRSP and normotensive Wistar-Kyoto rat (WKY) parents show an age-related increase in arterial BP up to borderline hypertensive levels. Renal transplantation studies in young rats indicate that the development of borderline hypertension in (SHRSP x WKY)-F1 hybrids can be blunted by bilateral nephrectomy and transplantation of a WKY kidney. Clinical studies in human renal transplant patients also indicate that the genetic background of the kidney donor with respect to predisposition for genetic hypertension significantly influences BP and/or the need for antihypertensive medication in the recipients. Together, the results of renal transplantation studies in animals and humans suggest that a genetic defect in the kidney plays a major role in the pathogenesis of primary hypertension.
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PMID:Does the kidney play a role in the aetiology of primary hypertension? Evidence from renal transplantation studies in rats and humans. 851 91

Ingestion of sugars (sucrose, fructose, glucose) by various rat strains is associated with perturbations in the glucose/insulin system and higher systolic blood pressure (SBP). The association suggests causality, because alterations in insulin metabolism have been found in essential hypertension and many experimental forms of hypertension. To test the hypothesis that sugar-induced SBP elevation is secondary to perturbed insulin metabolism, we examined in 2 experiments effects of chromium and guar, substances known to affect insulin metabolism, on SBP of Spontaneously Hypertensive Rats (SHR). In both studies, sucrose compared to starch ingestion caused significant elevation of SBP; but addition of 2 chromium nicotinate complexes and guar prevented development of sugar-induced SBP elevations. The basal, genetic hypertension of the SHR was not affected by either nutrient. An additional finding in the first study was that sugar-consuming SHR supplemented with chromium had greater BW and increased organ weight (kidney, spleen, and liver) than nonsupplemented SHR. Accordingly, we have shown that two different mechanisms known to ameliorate insulin perturbations, use of chromium and guar, prevent sugar-induced SBP elevations. Since essential hypertension may be due to insulin perturbations and high dose chromium supplementation seems nontoxic, this may prove to be a useful means to lower blood pressure (BP) in some essential hypertensives, as well as diabetic hypertensives. Soluble fiber in the form of guar is also quite effective in favorably influencing sugar-induced SBP elevations.
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PMID:Effects of chromium and guar on sugar-induced hypertension in rats. 855 33

There is circumstantial evidence that disturbances of calcium metabolism are implicated in primary hypertension. From a large number of observational epidemiological studies, data have shown that a low dietary calcium intake increases the risk for high blood pressure. There is no general sensitivity for the effects of inadequate calcium intake, but subgroups of hypertensive patients have been described characterized by reduced serum ionized calcium levels, increased urinary excretion of calcium, raised intracellular calcium levels, reduced cellular membrane calcium binding, and other indicators of a relative calcium need. Some of these changes, however, may be secondary to blood pressure elevation. The family history approach enables to study the pathophysiology of early primary hypertension, at a stage at which blood pressure differences between future hypertensive subjects and normotensive subjects are still limited. In the Dutch Hypertension and Offspring Study, young normotensive subjects were studied selected on the basis of presence or absence of familial predisposition for hypertension. The findings show that disturbances in calcium metabolism are present in the early phase of primary hypertension and may precede the development of high blood pressure. Moreover, they suggest that changes in calcium metabolism may be a characteristic of familial hypertension and could reflect a genetic basis for calcium sensitive hypertension. The presence of a relatively reduced serum calcium and increased plasma PTH [1-84] level in the offspring of hypertensive parents indicates that calcium balance in prehypertensive subjects is maintained at a higher level of circulating PTH. The implications of these findings in relation to other available data are discussed.
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PMID:Calcium metabolism and familial risk of hypertension. 858 11


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