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

To assess the participation of cardiovascular eicosanoids (prostaglandins and thromboxanes) system in the initiation of genetic hypertension, we examined eicosanoids metabolism in the heart, aortic wall and kidney in prehypertensive and hypertensive rat models for spontaneous hypertension (SHR). Vasoconstrictor thromboxane A2 (TXA2) generation in the aortic wall was significantly enhanced by 49% in the prehypertensive and by 18% in the hypertensive SHR when compared to the respective normotensive Wistar-Kyoto rats. Cardiac TXA2 content was significantly increased as well by 14% in the prehypertensive and by 30% in the hypertensive SHR. Moreover, vascular vasodepressor eicosanoids generation was decreased by 10% for PGI2 and by 29% for PGD2 in the prehypertensive SHR although the alterations were eliminated in the hypertensive SHR. In contrast to the cardiovascular eicosanoids system, there was no difference in renocortical TXA2 content in either young or adult SHR while vasodepressor prostaglandins contents were decreased by 29% for PGE2 and by 33% for PGD2 in SHR when they were in the prehypertensive stage. Thus, in the prehypertensive stage of SHR, the cardiovascular eicosanoids system exhibited enhanced vasoconstrictor TXA2 and decreased vasodepressor prostaglandins, thereby producing a vasoconstrictor state. These data indicate that the alterations in the cardiovascular eicosanoids system partially contribute to the initiation of hypertension in SHR.
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PMID:Alterations of the cardiovascular and renal prostaglandins and thromboxanes system in prehypertensive spontaneously hypertensive rats. 266 86

The hereditary nature of familial hypertension has been clearly established by a number of clinical studies. Most of the present work has been concentrated on the correlation between various phenotypic traits and the level of blood pressure. The development of molecular genetics allow now to establish a link between high blood pressure and specific phenotypes. As analyzed in this paper, several strategies can be used for the genetic study of arterial hypertension: linkage studies in informative families, population association studies, analysis of subjects with contrasted predisposition to high blood pressure, affected sib-pair method. The identification of the loci implicated in blood pressure regulation and which contribute to the development of arterial hypertension can then be performed in this clinical material by two main approaches. One is based on the study of candidate genes, genes whose products are known to participate in blood pressure regulation, such as those of the renin-angiotensin system which are examplified. The other involves testing a series of markers distributed randomly throughout the genome in order to establish a link between increased blood pressure and a particular region of the genome.
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PMID:The application of molecular genetics to the study of familial arterial hypertension. 267 50

This study attempted to investigate the possible involvement of the brain stem noradrenergic system in the development of hypertension in spontaneously hypertensive rats. Steady-state norepinephrine, dopamine, serotonin and 5-hydroxyindoleacetic acid concentrations and norepinephrine turnover were determined in the individual brain stem nuclei using high performance liquid chromatography with electrochemical detection. Decreased norepinephrine contents in the nucleus tractus solitarii in spontaneously hypertensive rats compared with Wistar-Kyoto rats at the age of 4, 8, and 16 weeks were demonstrated. In later stages (8 and 16 weeks), increased norepinephrine levels were observed in the nucleus reticularis gigantocellularis, the A1 and A5 areas. Norepinephrine turnover was not different between spontaneously hypertensive rats and Wistar-Kyoto rats in the nucleus tractus solitarii at the age of 4 and 16 weeks and increased in the nucleus reticularis gigantocellularis of spontaneously hypertensive rats at 16 weeks. Our results indicate that altered norepinephrine metabolism in the specific brain stem nuclei, especially the consistently decreased norepinephrine in the nucleus tractus solitarii of spontaneously hypertensive rats, contribute to the development of genetic hypertension.
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PMID:Involvement of brain stem noradrenergic neurons in the development of hypertension in spontaneously hypertensive rats. 271 Feb 80

Twenty clinically healthy subjects were studied to identify normotensive adults with a predisposition to arterial hypertension by monitoring blood pressure (BP) and restricting dietary sodium intake. Short-term restriction in sodium intake resulted in a decrease of the mean level for the circadian rhythm of BP. The phenomenon is visible in subjects without familial hypertension but not in individuals with a positive history for high BP. The response of the 24-hour BP patterns to abrupt sodium deprivation seems to be an indicator for discovering normotensive subjects at risk of developing arterial hypertension.
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PMID:Usefulness of twenty-four-hour blood pressure patterns and response to short-term sodium restriction in normotensive subjects in detecting a predisposition to systemic arterial hypertension. 278 50

Several abnormalities have been described in the blood-cell handling of calcium in patients with hypertension and rats with genetic hypertension. We have suggested elsewhere that the multiple abnormalities of monovalent and divalent ion handling by blood cells in hypertension, which are loosely and variably associated with blood pressure, reflect a global variability of cell membrane lipids. In the light of this suggestion we tested the relevance of decreased membrane binding of calcium by examining basal and maximal calcium binding in hypertensive patients and in normotensive subjects with and without a family history of hypertension. Calcium binding was reduced to a similar degree in both hypertensive subjects and those with a family history of hypertension. To examine the role of membrane lipids we examined calcium binding in relation to erythrocyte membrane composition, and found a negative correlation between the palmitic:linoleic acid ratio and calcium binding. This is consistent with the observation of a reduction in the unsaturated fatty acid, linoleic acid, in the erythrocyte membrane of hypertensive subjects, and this may therefore be of functional significance. In further studies, although there was no net difference in leucocyte cytosolic calcium between essential hypertensive subjects and normotensive controls, there was a positive relationship between leucocyte calcium and membrane palmitic:linoleic acid ratio only in normotensives. To test further the role of membrane lipids in calcium handling we administered linoleic acid (4 g daily safflower seed oil) to 13 normotensive volunteers in a double-blind crossover trial. Four weeks of administration of the linoleic acid produced a significant decrease in leucocyte calcium (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Membrane handling of calcium in essential hypertension. 283 20

Renal sympathetic antidiuretic, antinatriuretic, and vasoconstrictor responses are mediated by alpha 1-adrenergic receptors in the normal rat. Since the renal nerve has been implicated in the pathogenesis of rat genetic hypertension, we investigated renal alpha 1-adrenergic receptor coupling to phosphoinositide turnover in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). In cortical slices from adult (13-week-old) SHR and WKY, stimulation with norepinephrine (10(-7)-10(-3) M) caused a concentration-dependent increase in accumulation of [3H]inositol phosphates. However, dose-response curves for SHR characteristically displayed a depression of the maximum response as compared with those for WKY. Baseline accumulation of [3H]inositol phosphates was not different between strains (39.4 +/- 2.2 cpm/mg tissue/hr for WKY and 34.4 +/- 2.1 cpm/mg tissue/hr for SHR slices; n = 5 rats/group, determined in triplicate). Antagonist competition studies revealed that norepinephrine-stimulated (10(-4) M) [3H]inositol phosphate accumulation was mediated by alpha 1-adrenergic receptors (IC50) for prazosin: 65 +/- 11 nM for SHR and 64 +/- 5 nM for WKY). The reduction in norepinephrine-stimulated [3H]inositol phosphate accumulation in SHR cortex was not the result of the hypertension, since it was also present in cortical slices from young (4-week-old) SHR in which the blood pressure was not yet significantly different from that in WKY and since [3H]inositol phosphate accumulation was unchanged from control values in rats made hypertensive by treatment with deoxycorticosterone acetate. Scatchard analysis of [3H]prazosin binding in renal cortical membranes of young and adult SHR and WKY revealed no significant differences in alpha 1-adrenergic receptor density or affinity between strains at either age. Our results suggest that renal alpha 1-adrenergic receptor coupling to phospholipase C is less efficient in SHR than in WKY. This impaired response is not the result of hypertension or changes in receptor density; this defect may play a role in increased renal sympathetic nerve activity and in the development or maintenance of hypertension in SHR.
Hypertension 1988 Jul
PMID:Renal alpha 1-adrenergic receptor response coupling in spontaneously hypertensive rats. 284 Mar 96

Cardiacneurovegatative assessment was studied in 60 subjects divided into three groups consisting of 20 normotensive subjects without familial hypertension, 20 normotensive subjects with familial hypertension, and 20 patients with mild hypertension. Cardiacneurovegetative function was investigated by evaluations of these parameters: systolic, diastolic, and mean blood pressure, heart rate, skin temperature, skin conductance, and muscular contraction. These measurements were taken before and after psychological stress (mathematical, Sacks' incomplete sentences, electrical, auditory) and after physical stress (cold, hand grip, head-up tilt, lying, and standing). The results showed a significant difference of the psychophysiologic profiles among the three groups. On the contrary, the cardiovascular variables were not very sensitive or well-discriminating, especially when response amplitude was considered. In conclusion we propose the hypothesis that identification of the psychophysiologic profile in certain individuals may be a better marker for future development of hypertension in subjects with a genetic risk.
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PMID:Neurovegetative assessment in subjects with a risk for hypertension. 292 93

Renal damage is systemic hypertension has traditionally been related to an ischemic glomerular injury secondary to arteriosclerosis and arteriolosclerosis of preglomerular vessels. The use of micropuncture techniques with histopathologic studies have suggested non ischemic mechanisms of renal damage in systemic hypertension. Indeed in experimental models of hypertension which include DOCA-Salt, Goldblatt hypertension or genetic hypertension, the development of glomerular damage is associated with hyperfiltration secondary to increases in flow and pressure to the glomerular capillary. Hyperfiltration as a mechanism of renal damage in human systemic hypertension has not been established. Recent studies from our group have demonstrated lack of renal functional reserve in patients with systemic hypertension, reserve which is reestablished after 3 days of antihypertensive treatment. These data suggest therefore the presence of hyperfiltration as a possible mechanism of renal damage in patients with essential hypertension.
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PMID:[Is the kidney lesion caused by hypertension really ischemic?]. 294 50

Atrial natriuretic peptides (atrial natriuretic factor, ANF) are present in a great number of brain areas inside and outside of the blood-brain barrier. The pattern of distribution implies the involvement of ANF in different physiological functions, such as blood pressure regulation, electrolyte and fluid homeostasis, and modulation of the neuroendocrine system. To further investigate a possible involvement of central ANF in spontaneous hypertension, we measured levels of ANF in 18 selected, microdissected brain areas of prehypertensive (4-week-old) and hypertensive (12-week-old) spontaneously hypertensive rats (SHR) and their normotensive control, Wistar-Kyoto rats (WKY), by radio-immunoassay. ANF was significantly decreased in seven brain areas in SHR at both ages investigated; the most pronounced decreases were found in the subfornical organ, in the perifornical and periventricular hypothalamic nuclei, and in the medial preoptic nucleus. In addition, in young SHR ANF was significantly decreased in the organum vasculosum laminae terminalis and increased in the median eminence. After the development of hypertension, a significant decrease of ANF could be detected in four more brain areas (bed nucleus of the stria terminalis, paraventricular and arcuate nuclei, dorsal raphe nucleus) of SHR, as compared with normotensive controls, and the increase in the median eminence was no longer detectable. These results suggest a role for ANF in genetic hypertension and the specific importance of certain brain regions.
Hypertension 1988 Nov
PMID:Atrial natriuretic factor in specific brain areas of spontaneously hypertensive rats. 297 39

The ability of plasma extracts to inhibit Na+-K+ ATPase in vitro (P.I.A.) was tested in 20 normotensives, 10 without (F-) and 10 with (F+) familial hypertension, in 20 borderlines (BL) and in 21 essential hypertensives (EH). In these subjects we also measured intralymphocytic sodium (ILSC) and potassium (ILKC) content, P.R.A. urinary aldosterone and Na+(Na+u), and blood pressure. P.I.A. of EH, BL and F+ subjects was significantly higher than that of F-. 60% of EH and BL and 40% of F+ had P.I.A. values greater than the highest found in F-. P.I.A. was significantly related to mean blood pressure (r = 0.63), to ILSC (r = 0.56), to ILKC (r = -0.56), to ILSC/ILKC ratio (r = 0.71) and to Na+u (r = 0.39) but not to P.R.A. or aldosterone. These data demonstrate that plasma extracts from young subjects prone to hypertension may inhibit sodium pump and that this inhibitor may affect blood pressure by altering the Na+/K+ intracellular ratio.
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PMID:Plasma Na+-K+ ATPase inhibitory activity in normal and hypertensive subjects: relationship to intracellular electrolytes and blood pressure. 299 Jul 69


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