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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 employed 31P nuclear magnetic resonance (NMR) spectroscopy to examine the relationship between cytosolic free Mg2+ ([Mg2+]in), intracellular pH, high energy phosphates, and genetic hypertension using the Wistar-Kyoto rat (WKY) as a control and the spontaneously hypertensive rat (SHR) as a model for essential hypertension. The mean systolic blood pressures (measured using the tail cuff method) of control and hypertensive rats (aged 7 to 12 weeks) were 113 +/- 4 mm Hg (mean +/- 2 SE, n = 14) and 162 +/- 5 mm Hg (mean +/- 2 SE, n = 17), respectively. Intracellular free Mg2+ levels were significantly depleted in the isolated Langendorff perfused hypertensive rat hearts (452 +/- 39 mumol/L, mean +/- 2 SE, n = 17) compared to control hearts (756 +/- 52 mumol/L, n = 14); however, intracellular pH did not differ in the SHR hearts (7.02 +/- 0.03, mean +/- 2 SE, n = 7) compared with controls (7.03 +/- 0.03, n = 7). Although we could not demonstrate a statistically significant difference in the levels of P-creatine or ATP, intracellular Pi was two-fold higher (5.71 +/- 2.28 mmol/L v 2.92 +/- 0.66 mmol/L, n = 4) and the phosphorylation potential, [MgATP]/[MgADP][Pi], was correspondingly lower (3.0 X 10(4) +/- 1.6 x 10(4) v 8.3 X 10(4) +/- 1.4 X 10(4) (mol/L)-1, n = 4) in SHR compared to WKY hearts. These data demonstrate free magnesium depletion in heart muscle and indicate an alteration in cardiac bioenergetics in essential hypertension.
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PMID:Intracellular free magnesium and high energy phosphates in the perfused normotensive and spontaneously hypertensive rat heart. A 31P NMR study. 202 44

Increased sympathoadrenal activity appears to play an important role in the development or maintenance of elevated blood pressure in hypertensive patients and various animal models of hypertension. Alterations of adrenergic receptor number or responsiveness might contribute to this increased activity. We therefore reviewed the data on adrenergic receptor alterations in hypertension with special emphasis on several key cardiovascular tissues (i.e., heart, vascular smooth muscle, and kidney) and on lymphocytes and platelets as human tissues available for such studies. The data suggest that the number of alpha-adrenergic receptors in hypertension is regulated by catecholamines, dietary salt intake, and genetic factors. Increases in renal alpha-adrenergic receptor number may be etiologic in genetic forms of essential hypertension. beta-Adrenergic receptor alterations in states of elevated blood pressure do not appear to be specific for genetic hypertension. Desensitization of beta-adrenergic receptor function in hypertensive animals and patients contrasts with reports of decreased, unchanged, and increased beta-adrenergic receptor number, suggesting that signal transduction of beta-adrenergic (and possibly other) receptors that stimulate adenylyl cyclase is disturbed in hypertension. The mechanisms of such heterologous desensitization in states of elevated blood pressure remain to be elucidated.
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PMID:Peripheral adrenergic receptors in hypertension. 216

Primary hypertension in animals and humans probably represents several different pathophysiological states rather than being a uniform nosological entity. Among other factors, renal mechanisms may be primarily and secondarily involved. The availability of genetically homologous animal models for hypertension has greatly promoted studies on the etiology and pathogenesis of high blood pressure disease. In particular, renal transplantation studies between genetically hypertensive and normotensive rats from three different models have provided strong evidence for a primary role of the kidney in genetic hypertension. Other factors, such as vascular, neural, and humoral mechanisms have also been shown to be involved and may be particularly effective in increasing blood pressure, when they act through the kidney. Several functional and biochemical differences have been identified between kidneys from genetically hypertensive and normotensive animals. However, the relative contribution of each of these factors to the development of primary hypertension remains to be determined. Evidence from studies on human renal graft recipients also indicates that, among other factors, the kidney plays an important role in the development of primary hypertension in humans.
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PMID:Role of the kidney in the pathogenesis of primary hypertension. 224 18

We have utilized multinuclear NMR spectroscopy to examine the relationship between cytosolic free Ca2+ ([Ca2+]in), free Mg2+ ([Mg2+]in) and intracellular Na+ ([Na+]in) levels of the intact thoracic aorta and primary hypertension using the Wistar-Kyoto and Sprague-Dawley rats as controls and the spontaneously hypertensive rat as a model for genetic hypertension. Cytosolic free [Ca2+] was measured using 19F NMR of the intracellular Ca2+ indicator 5,5'-difluoro-1,2-bis-(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, free [Mg2+] using the 31P resonances of intracellular ATP, and intracellular [Na+] by 23Na NMR in combination with the extracellular shift reagent dysprosium tripolyphosphate. We have found that both the [Na+]in and [Ca2+]in levels were significantly increased in the hypertensive animals relative to normotensive controls (p less than 0.01). Mean systolic blood pressures (using tail cuff method) of control and hypertensive rats were 123 +/- 8 mm Hg (mean +/- 2 S.E., n = 7) and 159 +/- 6 mm Hg (mean +/- 2 S.E., n = 7), respectively. [Na+]in and [Ca2+]in were 21.9 +/- 6.4 mM (mean +/- 2 S.E., n = 7) and 277 +/- 28 nM (mean +/- 2 S.E., n = 5) for the spontaneously hypertensive rats versus 10.1 +/- 1.8 mM (mean +/- 2 S.E., n = 7) and 151 +/- 26 nM (mean +/- 2 S.E., n = 5) for control rats, respectively. A slight difference observed between intracellular free Mg2+ levels in hypertensives (180 +/- 38 microM, mean +/- 2 S.E., n = 4) and controls (246 +/- 76 microM, mean +/- 2 S.E., n = 4) was not statistically significant (p greater than 0.1). These data indicate alterations in the cell membrane ion transport function of the aortic smooth muscle in primary hypertension.
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PMID:NMR measurement of cytosolic free calcium, free magnesium, and intracellular sodium in the aorta of the normal and spontaneously hypertensive rat. 229 35

Recent studies in essential hypertensive patients and rats with genetic hypertension strongly suggested that the development of primary hypertension takes place by a transient and chronic "cascade" of events (i) excess Na+ intake, (ii) secretion of natriuretic factors, (iii) abnormal cells Na+ homeostasis in the vascular wall, due to the presence of inherited abnormalities in different Na+ transport systems, and (iv) increase in cytosolic free Ca2+ content and catecholamines. Canrenone, an antihypertensive drug, behaves like a partial agonist at the digitalis-receptor site of the Na+, K+ pump. We observed here that (i) a 4 hr preincubation of human red cells with this compound increases its antagonistic properties against ouabain, (ii) in cultured smooth muscle cells, canrenone counterbalances the increase in cytosolic free Ca2+ induced by ouabain, and (iii) in a model of experimental hypertension with increased endogenous "ouabain-like" factors (rats with reduced renal mass), the administration of canrenone tends to normalize Na+, K+-pump activity and decrease blood pressure.
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PMID:Involvement of natriuretic hormones and Na+ transport in the antihypertensive action of canrenone. 242 26

Glomerular and fascicular zones of the adrenal gland and the incretory renal structures of patients who had died from benign (20) and malignant (10) forms of essential hypertension, chronic glomerulonephritis (10) and of rats with a genetic hypertension (10) were examined by morphometric methods. Hypertrophy of glomerular and fascicular zones is observed in both forms of the hypertension disease, spontaneous hypertension and chronic glomerulonephritis. Correlation analysis revealed moderate and strong links between the volumes of nuclei and nucleoli; within each zone and between the zones. This may indicate an increased functional activity of the two zones and their close interaction. Factorial analysis revealed a sign indicator--nucleus volume of the glomerular zone cells. Numerous moderate and strong correlations between the incretory renal structures and the adrenal cortex in the malignant form of the hypertension disease may indicate not only the involvement of the renin-angiotensin-aldosteron- and prostaglandin-synthesizing systems in the pathogenesis of this disease but their interaction as well.
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PMID:[The morphology of the adrenals and kidney incretory structures in arterial hypertension]. 261 Jun 2

Circulating digitalis-like compounds have been found elevated in some experimental sodium--and volume--dependent hypertensions, as well as in human essential hypertension. As few studies have been undertaken to assess their enhancement in the genetic hypertension of Okamoto (SHR) we have investigated their presence in plasma using 4 criteria: their apparent immunoreactivity with antidigoxin antibodies, their competition with tritiated ouabain binding to the sodium pump of human red blood cells,-their ability to inhibit the Na+, K+ ATPase activity of rat kidney membranes, and the Na+ fluxes from rat red blood cells. When compared to ordinary Wistar (W) and Wistar Kyoto rats (WKY), SHR exhibited a markedly enhanced apparent immunoreactivity with antidigoxin-antibodies (138 +/- 8; 59 +/- 3; 61 +/- 4 pg/ml, n = 15, 6 et 15, p less than 0.001, and p less than 0.001 respectively). The inhibition of ouabain binding by plasma extracts of the three strains did not differ (10.3 +/- 1.6, 9.9 +/- 1.7 and 12.9 +/- 1.4 ng/ml, n = 9, 18 and 14 respectively). When compared to WKY, SHR plasma extracts inhibited the renal Na+, K+ ATPase activity (75.6 +/- 2.6 vs 89.3 +/- 2.4 mumoles Pi . mg-1 . h-1, n = 11 and 10, p less than 0.01, respectively). When incubated in SHR plasma for one hour, net sodium effluxes from Wistar erythrocytes were inhibited compared to that measured in the presence of W or WKY plasma: (5.91 +/- 0.20 vs 7.68 +/- 0.25 and 7.52 +/- 0.15 mmol/l cells, n = 5, 3 and 5, p less than 0.001, and p less than 0.001 respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Genetic hypertension in the SHR rat and circulating digitalis compounds]. 282 51

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

Recent studies in essential hypertensive patients and rats with genetic hypertension strongly suggested that the development of primary hypertension results from a transient and chronic "cascade" of events; I) excess Na+ intake, II) secretion of natriuretic factors, III) abnormal cell Na+ homeostasis in the vascular wall, due to the presence of inherited and induced abnormalities in different Na+ transport system and IV) increase in cytosolic free Ca2+ content and sympathetic drive. In vitro studies have previously shown that canrenone, an antihypertensive antialdosterone drug, behaves like a partial agonist at the digitalis-receptor site of the Na+, K+-pump. In particular, it has been shown that canrenone counterbalances the increases in internal Na+ and cytosolic free Ca2+ contents induced by ouabain in cultured smooth muscle cells. We thus investigated the effect of canrenone administration in a model of experimental hypertension with increased endogenous "ouabain-like" factors (rats with reduced renal mass under excess Na+ intake: RRM-salt rats). Results presented here confirm that RRM-salt rats exhibit: volume expansion, strongly decreased plasma renin activity, increased endogenous "ouabain-like" factors and (IV) decreased Na+, K+-pump activity and increased Na+ content in erythrocytes. In addition, we found that canrenone is antihypertensive in this model and this is associated with a tendency to normalize volume expansion, plasma levels of endogenous "ouabain-like" factors, Na+, K+-pump activity and Na+ content in erythrocytes. In conclusion, our results suggest that administration of canrenone to RRM-salt rats may induce a lowering of blood pressure by antagonism with endogenous "ouabain-like" factors at the vascular wall.
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PMID:[Canrenone: an effective antihypertensive in an experimental model of hypertension in which the active transport of sodium is diminished]. 309 4

The systemic and renal hemodynamic effects of diltiazem were determined in patients with mild to moderately severe essential hypertension and in rats with spontaneous hypertension (SHR). Seven patients were treated for one full year (300 mg/day, average dose) and 10 SHR and 10 normotensive Wistar-Kyoto (WKY) rats received 1 and 2 mg/kg, intravenously. In both man and rat with genetic hypertension, arterial pressure was reduced through a fall in total peripheral resistance without associated reflexive increases in heart rate and cardiac index; and the patients demonstrated no change in plasma volume. In both man and the SHR: renal blood flow increased (in SHR not statistically significant) as arterial pressure and renal vascular resistance fell; glomerular filtration rate (GFR) remained unchanged and the filtration fraction (FF) significantly fell; and calculated intrarenal hemodynamic indices (using the Gomez formulae) demonstrated falls in afferent and efferent glomerular arteriolar pressures and resistances and in intraglomerular pressures, thereby explaining the unchanged GFRs and the decline in FF. These findings in both hypertensive man and rat are in contrast with those of the normotensive WKY that only demonstrated a fall in afferent glomerular arteriolar resistance. Thus, these data demonstrate that diltiazem controlled arterial pressure in both forms of genetic hypertension associated with falls in systemic and renal arteriolar resistances and with improved intrarenal hemodynamics without glomerular hyperfiltration.
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PMID:Diltiazem maintains renal vasodilation without hyperfiltration in hypertension: studies in essential hypertension man and the spontaneously hypertensive rat. 315 72


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