Hypertension Research
Online ISSN : 1348-4214
Print ISSN : 0916-9636
ISSN-L : 0916-9636
Volume 17 , Issue 2
Showing 1-9 articles out of 9 articles from the selected issue
  • Anna F. Dominiczak, Anne O. Davidson, David F. Bohr
    1994 Volume 17 Issue 2 Pages 79-86
    Published: 1994
    Released: August 10, 2006
    JOURNALS FREE ACCESS
    Over the past decade the possibility of membrane abnormalities in hypertension has been studied very extensively. These studies reflect the putative significance of membrane abnormalities in the pathogenesis of this disease, and the need for resolution of the great divergence of the results that have been reported. Nevertheless, two sound generalizations have emerged from studies of the plasma membrane in hypertension: 1) The microviscosity of the plasma membrane is elevated (fluidity is decreased). However, genetic studies have cast doubt on the possibility that the decreased fluidity of the plasma membrane plays a role in the cause of experimental hypertension. 2) The stabilizing influence of calcium is diminished. The roles, if any, of these two abnormalities in the pathogenesis of hypertension require further study. Specific abnormalities, such as that of the Na/Li countertransport or Na/H exchange activity, may be useful phenotypic markers of subgroups of patients with essential hypertension. (Hypertens Res 1994; 17: 79-86)
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  • Tadashi Inagami, Yutaka Kitami
    1994 Volume 17 Issue 2 Pages 87-97
    Published: 1994
    Released: August 10, 2006
    JOURNALS FREE ACCESS
    Angiotensin II receptors are diverse and mediate complex signaling mechanisms. Their isoforms AT1 and AT2 have been cloned. AT1 consists of two closely related subtypes, AT1A and AT1B, in rodents. AT1A is expressed preferentially in the kidney, liver and cardiovascular tissues, whereas, AT1B is found mainly in endocrine tissues like the adrenal and pituitary glands. In higher mammals only a single isoform of AT1 has been reported. AT1 accounts for the majority of actions traditionally ascribed to angiotensin II that include the Gq-protein coupled activation of phospholipase C, Gi-coupled opening of an L-type calcium channel. AT2 was cloned recently from rat tissues and cell lines. It has a structure compatible with a seven transmembrane domain receptor in spite of the lack of internalization or shift to the low affinity state by stable GTP analogs. AT2 was found to inhibit certain phosphotyrosine phosphatase(s) by a pertussis toxin-sensitive mechanism. These cloned cDNAs and their mutated cDNAs have been expressed in mammalian cells to identify various functional domains such as ligand binding sites, domains for interaction with various G-proteins, and for desensitization. Both AT1 and AT2 genes consist of 3-5 exons. Their coding regions are contained in a single exon. Angiotensin II down-regulates the expression of the AT1 gene by two different mechanisms, whereas, glucocorticoids up-regulates it. (Hypertens Res 1994; 17:87-97)
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  • Philippe Gosse, Pascal Guillo, Jacques Clementy
    1994 Volume 17 Issue 2 Pages 99-104
    Published: 1994
    Released: August 10, 2006
    JOURNALS FREE ACCESS
    Predominant or septal hypertrophy is observed on echocardiographic examination of certain hypertensive patients. It is not yet established whether asymmetric septal hypertrophy is a particular form of hypertensive cardiopathy or is coincidentally associated with high blood pressure. We examined the effect of antihypertensive treatment on wall thickness and left ventricular mass in previously untreated hypertensive patients with either asymmetric septal hypertrophy or symmetrical wall thickening. Echocardiograms were recorded before and after 6 months of antihypertensive treatment in 112 patients. A septum/posterior wall thickness ratio over 1.3 was found in 15 of these patients. All echocardiograms were recorded by the same doctor and read blindly according to the Penn convention. Similar reductions in left ventricular mass were observed in the two groups after 6 months of antihypertensive therapy. In the group with asymmetric septal hypertrophy, the reduction was most marked in the septum. Asymmetric septal hypertrophy in hypertensive patients can be reduced by antihypertensive treatment, indicating that it is a reversible form of hypertensive cardiopathy. (Hypertens Res 1994; 17: 99-104)
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  • Gian Paolo Rossi, Lucia Zanin, Renzo de Toni, Roberta Venturini, Giova ...
    1994 Volume 17 Issue 2 Pages 105-115
    Published: 1994
    Released: August 10, 2006
    JOURNALS FREE ACCESS
    To assess the role of dopaminergic inhibition of aldosterone secretion in primary aldosteronism (PA) we studied the effect of dopaminergic DA2 blockade and stimulation in a series of consecutive cases of PA, and of primary hypertension (PH) as controls. Thirteen patients with confirmed PA (11 adenoma, 2 idiopathic hyperaldosteronism) and 8 primary hypertensive subjects (PH) were studied while on a 100 mmol/day sodium diet. Patients with aldosterone-producing adenoma were studied before, 1-2wk after, and 6 months after surgery. The DA2-antagonist metoclopramide (10mg i.v.) and the DA2-agonist dihydroergotoxine (6μg/Kg b.w. i.v.) were administered on different days. The effect of the latter on adrenal vein aldosterone and cortisol levels was also studied in selected cases. Plasma aldosterone, prolactin, cortisol, renin activity, free catecholamines, ACTH, Na+, K+, heart rate, and blood pressure were measured before and repeatedly after administration of each drug. In both groups, metoclopramide significantly increased aldosterone, prolactin, and cortisol (p<0.01), slightly decreased K+, and did not change the other variables. In PA patients, the aldosterone output was significantly (p<0.05) greater than in PH, and fell after surgery. There was no difference, however, in responsiveness to metoclopramide between PA and control patients. Dihydroergotoxine significantly decreased plasma prolactin and aldosterone levels and adrenal vein aldosterone in patients with PH. In contrast, despite a similar decrease in prolactin, in PA a significant (p<0.05) increase in aldosterone was seen, both peripherally and in adrenal vein blood. Thus, in PA: 1) the response to DA2 blockade is qualitatively normal but quantitatively enhanced; 2) this enhancement disappears after removal of the adenoma and thus appears related to increased aldosterone-secreting tissue rather than to enhanced responsiveness; 3) the response stimulation by dihydroergotoxine is paradoxical in PA, and may be mediated through ACTH stimulation. (Hypertens Res 1994; 17: 105-115)
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  • Naoharu Iwai, Nobuyuki Ohmichi, Yasuyuki Nakamura, Kenichi Mitsunami, ...
    1994 Volume 17 Issue 2 Pages 117-121
    Published: 1994
    Released: August 10, 2006
    JOURNALS FREE ACCESS
    Association between hypertension and molecular variants of angiotensinogen (AGT) has been confirmed in Caucasian populations. The present study was conducted in a Japanese population. Eighty-two hypertensive and eighty-three normotensive subjects were analyzed. The region of interest in the AGT gene was amplified by the polymerase chain reaction method, the molecular variant of T174M was detected with the use of a restriction enzyme Nco I, and the molecular variant of M235T was detected with the use of allele-specific oligonucleotide probes. The allele frequency of the M174 in the hypertensive group (HT) was 0.141, while that in the normotensive group was 0.079 (0.05<p<0.1). The allele frequency of the T235 in HT was 0.859, while that in NT was 0.771 (p<0.05). A higher frequency of the T235 allele was observed in the hypertensive subjects with ECG-LVH than in those without ECG-LVH (p<0.05). The molecular variant of the angiotensinogen gene T235 seem to be a predisposing factor for hypertension in the Japanese population. (Hypertens Res 1994; 17: 117-121)
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  • Makoto Suzuki, Mareomi Hamada, Kunio Hiwada
    1994 Volume 17 Issue 2 Pages 123-131
    Published: 1994
    Released: August 10, 2006
    JOURNALS FREE ACCESS
    Left ventricular elastance is the intrinsic mechanical property of the chambers that generates pressure for a given volume, but the dynamics of the ejection flow are characterized by the ventricular impulse in early systole. The purpose of this study was to characterize the ejection dynamics in the human hypertensive heart according to the concept of ventricular impulse and elastance. Nineteen hypertensive patients without left ventricular hypertrophy (HT-I), 42 hypertensive patients with left ventricular hypertrophy (HT-II), and 43 normotensive subjects (NT) were studied by pulsed Doppler echocardiography. The maximum ejection force (Fmax; kdyne) and the end-systolic wall stress/end-systolic volume index (ESWS/ESVI; kdyne/cm2/ml/m2)were examined as indexes of maximal impulse and elastance, respectively. Fmax was calculated on the basis of the unsteady Bernoulli equation. With regard to impulse and elastance in NT, Fmax was 43.7±6.1 and ESWS/ESVI was 2.26±0.78. In the hypertensive groups, HT-I showed normal Fmax (46.0±5.5) with a significantly higher ESWS/ESVI (3.52±1.12, p<0.01 vs. NT), and HT-II showed a significantly lower Fmax (34.4±7.2, p<0.01 vs. NT) with normal ESWS/ESVI (2.65±1.38). There was a significant inverse correlation between Fmax and left ventricular mass index (r =-0.45, p<0.001). This study shows for the first time the dissociation of maximum impulse and maximum elastance in the human hypertensive heart. The characteristics of elastance are well preserved, but those of the impulse are not preserved in the hypertensive hypertrophied heart. Further more, this dissociation is observed from the undetected hypertrophic state in the human hypertensive heart. (Hypertens Res 1994; 17: 123-131)
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  • Hiroshi Kawabe, Ikuo Saito, Motoko Nishino, Hideki Wainai, Shiro Nagan ...
    1994 Volume 17 Issue 2 Pages 133-136
    Published: 1994
    Released: August 10, 2006
    JOURNALS FREE ACCESS
    We investigated whether hyperinsulinemia and insulin resistance were associated with hypertension independent of obesity in young (mean age 20 years) Japanese men. Subjects were classified as hypertensive if their systolic or diastolic blood pressure (BP) was≥40 or≥90mm Hg, respectively. Subjects were classified as obese if their body mass index (BMI) was≥26. We divided 88 subjects into four groups: 29 nonobese normotensives (NONT), 12 nonobese hypertensives (NOHT), 28 obese normotensives (ONT), and 19 obese hypertensives (OHT). We conducted a 75g oral glucose tolerance test (OGTT) and measured plasma glucose and serum insulin at 0, 30, and 60min. We found similar glucose levels at fasting and during OGTT in all groups. Compared with the NONT group, the insulin levels at fasting and during OGTT were significantly higher in the NOHT group. No difference was found between the NOHT and ONT groups. The glucose/insulin ratios and the ratio of glucose area to insulin area were significantly lower in the NOHT group than in the NONT group; no difference was found between the NOHT and ONT groups. The OHT group had higher fasting insulin levels and lower fasting glucose/insulin ratios than the NOHT or ONT group. The fasting glucose/insulin ratio was correlated with the mean BP when the normotensives and hypertensives were combined. In a multiple regression analysis including BMI, the mean BP was still significantly related to the fasting glucose/insulin ratio. Our data indicate that hyperinsulinemia is associated with hypertension and is independent of obesity in young Japanese men. (Hypertens Res 1994; 17: 133-136)
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  • Judith A. Whitworth, Paula M. Williamson, David Ramsay
    1994 Volume 17 Issue 2 Pages 137-142
    Published: 1994
    Released: August 10, 2006
    JOURNALS FREE ACCESS
    To examine the proposition that vasoconstriction is essential for onset of cortisol hypertension using the calcium channel blocking drug, felodipine. Six normal male volunteers in random order, 4 weeks apart received placebo (Study A) or 5mg felodipine ER, orally daily (Study B) for 9 days, plus 50mg cortisol orally, 6 hourly for 5 days, commencing day 4. Minute distance (cm/min) determinations were made using Doppler and total peripheral resistance calculated as: mean arterial pressure (MAP) (mmHg)/minute distance. There were no differences between placebo and felodipine alone (Day 1-3). On both treatments, cortisol increased blood pressure (BP), weight, white cell count, sodium and cortisol concentrations and decreased potassium, albumin, hematocrit and eosinophil count. BP was similar on both treatments. Minute distance in felodipine pre-treated subjects prior to cortisol was 1, 518±66cm/min and rose with cortisol to 1, 644±83cm/min (p=0.030) but the increase in placebo pre-treated subjects was not significant. Calculated total peripheral resistance was unchanged following cortisol. Felodipine pretreatment failed to modify cortisol-induced rises in BP. An increase in peripheral resistance is not essential for production of cortisol-induced hypertension. (Hypertens Res 1994; 17: 137-142)
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  • Eiji Kaneko, Yasushi Kobayashi, Yukio Yasukochi, Yukio Kishi, Fujio Nu ...
    1994 Volume 17 Issue 2 Pages 143-147
    Published: 1994
    Released: August 10, 2006
    JOURNALS FREE ACCESS
    17α-hydroxylase/17, 20-lyase deficiency is an autosomal recessive disorder, which causes mineralcorticoid hypertension. Here we report two Japanese siblings, male and female, affected by 17α- hydrOxylase/17, 20-lyase deficiency. To clarify the molecular mechanism of the enzyme deficiency, we isolated the gene encoding 17α-hydroxylase/17, 20-lyase (CYP17) by polymerase chain reaction (PCR) from these patients, and compared its nucleotide sequences with those of normal CYP17. We confirmed only one difference: a TTC of codon 53 or 54 was deleted in the exon 1 of CYP17 of the propositus, resulting in deletion of phenylalanine at either 53 or 54. Dot blot hybridization of the amplified DNA with allele-specific oligonucleotide probes showed that the two patients were homozygous and their parents were heterozygous for this mutation. The reduced activity of 17α-hydroxylase/17, 20-lyase was probably caused by this mutation. (Hypertens Res 1994; 17: 143-147)
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