Hypertension Research
Online ISSN : 1348-4214
Print ISSN : 0916-9636
ISSN-L : 0916-9636
Volume 15 , Issue 1
Showing 1-8 articles out of 8 articles from the selected issue
  • Norman K. Hollenberg, Caroline Coletti, Diane Passan
    1992 Volume 15 Issue 1 Pages 3-10
    Published: 1992
    Released: August 10, 2006
    JOURNALS FREE ACCESS
    The concept of volume and vasoconstriction as polar elements in a model of the pathogenesis of hypertension has proven to be very useful. Many lines of investigation also suggest that the kidney must be involved in sustaining hypertension, whatever the primary pathogenetic mechanism. There are few studies, however, to link the status of renal perfusion and function to models of vasoconstriction and volume. We assessed the renal vascular (electromagnetic flowmeter) and depressor responses to two classes of agent, manidipine (a calcium antagonist) and enalaprilat (an ACE inhibitor), in rats with two models of hypertension. The spontaneously hypertensive rat (SHR) in comparison to its genetic mate, the normotensive WKY, was studied as a model in which vasoconstriction dominates pathogenesis. DOCA-salt hypertension was induced in rats as a model of volume-dependent hypertension. In SHR and WKY, enalaprilat and manidipine induced similar depressor responses and similar renal vasodilatation: internal evidence suggested that enalaprilat acted primarily by reducing angiotensin II (All) formation. The similarity of the response to manidipine may reflect its ability to block renal vasoconstriction induced by All. In the DOCA-salt model, on the other hand, manidipine was much more effective both as a depressor agent and as a renal vasodilator than enalaprilat. Indeed, the renal vasodilatation induced by manidipine in the DOCA-salt model exceeded substantially the vasodilatation induced by either class of agent in SHR. The results are consistent with an action of manidipine in the volume-dependent model that reverses the action of an agent that leads to increased vascular smooth muscle intracellular calcium -perhaps the digitalis-like factor. We conclude that quantitatively important renal vascular changes occur in both models of volume and vasoconstriction, and that the model determines the renal response to calcium antagonists and ACE inhibitors. (Hypertens Res 1992; 15: 3-11)
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  • Mitsuhide Naruse, Noriko Nakamura, Kiyoko Naruse, Kazuo Kubo, Mariko K ...
    1992 Volume 15 Issue 1 Pages 11-16
    Published: 1992
    Released: August 10, 2006
    JOURNALS FREE ACCESS
    To elucidate the mechanism responsible for the hypertension following recombinant human erythropoietin (rhEpo) therapy in hemodialysis patients, we determined plasma immunoreactive (ir-) endothelin-1 (ET-1) in Epo-induced hypertension. Sixteen hemodialysis patients (54±3 years) were studied. RhEpo was administered (30-120IU/kg/week) for 12 weeks. Blood pressure, hematocrit (Ht), plasma ir-ET-1, renin, aldosterone, norepinephrine, epinephrine, and atrial natriuretic peptide (ANP) were determined. Ht increased significantly in all patients. Based upon the changes in mean blood pressure (MBP) after rhEpo therapy, patients were classified into two groups: hypertensive (n=9) with ΔMBP >10mmHg, and normotensive (n=7) with ΔMBP≤10mmHg. Plasma ir-ET-1 in the hypertensive group increased significantly from 0.52±0.08pmol/liter to 0.88±0.08pmol/liter, while that in the normotensive group did not change. There was a positive correlation between changes in plasma ir-ET-1 and MBP in the hypertensive group. After cessation of rhEpo therapy, the decrease in plasma ir-ET-1 level paralleled the decreases in Ht and MBP. There were no significant changes in plasma renin, aldosterone, norepinephrine, epinephrine, and ANP between the two groups after rhEpo therapy. These results suggest that ET-1 participates to some extent in the pathogenesis of hypertension following rhEpo therapy. (Hypertens Res 1992; 15: 11-16)
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  • Yoshio Uehara, Yukari Kawabata, Hiroaki Shirahase, Katsuo Wada, Yukiko ...
    1992 Volume 15 Issue 1 Pages 17-26
    Published: 1992
    Released: August 10, 2006
    JOURNALS FREE ACCESS
    We have found that indapamide has free radical scavenging properties and stimulates prostacyclin generation in vascular smooth muscle cells. In this study, we investigated whether indapamide exhibits radical scavenging effects in vivo and whether these properties are related to renal protection in Dahl salt-sensitive (Dahl S) rats. Indapamide (4mg/kg body weight per day for 5 weeks) ameliorated the development of hypertension in Dahl S rats fed a high salt (6% NaCl) diet. The blood pressure reduction was associated with a decrease in proteinuria, a decrease in urinary n-acetyl-β-D-glucosaminidase excretion, and an increase in glomerular filtration rate. Moreover, morphological investigation revealed improvement in glomerulosclerosis, renal tubular damage and intrarenal arterial injuries, seen in the salt-induced hypertension. These beneficial properties were accompanied by a significant decrease in the capacity for lipid peroxide formation in the renal homogenates. In contrast, trichloromethiazide, which reduced the blood pressure to the same extent as indapamide, did not lower lipid peroxide formation in the kidney or exert protective effects on the renal glomeruli or arteries. Thus, the evidence suggests that the diuretic indapamide exhibits radical scavenging effects on the kidney which may contribute to attenuating the renal injuries seen in salt-induced hypertension in Dahl S rats. (Hypertens Res 1992; 15: 17-26)
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  • Shinjiro Muneta, Yasunobu Dazai, Takeru Iwata, Kunio Hiwada, Katsuyuki ...
    1992 Volume 15 Issue 1 Pages 27-32
    Published: 1992
    Released: August 10, 2006
    JOURNALS FREE ACCESS
    We examined baroreflex sensitivity (BRS) and blood pressure response to stress tests in climacteric hypertensive women (CHW) and ovariectomized hypertensive women (OxHW) and compared the results with those obtained in climacteric normotensive women (CNW) and essential hypertensive women (EHW). BRS was markedly reduced in CHW and OxHW compared with CNW and EHW. The blood pressure response to mental arithmetic test was significantly higher in CHW and OxHW than in CNW. On the other hand, the blood pressure response to isometric handgrip exercise in CHW and OxHW was similar to that in CNW. Aortic pulse wave velocity, used as an indicator of arteriosclerosis, in CHW and OxHW was similar to that in CNW. The blood pressure response to mental arithmetic test showed a significant inverse correlation with BRS. After estrogen replacement therapy in CHW and OxHW for one month, the clinic blood pressure fell significantly with marked improvement of BRS and attenuation of the blood pressure response to mental arithmetic test. Thus, impaired baroreflex and hyperresponsiveness of blood pressure to mental stress due to the deprivation of estrogen are considered to be important factors in the pathophysiology of hypertension in climacteric state. (Hypertens Res 1992; 15: 27-32)
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  • Hironosuke Sakamoto, Kouji Imataka, Hiroshi Nishimura, Jun Fujii
    1992 Volume 15 Issue 1 Pages 33-39
    Published: 1992
    Released: August 10, 2006
    JOURNALS FREE ACCESS
    We carried out both mental stress (MS) and isometric handgrip exercise (IHG) tests in 20 mild hypertensive patients to compare responses of blood pressure, heart rate, blood cell count and pressor hormones between the two tests. Increments of blood pressure and heart rate by MS (mean±SEM, 42± 2/17±1mmHg and 8±1beats/mm) were similar to those by IHG (39 ±3/17±2mmHg and 6±1beats/ min). Packed cell volume, erythrocytes, leukocytes, and platelets significantly increased in the MS test (1.3±0.3%, 1.7±0.3%, 10.3±2.1% and 2.8±1.6%, respectively) and in the IHG test (1.3±0.3%, 1.0 ±0.3%, 6.2±1.2% and 1.9±0.8% respectively). In both tests the percent increase was significantly greater in leukocytes than in erythrocytes and platelets (p<0.01). A comparison between the two tests revealed that the increase in leukocyte count was significantly greater in the MS than in the IHG test (p <0.05). Plasma noradrenaline, adrenaline and vasopressin levels significantly increased in both tests and there were no significant differences in responses of these pressor hormones between the two tests. Plasma active renin and aldosterone levels significantly increased in the MS test, but remained unchanged in the IHG test. Although the responses to both stressors are mainly induced by the sympathoadrenal excitation, there are some differences in details between the two tests. We concluded that MS induced a greater increase in leukocyte count than IHG with equipressor response and activated the renin-angiotensin-aldosterone system, which was not stimulated by the latter. (Hypertens Res 1992; 15: 33-39)
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  • Eiki Murakami, Tatsuo Kokubu, Yasuko Ii, Kunio Hiwada, Shigeki Muramat ...
    1992 Volume 15 Issue 1 Pages 41-44
    Published: 1992
    Released: August 10, 2006
    JOURNALS FREE ACCESS
    Repeated oral doses (120mg or 240mg, once daily) of the human renin inhibitor ES-8891 were given for 10 days to 16 normotensive male subjects on a normal sodium diet. Both doses produced significant inhibition of plasma renin activity (complete inhibition at 0.5 and 1 hour, 50% inhibition at 2 hours) which was inversely correlated with the plasma level of ES-8891. Plasma immunoreactive active renin was not enhanced in spite of significant decreases in plasma angiotensin I and aldosterone levels. There was no significant change in blood pressure or heart rate. No adverse reactions were evident. These results suggest that ES-8891 is an orally active human renin inhibitor which may be clinically useful. (Hypertens Res 1992; 15: 41-44)
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  • Shunsaku Mizushima, Emilio Hideyuki Moriguchi, Yasuhiko Nakada, Maria ...
    1992 Volume 15 Issue 1 Pages 45-55
    Published: 1992
    Released: August 10, 2006
    JOURNALS FREE ACCESS
    To investigate the relationship of dietary factors to cardiovascular diseases, we conducted a study of 234 middle-aged Japanese men and women in Okinawa (JJ), and 160 Japanese immigrants of similar age, originally from Okinawa, in Brazil (JB). JB showed double the prevalence (%) of ST-T changes in the electrocardiogram (ECG) (JJ: M3.4, F4.4, JB: M8.3, F10.1) and of hypertension (HT) (JJ: M15.9, F18.4; JB: M32.8, F36.4, p<0.05) when this was assessed on BP≥160/95 and/or the taking of antihypertensive medication; however the mean level of blood pressure did not differ. A gradient in the rate of HT in men and of ECG ST-T changes in both sexes was observed from JJ to JB of first-generation and to JB of second-generation. JB had much higher body mass index (kg/m2) (JJ: M24.8±0.3, F24.8± 0.4; JB:M26.2±0.4, F26.5±0.4, p<0.01) in both sexes, and an 8-fold higher rate of oral contraceptive usage (p<0.001). Total cholesterol level showed no significant difference between JJ and JB. 24-hour urinary taurine excretion in both sexes and plasma phospholipid n-3 fatty acid level in men were significantly higher in JJ than in JB. The dietary pattern in Japanese immigrants in Brazil, characterized by low fish and large meat intake, is possibly responsible for the higher risk of HT and ECG ST-T changes, indicating the importance of dietary rather than genetic factors. (Hypertens Res 1992; 15: 45-55)
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  • Robert Y. L. Zee, Brian J. Morris, Lyn R. Griffiths
    1992 Volume 15 Issue 1 Pages 57-60
    Published: 1992
    Released: August 10, 2006
    JOURNALS FREE ACCESS
    Adrenoceptor stimulation has an important role in normal cardiovascular regulation and a genetic defect could be a cause of essential hypertension (HT). The present study examined the relationship with HT of RFLPs for the α2-adrenoceptor gene (ADRA2R) and β1-adrenoceptor gene (ADRB1R), which share the same chromosomal locus (10q24-26). Subjects were HTs and normotensives (NTs) whose parents had a similar blood pressure status at age ≥50. The frequency of the minor allele of the DraI RFLP of ADRA2R was 0.17 in HTs (n=76) and 0.17 in NTs (n=87). For the BglI RFLP of ADRBIR, frequency of the minor allele was 0.10 in HTs (n=62) and 0.12 in NTs (n=88). x2 analysis showed no difference between HT and NT groups. Thus the present study provides no basis for involvement of the α2- or β1- adrenoceptor genes in essential hypertension. (Hypertens Res 1992; 15: 57-60)
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