Decreased plasma levels of nitric oxide metabolites, angiotensin II, and aldosterone in spontaneously hypertensive rats exposed to 5 mT static magnetic field

Previously, we found that whole body exposure to static magnetic fields (SMF) at 10 mT (B(max)) and 25 mT (B(max)) for 2-9 weeks suppressed and delayed blood pressure (BP) elevation in young, stroke resistant, spontaneously hypertensive rats (SHR). In this study, we investigated the interrelated antipressor effects of lower field strengths and nitric oxide (NO) metabolites (NO(x) = NO(2)(-) + NO(3)(-)) in SHR. Seven-week-old male rats were exposed to two different ranges of SMF intensity, 0.3-1.0 mT or 1.5-5.0 mT, for 12 weeks. Three experimental groups of 20 animals each were examined: (1) no exposure with intraperitoneal (ip) saline injection (sham-exposed control); (2) 1 mT SMF exposure with ip saline injection (1 mT); (3) 5 mT SMF exposure with ip saline injection (5 mT). Arterial BP, heart rate (HR), skin blood flow (SBF), plasma NO metabolites (NO(x)), and plasma catecholamine levels were monitored. SMF at 5 mT, but not 1 mT, significantly suppressed and retarded the early stage development of hypertension for several weeks, compared with the age matched, unexposed (sham exposed) control. Exposure to 5 mT resulted in reduced plasma NO(x) concentrations together with lower levels of angiotensin II and aldosterone in SHR. These results suggest that SMF may suppress and delay BP elevation via the NO pathways and hormonal regulatory systems.     

Effects of 25 mT static magnetic field on blood pressure in reserpine-induced hypotensive Wistar-Kyoto rats

We investigated the interrelated antihypotensive effects of static magnetic fields (SMF) and plasma catecholamine levels in reserpine-induced hypotensive Wistar-Kyoto rats. Seven-week-old male rats were exposed to two different ranges of SMF intensities, 3.0-10 mT (Bmax) or 7.5-25 mT (Bmax) for 12 weeks. Six experimental groups of 10 animals each were examined: (1) no exposure with intraperitoneal (ip) saline injection (sham exposed control); (2) 10 mT SMF exposure with ip saline injection (10 mT); (3) 25 mT SMF exposure with ip saline injection (25 mT); (4) no exposure with ip reserpine injection (RES); (5) 10 mT SMF exposure with ip reserpine injection (10 mT + RES); (6) 25 mT SMF exposure with ip reserpine injection (25 mT + RES). Reserpine (5 mg/kg) was administered three times a week for 12 weeks, and 18 h after each injection, arterial blood pressure (BP), heart rate, skin blood flow, plasma nitric oxide metabolites, plasma catecholamine levels, and behavioral parameters of a functional observational battery (FOB) were monitored. The action of reserpine significantly decreased BP, reduced plasma norepinephrine (NE), increased the FOB hunched posture score and decreased the number of rearing events in the RES group, compared with the respective age-matched control group. Exposure to 25 mT, but not 10 mT, for 2-12 weeks significantly prevented the reserpine-induced decrease of BP in the 25 mT + RES group compared with the respective RES group. Moreover, exposure to 25 mT for 5 weeks partially suppressed the reserpine-induced NE reduction, but did not bring about a complete reversal of reserpine effects. NE levels for the 25 mT + RES group for 5 weeks were significantly higher compared with the RES group, but still lower compared with the control group. In addition, the FOB hunched posture score for the 25 mT + RES group was significantly lower and the number of rearing events was higher compared with the RES group, but these behavioral parameters did not revert to control levels. There were no significant differences in any of the physiological or behavioral parameters measured between the 10 mT + RES and RES groups, nor between the two different SMF groups and the control group. These results indicate that 25 mT SMF with spatial gradients significantly suppressed the reserpine-induced hypotension and bradykinesia. The antihypotensive effects of SMF on the reserpine-treated group might be at least partially related to the inhibition of NE depletion.     

Effects of static magnetic fields on plasma levels of angiotensin II and aldosterone associated with arterial blood pressure in genetically hypertensive rats

Effects of static magnetic fields (SMFs) on development of hypertension were investigated using young male, stroke resistant, spontaneously hypertensive rats (SHRs) beginning at 7 weeks of age. SHRs were randomly assigned to two different exposure groups or an unexposed group. The SHRs in the exposure groups were constantly exposed to two different types of external SMFs of 3.0-10.0 mT or 8.0-25.0 mT for 12 weeks. The SMFs were generated from permanent magnetic plates attached to the rat cage. The blood pressure (BP) of each rat was determined at weekly intervals using indirect tail-cuff method. The SMFs suppressed and retarded the development of hypertension in both exposed groups to a statistically significant extent for several weeks, as compared with an unexposed group. The antipressor effects were related to the extent of reduction in plasma levels of angiotensin II and aldosterone in the SHRs. These results suggest that the SMFs of mT intensities with spatial gradients could be attributable to suppression of early BP elevation via hormonal regulatory system.     

No effect of exposure to static and sinusoidal magnetic fields on nitric oxide production by macrophages

The effects of exposure to static (1–100 mT) or sinusoidal (1 Hz, 1.6 mT) magnetic fields on the production of nitric oxide (NO) by murine BCG-activated macrophages were investigated. In these cells, the inducible isoform of NO synthase is present. No significant differences were observed in nitrite levels among exposed, sham-exposed, or control macrophages after exposure for 14 h to static fields of 1, 10, 50, and 100 mT and to sinusoidal 1.6 mT, 1 Hz magnetic fields. © 1996 Wiley-Liss, Inc.     

Nitric oxide modulates the responses of osteoclast formation to static magnetic fields

Nitric oxide (NO) is involved in osteoclast differentiation. Our previous studies showed that static magnetic fields (SMFs) could affect osteoclast differentiation. The inhibitory effects of 16 T of high SMF (HiMF) on osteoclast differentiation was correlated with increased production of NO. We raised the hypothesis that NO mediated the regulatory role of SMFs on osteoclast formation. In this study, 500 nT of hypomagnetic field (HyMF), 0.2 T of moderate SMF (MMF) and 16 T of high SMF (HiMF) were utilized as SMF treatment. Under 16 T, osteoclast formation was markedly decreased with enhanced NO synthase (NOS) activity, thus producing a high level of NO. When treated with NOS inhibitor N-Nitro-L-Arginine Methyl Ester (L-NAME), NO production could be inhibited, and osteoclast formation was restored to control group level in a concentration-dependent manner. However, 500 nT and 0.2 T increased osteoclast formation with decreased NOS activity and NO production. When treated with NOS substrate L-Arginine (L-Arg) or NO donor sodium nitroprusside (SNP), the NO level in the culture medium was obviously elevated, thus inhibiting osteoclast differentiation in a concentration-dependent manner under 500 nT or 0.2 T. Therefore, these findings indicate that NO mediates the regulatory role of SMF on osteoclast formation.     

Effects of 12 mT static magnetic field on sympathetic agonist-induced hypertension in Wistar rats

We investigated the combined effects of a moderate-intensity static magnetic field (SMF) and two different sympathetic agonists, an alpha(1)-adrenoceptor agonist, phenylephrine and a beta(1)-adrenoceptor agonist, dobutamine, which induced hypertension and different hemodynamics in Wistar rats. Five-week-old male rats were continuously exposed to the SMF intensity of 12 mT (B(max)) with the peak spatial gradient of 3 mT/mm for 10 weeks. A loop-shaped flexible rubber magnet was adjusted to fit snugly around the neck region of a rat (diameter-adjustable to an animal size). Sham exposure was performed using a dummy magnet. Six experimental groups of six animals each were examined: (1) sham exposure with intraperitoneal (ip) saline injection (control); (2) SMF exposure with ip saline injection (SMF); (3) sham exposure with ip phenylephrine (1.0 microg/g) injection (PE); (4) SMF exposure with ip phenylephrine injection (SMF + PE); (5) sham exposure with ip dobutamine (4.0 microg/g) injection (DOB); (6) SMF exposure with ip dobutamine injection (SMF + DOB). Fifteen minutes after the injection of each agent, the first set of parameters, arterial blood pressure (BP) and heart rate (HR), the second set of parameters, skin blood flow (SBF) and skin blood velocity (SBV), or the third set of parameters, the number of rearing (exploratory behavior) responses and body weight was monitored. Each agent was administered three times a week for 10 weeks, and each set of parameters was monitored on different days, once a week. The dose of phenylephrine significantly increased BP and decreased HR, SBF, SBV, and the number of rearing responses in the PE group compared with those in the respective age-matched control group. The dose of dobutamine significantly increased BP and HR, increased SBF, SBV, and the number of rearing responses in the DOB group compared with those in the control group. Continuous neck exposure to the SMF alone for up to 10 weeks induced no significant changes in any of the measured cardiovascular and behavioral parameters. The SMF exposure for at least 2 weeks (1) significantly depressed phenylephrine effects on BP, SBF, SBV, and rearing activity (SMF + PE group vs. PE group); (2) significantly depressed dobutamine effects on BP, SBF, and SBV, and suppressed dobutamine-induced increase in the rearing activity (SMF + DOB group vs. DOB group). These results suggest that continuous neck exposure to 12 mT SMF for at least 2 weeks may depress or suppress sympathetic agonists-induced hypertension, hemodynamics, and behavioral changes by modulating sympathetic nerve activity.     

Lack of an effect of static magnetic field on calcium efflux from isolated chick brains

45Ca2+ efflux from neonatal isolated chick brains was measured. The brains were exposed to uniform or nonuniform static magnetic fields. The field intensity ranged from 200-900 mT. The exposure took place during incubation and/or when efflux was being measured. No difference appeared in the 45Ca2+ efflux between controls and exposed brains.     

Exposure to strong static magnetic field slows the growth of human cancer cells in vitro

Proposals to enhance the amount of radiation dose delivered to small tumors with radioimmunotherapy by constraining emitted electrons with very strong homogeneous static magnetic fields has renewed interest in the cellular effects of prolonged exposures to such fields. Past investigations have not studied the effects on tumor cell growth of lengthy exposures to very high magnetic fields. Three malignant human cell lines, HTB 63 (melanoma), HTB 77 IP3 (ovarian carcinoma), and CCL 86 (lymphoma; Raji cells), were exposed to a 7 Tesla uniform static magnetic field for 64 hours. Following exposure, the number of viable cells in each group was determined. In addition, multicycle flow cytometry was performed on all cell lines, and pulsed-field electrophoresis was performed solely on Raji cells to investigate changes in cell cycle patterns and the possibility of DNA fragmentation induced by the magnetic field. A 64 h exposure to the magnetic field produced a reduction in viable cell number in each of the three cell lines. Reductions of 19.04 ± 7.32%, 22.06 ± 6.19%, and 40.68 ± 8.31% were measured for the melanoma, ovarian carcinoma, and lymphoma cell lines, respectively, vs. control groups not exposed to the magnetic field. Multicycle flow cytometry revealed that the cell cycle was largely unaltered. Pulsed-field electrophoresis analysis revealed no increase in DNA breaks related to magnetic field exposure. In conclusion, prolonged exposure to a very strong magnetic field appeared to inhibit the growth of three human tumor cell lines in vitro. The mechanism underlying this effect has not, as yet, been identified, although alteration of cell growth cycle and gross fragmentation of DNA have been excluded as possible contributory factors. Future investigations of this phenomenon may have a significant impact on the future understanding and treatment of cancer. © 1996 Wiley-Liss, Inc.     

Anti-pressor effects of whole body exposure to static magnetic field on pharmacologically induced hypertension in conscious rabbits

Acute effects of whole body exposure to static magnetic field (SMF) on pharmacologically induced hypertension in a conscious rabbit were evaluated. Hypertensive and vasoconstrictive actions were induced by norepinephrine (NE) or a nonselective nitric oxide synthase (NOS) inhibitor, N(omega)-nitro-l-arginine methyl ester (l-NAME). The hemodynamics in a central artery of the ear lobe was measured continuously and analyzed by penetrating microphotoelectric plethysmography (MPPG). Concurrently, blood pressure (BP) changes in a central artery, contralateral to that of the MPPG measured ear lobe, were monitored. Magnetic flux densities were 5.5 mT (Bmax), the magnetic gradient peaked in the throat at the level of approximately 0.09 mT/mm, and the duration of exposure was 30 min. The results demonstrated that under normal physiological conditions without treatment of pharmacological agents, there were no statistically significant differences in the hemodynamics and BP changes between the sham and the SMF exposure alone. Under pharmacologically induced hypertensive conditions, the whole body exposure to nonuniform SMF with peak magnetic gradient in the carotid sinus baroreceptor significantly attenuated the vasoconstriction and suppressed the elevation of BPs. These findings suggest that antipressor effects of the SMF on the hemodynamics under NE or l-NAME induced high vascular tone might be, in part, dependent on modulation of NE mediated response in conjunction with alteration in NOS activity, thereby modulating BPs.     

Neuropathology and behavioral impairments in Wistar rats with a 6-OHDA lesion in the substantia nigra compacta and exposure to a static magnetic field

Studies have sought to assess various potential neuroprotective therapeutics in Parkinson's disease. The aim of this study was to evaluate the effects of static magnetic field stimulation 14 days after a 6-Hydroxydopamine (6-OHDA) substantia nigra compacta (SNc) lesion on motor behavior, as assessed by the rotarod (RR) test and brain tissue morphology. Forty male Wistar rats were used and were divided into five groups: control group, sham group (SG), lesion group (LG), lesion north pole group (LNPG) and lesion south pole group (LSPG). In groups with magnetic stimulation, a 3200-gauss magnet was fixed to the skull. After the experiments, the animals were anesthetized for brain perfusion. Coronal sections of the SNc were stained with Nissl. The RR test showed a decrease in the time spent on the apparatus in the LG compared with all groups. The LNPG and LSPG had significant increases in the time spent when compared to the LG. A morphometric analysis revealed a significant reduction in the number of neurons in the LG, LNPG and LSPG in relation to the SG. There were a higher number of neurons in the LNPG and LSPG than the LG, and a higher number of neurons in the LSPG than the LNPG. We observed that the LG, LNPG and LSPG showed a higher number of glial cells than the SG, and the LNPG and LSPG showed a lower number of glial cells than the LG. Our results demonstrate a potential therapeutic use of static magnetic fields for the preservation of motor behavior and brain morphology in the SNc after 14 days with 6-OHDA lesion.     

Development of xenopus laevis embryos in a static magnetic field

Xenopus laevis embryos were exposed to a DC magnetic field (2.5 kG) for periods up to 1 week. The previously reported stabilization of cell membranes by stationary magnetic fields could not be demonstrated.     

Beneficial effect of enalapril in spontaneously hypertensive rats cardiac remodeling with nitric oxide synthesis blockade

Aims . To study the efficiency of an angiotensin converting enzyme inhibitor on the blood pressure (BP) and the myocardium remodeling when spontaneously hypertensive rats (SHRs) are submitted to nitric oxide synthesis (NOs) blockade (with L-NAME) and simultaneously treated.
Methods . Young adult male SHRs were separated in four groups (n = 5) and treated for 20 days: Control, L-NAME, L-NAME+Enalapril, and Enalapril. The alterations of the BP, heart mass/body mass ratio and stereological parameters for myocytes, connective tissue and intramyocardial vessels were studied among the groups.
Results . The SHRs with NOs blockade showed a great modification of the myocardium with extensive areas of reparative and interstitial fibrosis and accentuated hypertrophy of the cardiac myocytes (cross sectional area 60% higher in animals taking L-NAME than in Control SHRs). Comparing the SHRs with NO deficiency (L-NAME group), the Control SHRs and the Enalapril treated SHRs significant differences were found in the BP and in all stereological parameters. The NO deficiency caused an important BP increment in SHRs that was partially attenuated by Enalapril. This Enalapril effect was more pronounced in Control SHRs. A significant increment of the intramyocardial vessels was observed in NO deficient SHRs and Control SHRs treated with Enalapril demonstrated by the stereology (greater microvascular densities in treated SHRs).
Conclusion . Enalapril administration showed a beneficial effect on vascular remodeling and myocardial hypertrophy in SHRs. In SHRs with NO blockade, however, the beneficial effect of Enalapril occurred only in vascular remodeling.     

Blockade of sensory neuron action potentials by a static magnetic field in the 10 mT range

To characterize the inhibitory effect of a static magnetic field, action potentials (AP) were elicited by intracellular application of 1 ms depolarizing current pulses of constant amplitude to the somata of adult mouse dorsal root ganglion neurons in monolayer dissociated cell culture. During the control period, <5% of stimuli failed to elicit AP. During exposure to an ?11 mT static magnetic field at the cell position produced by an array of four permanent center-charged neodymium magnets of alternating polarity (MAG-4A), 66% of stimuli failed to elicit AP. The number of failures was maximal after about 200-250 s in the field and returned gradually to baseline over 400–600 s. A direct or indirect effect on the conformation of AP generating sodium channels could account for these results because (I) failure was preceded often by reduction of maximal rate of rise, an indirect measure of sodium current; (2) recovery was significantly prolonged in more than one-half of neurons that were not stimulated during exposure to the MAG-4A field; and (3) resting membrane potential, input resistance, and chronaxie were unaffected by the field. The effect was diminished or prevented by moving the MAG-4A array along the X or Z axis away from the neuron under study and by increasing the distance between magnets in the XY plane. Reduction of AP firing during exposure to the ?0.1 mT field produced by a MAG-4A array of micromagnets was about the same as that produced by a MAG-4A array of the large magnets above. The ?28 mT field produced at cell position by two magnets of alternating polarity and the ?88 mT field produced by a single magnet had no significant effect on AP firing. These findings suggest that field strength alone cannot account for AP blockade. © 1995 Wiley-Liss, Inc.     

自发性高血压大鼠心脏与红细胞L-Arg转运的改变

研究自发性高血压大鼠 (spontaneouslyhypertensiverats ,SHR)心脏L 精氨酸 /一氧化氮 (L Arg/NO)系统的改变及其与红细胞L Arg转运的关系。检测 12周龄 (W)、16W、captopril治疗 4周后的 16WSHR (SHR C)及同龄Wistar Kyoto (WKY)大鼠心脏的L Arg转运、tNOS活性、NO 2 NO 3 和cGMP含量以及红细胞L Arg转运的改变。结果显示 ,SHR心室肌组织L Arg高亲和转运成分的最大转运速率 (Vmax)及低亲和转运成分的米氏常数 (Km)均明显低于WKY大鼠 ;但高亲和转运成分的Km 值和低亲和转运成分的Vmax则无明显改变 ;SHR C组的改变基本同 12W组。心肌组织tNOS活性的变化无统计学意义。NO 2 NO 3 及cGMP含量则分别较WKY组降低 2 4 6 %、19 8% (P >0 0 5 ,P <0 0 5 ,12W组 ) ,5 2 5 %、6 0 4% (P <0 0 1,P <0 0 1,16W组 )和 14 8%、2 3 % (P >0 0 5 ,P <0 0 5 ,SHR C组 )。tNOS活性、cGMP含量与LVW/BW呈负相关 ,r=0 45 0 7,P =0 0 5 (NOS) ,r=0 6 898,P <0 0 1(cGMP)。红细胞L Arg转运的改变与心脏一致 ,且其Vmax与心肌组织高亲和转运成分的Vmax呈正相关 ,r=0 5 6 0 6 ,P =0 0 1;与LVW /BW呈负相关 ,r=- 0 6 2 31,P <0 0 1。以上结果表明 ,SHR心室肌组织L Arg/NO系统活动被抑制 ,其抑制程度与心肌肥厚     

Effects of a moderate-intensity static magnetic field on VEGF-A stimulated endothelial capillary tubule formation in vitro

Effects of a moderate-intensity static magnetic field (SMF) on the early-stage development of endothelial capillary tubule formation were examined during the initial cell growth periods using co-cultured human umbilical vein endothelial cells and human diploid fibroblasts. The co-cultured cells within a well (16 mm in diameter) were exposed to SMF intensity up to 120 mT (Bmax) with the maximum spatial gradient of 21 mT/mm using a disc-shaped permanent magnet (16 mm in diameter and 2.5 mm in height) for up to 10 days. Control exposure was performed without magnet. Some vascular endothelial cells were treated with vascular endothelial growth factor (VEGF)-A (10 ng/ml) to promote the tubule formation every 2-3 days. Four experimental protocols were performed: (1) non-exposure (control); (2) SMF exposure alone; (3) non-exposure with VEGF-A; (4) SMF exposure with VEGF-A. Photomicrographs of tubule cells immunostained with an anti-platelet-endothelial cell adhesion molecule-1 (PECAM-1 [CD31[) antibody as a pan-endothelial marker, were analyzed after culture at 37 degrees C for 4, 7, and 10 days. The mean values of the area density and the length of tubules (related mainly to arteriogenesis) as well as the number of bifurcations (related mainly to angiogenesis) were determined as parameters of tubule formation and were compared between the groups. After a 10 day incubation, in the peripheral part of the culture wells, SMF alone significantly promoted the tubule formation in terms of the area density and the length of tubules, compared with control group. In the central part of the wells, however, SMF did not cause any significant changes in the parameters of tubule formation. After a 7 day incubation, VEGF-A significantly promoted all the parameters of tubule formation in any part of the wells, compared with control group. With regard to the synergistic effects of SMF and VEGF-A on tubule formation, after a 10 day incubation, SMF significantly promoted the VEGF-A-increased area density and length of tubules in the peripheral part of the wells, compared with the VEGF-A treatment alone. However, SMF did not induce any significant changes in the VEGF-A-increased number of bifurcations in any part of the wells. The tubule cells observed in the wells had elongated, spindle-like shapes, and the direction of cell elongation was random, irrespective of the presence and direction of SMF. These findings suggest that the application of SMF to intact or VEGF-A-stimulated vascular endothelial cells leads mainly to promote or enhance arteriogenesis in the peripheral part of the wells, where the spatial gradient increases relative to the central part. The effects of SMF on the VEGF-A-enhanced tubule formation appear to be synergistic or additive in arteriogenesis but not in angiogenesis.     

Cardiac mitochondrial function and tissue remodelling are improved by a non-antihypertensive dose of enalapril in spontaneously hypertensive rats

Renal and cardiac benefits of renin-angiotensin system inhibition exceed blood pressure (BP) reduction and seem to involve mitochondrial function. It has been shown that RAS inhibition prevented mitochondrial dysfunction in spontaneously hypertensive rats (SHR) kidneys. Here, it is investigated whether a non-antihypertensive enalapril dose protects cardiac tissue and mitochondria function. Three-month-old SHR received water containing enalapril (10 mg/kg/day, SHR+Enal) or no additions (SHR-C) for 5 months. Wistar-Kyoto rats (WKY) were normotensive controls. At month 5, BP was similar in SHR+Enal and SHR-C. In SHR+Enal and WKY, heart weight and myocardial fibrosis were lower than in SHR-C. Matrix metalloprotease-2 activity was lower in SHR+Enal with respect to SHR-C and WKY. In SHR+Enal and WKY, NADH/cytochrome c oxidoreductase activity, eNOS protein and activity and mtNOS activity were higher and Mn-SOD activity was lower than in SHR-C. In summary, enalapril at a non-antihypertensive dose prevented cardiac hypertrophy and modifies parameters of cardiac mitochondrial dysfunction in SHR.     

核磁共振磁场照射对子代大鼠海马突触形态的影响

研究观察了孕期磁共振磁场照射对子代大鼠海马突触超微结构的影响。SD孕鼠妊娠第12-18d给予0．35T核磁共振(magnetic resonance imaging,MRI)磁场照射。测量1、2和5月龄雌性仔鼠海马CAl区和齿状回的突触结构参数,用立体计量学方法进行定量测定。结果显示,磁场照射可引起2月龄子代大鼠海马CAl区突触间隙增宽．齿状回突触活性区长度变短、突触界面曲率和活性区面密度减小;5月龄子代大鼠CAl区突触间隙增宽,突触后致密物变薄,突触界面曲率减小,齿状回突触间隙增宽。结果提示,妊娠期接受MRI磁场照射可引起海马突触超微结构的改变。对这些结构变化与行为损害之间的关系进行了讨论。     

Antihypertensive effect of roselle (Hibiscus sabdariffa) calyx infusion in spontaneously hypertensive rats and a comparison of its toxicity with that in Wistar rats

The LD₅₀ of roselle calyx extract and its effect on blood pressure were determined. The LD₅₀ was found to be above 5000 mg kg⁻¹. Roselle calyx infusion was found to lower significantly (p<0·05) both systolic and diastolic pressure in spontaneously hypertensive and normotensive Wistar–Kyoto rats at tested doses of 500 and 1000 mg kg⁻¹ body weight. The reduction in blood pressure in both groups was positively correlated with weight. Continuous consumption of the infusion at 1000 mg kg⁻¹ was discovered to lead to sudden death in spontaneously hypertensive rats but not in Wistar‐Kyoto rats. Water intake was not significantly different (p>0·05) in the control groups of the two strains of rats used, neither was there a significant difference in their urine output. The water intake in the treated spontaneously hypertensive and normotensive rats was not different from the corresponding control groups. However the urine output of the treated spontaneously hypertensive rats was significantly higher. A significant decrease in serum creatinine, cholesterol, and glucose in the treated rats compared with the control as well as a significant increase in serum uric acid was observed. The serum proteins (albumin and total protein) in the treated rats when compared with the control groups was not changed significantly. Copyright © 1999 John Wiley & Sons, Ltd.