bluuebunny/crossref_metadata_2025_split huggingface dataset:
EFFECT OF HAEMORRHAGE ON THE POWER OF LOW FREQUENCY BLOOD PRESSURE FLUCTUATIONS IN YOUNG SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Eliash S. , Oz O. , Akselrod S. , Cohen S. 
Published: June 2007

Summary1. Before the onset of hypertension low frequency (0.04– 0.1 Hz) MAP fluctuations are reduced in SHR when compared to WKY. We studied the effect of haemorrhage under α1 blockade or angiotensin converting enzyme inhibition (CEI) on the power spectra (PS) of each strain.2. MAP was recorded from the caudal artery in conscious, 1 month old SHR and WKY. Three groups of rats were studied. Group 1, acute 2 mL haemorrhage; groups 2 and 3, injection of prazosin (0.25–2.5 mg/kg) or captopril (O.5–4 mg/kg), followed by haemorrhage, as in group 1. The PS was divided into 3 frequency bands, 0.004–0.04,0.04–0.07 and 0.07–0.1 Hz.3. In SHR, although the baseline MAP levels were similar to those of WKY, the PS was significantly damped in each of the 3 frequency bands.4. Haemorrhage induced a similar MAP fall in both strains accompanied by an increase in the slow MAP fluctuations. However, in SHR the PS response was significantly greater than in WKY. The biggest response was in the slowest (0.004–0.04 Hz) frequency band, 8.7 ± 1.7 vs 1.5 ± 0.4 times baseline levels, respectively.5. The difference between the two strains in the PS response to haemorrhage was eliminated by α1 blockade. The exaggerated response observed in haemorrhaged, unblocked SHR was reduced in the 3 frequency bands.6. Captopril reduced the PS response to haemorrhage in SHR to the level observed in WKY in all 3 frequency bands.7. The enhanced amplification of the MAP fluctuations in haemorrhaged SHR may indicate that SHR requires greater recruitment of control mechanisms than WKY to maintain MAP at a similar level to WKY.
DEVELOPMENT OF POLYURIA IN TSUKUBA HYPERTENSIVE MICE CARRYING HUMAN RENIN AND ANGIOTENSINOGEN GENES
Authors: Uehara Sayuri , Mino Nobuyuki , Tsuchida Minoru , Nishikibe Masaru , Fukamizu Akiyoshi , Murakami Kazuo , Ikemoto Fumihiko 
Published: June 2007

Summary1. Tsukuba hypertensive mice (THM) carry both human renin and angiotensinogen genes, and develop hypertension. The animal has high levels of renin activity and angiotensin II concentration in the plasma.2. Urinary excretion in THM was greater than in the control animal, non‐transgenic C57/BL/6j. THM showed a greater amount of daily water intake. The osmolality of 24 h urine was lower than that of the control animal.3. When water was deprived for 12h and then loaded with 0.25mL/10g bodyweight, the osmolality of urine at the first 0–3 h period was the same in THM and control, but significantly lower in THM at the following 3–6 h period, indicating that the urine concentrating activity is insufficient in THM compared with the control animal.4. Urinary excretion of vasopressin was significantly higher in THM. Plasma aldosterone concentration and urinary excretion of aldosterone were also higher in THM. Plasma potassium level was significantly low.5. The mechanism underlying the pathophysiology of polyuria is not totally explained; however, hypokalaemia, which was probably the result of hyperaldosteronism, may be at least partially involved, since hypokalaemia is considered to be a factor hampering the action of vasopressin for concentration of urine at the site of the collecting duct of the kidney.
ROLE OF NITRIC OXIDE IN IMPAIRED CORONARY CIRCULATION AND IMPROVEMENT BY ANGIOTENSIN II RECEPTOR ANTAGONIST IN SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Fujita Hiroshi , Takeda Kazuo , Nakamura Kame , Uchida Atsushi , Takenaka Ken , Itoh Hiroshi , Nakata Tetsuo , Sasaki Susumu , Nakagawa Masao 
Published: June 2007

Summary1. To determine whether coronary flow regulation by nitric oxide (NO) is impaired in the hypertensive heart (HTH), coronary perfusion was measured in isolated rat hearts using NO synthesis inhibitor L‐NG‐monomethyl arginine (L‐NMMA) in Wistar‐Kyoto (WKY) rat and spontaneously hypertensive rat (SHR) with and without chronic Nω‐nitro‐L‐arginine‐methylester (L‐NAME) treatment. Moreover, the effect of angiotensin 11 receptor antagonist (AT1 receptor antagonist) (TCV‐116) on the impaired coronary circulation in HTH was examined.2. Coronary flow (CF) was decreased in HTH accompanied with cardiac hypertrophy. The decreased response of CF to L‐NMMA infusion was diminished in HTH. It is suggested that NO production was reduced in coronary vasculature in HTH.3. In chronic L‐NAME treated SHR, blood pressure and cardiac hypertrophy were accelerated. Although coronary flow resistance (CFR) was increased, the increased response of CFR to L‐NMMA infusion was not altered.4. The AT1 antagonist improved total minimal coronary flow resistance (MCFR) restoring CFR response in SHR, although it did not recover CFR response in chronic L‐NAME treated SHR.5. Taken together the findings suggest that NO production was exhausted in the coronary artery even in the developing stage of hypertension and this exhaustion could contribute to the impairment of coronary circulation of HTH.
A ROLE OF LYSINE‐43 IN THE INACTIVATION OF RAT PRORENIN
Authors: Suzuki Fumiaki , Tosaki Ikuko , Shiratori Yasuhiko , Nagai Miyuki , Murakami Kazuo , Nakamura Yukio 
Published: June 2007

Summary1. Lysine‐43 (Lys43) in the prosegment region was located within 3 × 10−1 of catalytic sites, Asp81 and Asp266, in a stereo structure model of rat prorenin.2. A mutant prorenin, Lys43Leu, was produced to elucidate a role of Lys43 in the inactivation of prorenin. Lys43Leu as well as the wild type were inactive at a neutral pH, and activated at an acidic pH. Its acid‐activation speed was three times higher than that of the wild type. The mutant prorenin was more labile than the wild type at 55°C and a neutral pH.3. These results indicate that Lys43 forms ionic bonds with Asp81 and Asp266 to inactivate and stabilize prorenin.
HAEMODYNAMIC EFFECTS OF NO‐SYNTHASE INHIBITORS, NG‐MONOMETHYL‐L‐ARGININE, NG‐NITRO‐L‐ARGININE AND NG‐NITRO‐L‐ARGININE METHYL ESTER, AND NO‐DONOR, GLYCERYL TRINITRATE, IN CONSCIOUS SHRSP AND WKY
Authors: Higashino H. , Simeonova K. , Lambev I. , Suzuki A. 
Published: June 2007

Summary1. The experiments were carried out by an ordinary and a microsphere method in order to clarify the effects of three nitric oxide‐synthase inhibitors and ‐donor on the circulating system between SHRSP and WKY.2. Intravenous administration of each compound possessing the nitric acid‐synthase inhibiting action markedly elevated the systolic blood pressure both in SHRSP and WKY, but more prominently in the former.3. The hypotensive and tachycardic responses to glyceryl trinitrate were more enhanced after treatment with NO‐nitro‐L‐arginine and NG‐nitro‐L‐arginine methyl ester but not with NG‐monomethyl‐L‐arginine compared with the non‐treated one.4. All peripheral organs except the brain decreased their regional blood flow after administration of NG‐nitro‐L‐arginine, indicating a crucial involvement of nitric oxide in the peripheral circulation.5. It was suggested that the nitric oxide system worked more sensitively and actively in SHRSP than in WKY in order to maintain the peripheral blood flow and systemic blood pressure.
VASCULAR ENDOTHELIAL GROWTH FACTOR: TISSUE DISTRIBUTION AND SIZE OF MULTIPLE mRNA SPLICE FORMS IN SHR AND WKY
Authors: Lan L. , Wilks A. , Morgan T. O. , Di Nicolantonio R. 
Published: June 2007

Summary1. We have determined the optimal polymerase chain reaction (PCR) conditions for the amplification and detection of mRNA for a new vascular growth factor—vascular endothelial growth factor (VEGF)–‐and determined its size and tissue distribution in genetically normotensive and hypertensive rats.2. Multiple VEGF mRNA subtypes were obtained which were 625, 520 and 480 base pairs in length.3. All three species of VEGF mRNA were found in heart, kidney, aorta, adrenal and brainstem and the size and tissue distribution of VEGF mRNA subtypes were not different between spontaneously hypertensive rats (SHR) of the Okamoto strain and normotensive Wistar‐Kyoto (WKY) controls.4. Thus multiple forms of VEGF mRNA can be readily detected by PCR in a variety of tissues. While these preliminary results suggest no difference in size and tissue distribution between SHR and WKY, sequencing and quantitative studies will be required to confirm this.
ETA AND ETB RECEPTORS ON VASCULAR SMOOTH MUSCLE CELLS FROM MESENTERIC VESSELS OF SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Schiffrin Ernesto L. , Larivière Richard , Touyz Rhian M. 
Published: June 2007

Summary1. To investigate the contribution of ETA and ETB receptors, calcium responses to the ETB agonist, IRL‐1620, to endothelin‐1 (ET‐1) and to the ETA antagonist, BQ‐123, were examined in primary cultured unpassaged vascular smooth muscle cells (VSMC) from mesenteric vessels of 3, 9 and 17 week old spontaneously hypertensive rats (SHR), Wistar and Wistar‐Kyoto (WKY) rats using Fura‐2 methodology.2. IRL‐1620 (10‐7mol/L) and ET‐1 (10‐9mol/L) increased [Ca2+]i in all strains and ages. Responses to ET‐1 and IRL‐1620 were blunted in 17 week SHR. BQ‐123 significantly reduced ET‐1‐stimulated [Ca2+]i. In endothelium‐denuded mesenteric vessels, ET‐1 and IRL‐1620 induced significant [Ca2+]i responses.3. Binding of ET‐1 was significantly lower in mesenteric artery membranes from 17 week SHR compared to controls.4. Thus, ETA and ETB receptors are present in rat mesenteric VSMC. In adult SHR, a reduced density of ET receptors results in decreased responses to IRL‐1620 and to ET‐1.
ENDOTHELIN‐INDUCED ACTIVATION OF MITOGEN‐ACTIVATED PROTEIN KINASES IN GLOMERULAR MESANGIAL CELLS FROM NORMOTENSIVE AND STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Kishimoto I. , Yoshimasa T. , Arai H. , Takaya K. , Miyamoto Y. , Yamashita J. , Suga S. , Komatsu Y. , Nakagawa O. , Tanaka I. , Itoh H. , Nakao K. 
Published: June 2007

Summary1. Kinase assay in myelin basic protein (MBP) containing polyacrylamide gels revealed that endothelin‐1 (ET‐1) and ET‐3 increased MBP kinase activities in glomerular mesangial cells (MC) from Wistar‐Kyoto (WKY) rats and spontaneously hypertensive rat (SHRSP). ET‐1 stimulated MBP kinase activities more potently than ET‐3.2. Immunoprecipitation with anti‐41‐kDa MAPK antiserum showed that the MBP kinases activated by ET‐1 correspond to 43‐ and 41‐kDa MAPK.3. Since Phorbol 12‐myristate 13‐acetate, a direct activator of protein kinase C, also activated MAPK, protein kinase C was suggested to mediate ET‐induced activation of MAPK.4. These results suggest that MAPK may mediate the ET actions in glomerular mesangial cells from normotensive rats as well as spontaneously hypertensive rats. Since ET is produced by vascular endothelial cells of the kidney and glomerular mesangial cells, the ET signalling pathway may have some physiological and pathophysiological significance in wivo glomerulus.
DEVELOPMENT OF HYPERTENSION IN SPONTANEOUSLY HYPERTENSIVE RATS: ROLE OF MILK ELECTROLYTES
Authors: MeCarty Richard , Tong Hongyun 
Published: June 2007

Summary1. Milk samples were collected from lactating spontaneously hypertensive rats (SHR) and Wistar‐Kyoto (WKY) normotensive females at 8, 14 or 18 days postpartum.2. Milk samples were later analysed for content of calcium (Ca++), sodium (Na+), potassium (K+), chloride (CI‐) and total protein.3. Milk samples from SHR females had significantly higher concentrations of Na+ (at 8 and 14 days) and CI‐ and significantly lower concentrations of Ca++, K+ (at 8 and 14 days) and total protein compared to milk samples from WKY females.4. Preweanling dietary content of several electrolytes implicated in the development of hypertension differred dramatically between SHR and WKY strains. This altered diet early in life may serve as an environmental trigger for progressive age‐related increases in arterial pressure in SHR.
INCREASED CA2+ INFLUX IN THE RESTING STATE MAINTAIN THE MYOGENIC TONE AND ACTIVATES CHARYBDOTOXIN‐SENSITIVE K+ CHANNELS IN FEMORAL ARTERIES FROM YOUNG SHR
Authors: Asano M. , Nomura Y. , Hayakawa M. , Ito K. M. , Ito K. , Uyama Y. , Imaizumi Y. , Watanabe M. 
Published: June 2007

Summary1. To determine the possible role of voltage‐dependent Ca2+ channels (VDCC) and Ca2+‐activated K+ (KCa) channels in the regulation of resting tone of arteries from young spontaneously hypertensive rats (SHR), mechanical responses to the agents which interact with these channels were examined in endothelium‐denuded strips of femoral arteries from 4 week old SHR and age‐matched normotensive Wistar‐Kyoto (WKY) rats. Systolic blood pressures at this age were not significantly different between SHR and WKY.2. The strips from SHR, but not from WKY, maintained a myogenic tone; that is, the resting tone decreased when nifedipine was added.3. Studies using 1 or 5 min pulse labelling of the strips with 45Ca showed that the basal Ca2+ influx was increased in SHR when compared with WKY, and this increase in SHR was abolished by nifedipine. Similar results were obtained when the cytoplasmic Ca2+ concentration ([Ca2+]i) in the resting state of the strips was measured by fura‐PE3.4. The addition of charybdotoxin (ChTX, a blocker of large conductance Kca channels) to the resting state caused a concentration‐dependent contraction, which was much greater in SHR than in WKY. The ChTX‐induced contraction in SHR was abolished by nifedipine.5. In strips preloaded with 86Rb, the basal 86Rb efflux rate constant was significantly greater in SHR than in WKY. The increase in 86Rb efflux in SHR was abolished by nifedipine.6. The results suggest that the Ca2+ influx via L‐type VDCC was increased in the resting state of the femoral artery from 4 week old SHR, and therefore the myogenic tone was maintained and ChTX‐sensitive K+ channels were highly activated.
WHAT IS THE DIFFERENCE OF BONE GROWTH IN SHR AND SD RATS?
Authors: Inoue Tsutomu , Moriya Atsuko , Goto Kosei , Tanaka Toshimitsu , Inazu Mizuho 
Published: June 2007

Summary1. Both sexes of spontaneously hypertensive rats (SHR) and Sprague‐Dawley (SD) rats were used in this study.2. At 6, 12, 18, 24, 30, 36, 42, 48, 54 and 60 weeks old, tibia length (L), volume (V), dry weight (DW), bone mineral density (BMD) in tibia and serum biochemical parameters (Ca2+, Ca, iP, ALP, TRAP) were measured.3. At the 18 and 48 weeks old, bone morphometry was performed (mineral apposition rate, trabecular bone volume and trabecular thickness). Serum PTH and osteocalcin level were determined in 18 week old rats.4. The time course change of DW, L and V were almost the same as the trends of bodyweight in each group, namely, male SD had the highest value, female SD and male SHR showed the same value and the lowest figures were obtained in female SHR.5. BMD of the middle area showed almost the same trends with the time course change of bodyweight. On the other hand, both sexes of SHR had lower BMD than that of SD in the proximal area.6. Serum biochemical parameters showed the same trends in both sexes of SD and SHR except for ALP (a marker of bone formation) which was higher in male than in female rats.7. Mineral apposition rate, trabecular bone volume and trabecular thickness were not different between the same sex of SD and SHR.8. These findings suggest that trabecular bone in SHR had a lower mineral status than that of SD rats not only in the adult but also in the young. This alteration may due to the abnormal mineralization mechanisms.
STROKE‐PRONE SHR AND ARTERIOLIPIDOSIS‐PRONE SHR AS MODELS FOR ATHEROSCLEROSIS: THEIR MECHANISMS AND APPLICATION FOR NUTRITIONAL AND PHARMACOLOGICAL STUDIES
Authors: Yamori Yukio , Murakami Shigeru , Nara Yasuo , Ikeda Katsumi 
Published: June 2007

Summary1. Peritoneal macrophages (Mø) were harvested from non‐stimulated 2 month old SHRSP and WKY, and incubated with acetyl LDL or [14C]‐oleate‐albumin complex to check total, free and esterified cholesterol (Cho) accumulation as well as acy coenzyme A‐cholesterol acyltransferase (ACAT) activity and its activation by hyperlipidaemic serum.2. Total and esterified Cho accumulation as well as ACAT activity were enhanced in Mø from SHRSP compared with those from WKY.3. To observe the dietary or pharmacological influence on atherogenesis, arteriolipidosis‐prone SHR (ALR) were given a high fat cholesterol diet with 3% taurine or a Ca blocker (Nilvadipine, N; 30 mg/kg), both of which significantly decreased serum Cho level and clearly attenuated arterial fat deposition.
DECREASED EXPRESSION OF THE VERY LOW DENSITY LIPOPROTEIN RECEPTOR mRNA IN THE CARDIAC VENTRICLE OF SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Jingami H. , Masuzaki H. , Matsuoka N. , Nakagawa O. , Ogawa Y. , Mizuno M. , Yamamoto T. , Nakao K. 
Published: June 2007

Summary1. To elucidate the functional implication of very low density lipoprotein (VLDL) receptor, we studied the gene expression of VLDL receptor in rats. The VLDL receptor mRNA was highly expressed in the cardiac ventricle and skeletal muscle. Intermediate amounts of VLDL receptor mRNA were detected in adipose tissue, adrenal gland, brain and lung. Thus the tissue distribution of VLDL receptor mRNA in rats was similar to that reported previously in rabbits.2. We studied the gene expression of the VLDL receptor in the heart of stroke‐prone spontaneously hypertensive rats (SHRSP), an animal model for hypertension‐induced cardiac hypertrophy. RNase protection assay showed that the level of ventricular VLDL receptor mRNA was already decreased to one half when hypertension was not fully developed, and further diminished to one fifth when cardiac hypertrophy was established.3. It is reported that energy utilization in SHRSP hypertrophied myocardium is impaired. Our results suggest that inactive fatty acid metabolism in the ventricle of SHRSP is related to the lowered expression of the VLDL receptor which is postulated as a gate for triglyceride‐rich lipoprotein particle.
ACCELERATION OF RENAL DISEASE IN OBESE SHR BY EXACERBATION OF HYPERTENSION
Authors: Koletsky Richard J. , Boccia Joseph , Ernsberger Paul 
Published: June 2007

Summary1. Obese SHR have lower blood pressures than lean litter‐mates on ad libitum diets of standard rat chow and develop spontaneous progressive kidney disease with marked proteinuria, whereas lean SHR have only mild proteinuria.2. On a high‐salt diet, obese SHR show dramatic elevations in blood pressure accompanied by accelerated renal disease and mortality. Lean SHR are also salt sensitive but to a lesser degree.3. Weight cycling elevates blood pressure in obese SHR to levels comparable to lean SHR littermates. This elevation in blood pressure is accompanied by an exacerbation of kidney disease relative to age‐matched controls.4. Ganglionic blockade reversed the elevation in blood pressure in obese SHR elicited by either high‐salt diet or weight cycling. Therefore, excess sympathetic nervous activity contributes to the impact of these hypertensive stimuli,5. Exacerbation of hypertension accelerates renal disease in obese SHR.
ALTERED PRODUCTION OF NERVE GROWTH FACTOR IN CULTURED VASCULAR SMOOTH MUSCLE CELLS FROM GENETICALLY HYPERTENSIVE RATS
Authors: Ueyama Takashi , Hamada Masanori , Hano Takuzo , Nishio Ichiro , Furukawa Shoei 
Published: June 2007

Summary1. Nerve growth factor (NGF) is a neurotrophic peptide for peripheral sympathetic nerves. Hypotrophy of sympathetic nerve ganglia and reduced content of neuropeptide Y were reported in genetically hypertensive (GH) rats. These facts led us to consider that production of NGF might be altered in GH rat cells.2. Vascular smooth muscle cells (VSMC) were prepared from the aortic media of 12 week old GH rats and age‐matched normotensive (NT) rats by enzyme digestion method. Growth rates and the maximum cell densities were fairly equivalent between GH cells and NT cells.3. The NGF content in the medium was measured using an enzyme immunoassay against mouse beta NGF. The amount of NGF secreted from VSMC of GH were 1.2pg/104 cells per 48 h in the progressive phase and 0.7 pgj 104 cells per 48 h in the quiescent phase, while those of NT were 8 pg/104 cells per 48 h and 1pg/104 cells per 48 h, respectively. The levels of NGF secretion per cells were greater in NT cells. In summary, NGF secretion from VSMC were reduced in GH.4. These results suggested that a reduced production of NGF from VSMC might be involved in the reported hypotrophy of sympathetic nerve cells in GH.
FIBRINOLYTIC ACTIVITY IN LIVER TISSUES OF STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Okada Kiyotaka , Yuasa Haruyuki , Hagiya Yasuhiro , Takaishi Tomoaki , Fukao Hideharu , Ueshima Shigeru , Matsuo Osamu 
Published: June 2007

Summary1. Plasminogen activator activity was detected in the extract solution of the liver tissues of both stroke‐prone spontaneously hypertensive rats (SHRSP) and Wistar‐Kyoto (WKY) rats by the synthetic substrate assay.2. The total PA activity in the liver extract of WKY (26.8 ± 8.3 i.u.) was about 1.5‐fold higher than that of SHRSP (18.5 ± 4.1 i.u., n = 8, P < 0.005).3. The enzymography of the liver extract revealed three lytic bands with a molecular weight of 67 kDa, 44 kDa and 38 kDa.4. The inhibitor activity of the liver extract was detected by the reverse fibrin autography method with one lytic resistance hand at 70 kDa.5. Thus, fibrinolytic components exist in the liver tissue of both strains of rats, but their contribution to the stroke requires further study.
GLIAL ENDOTHELIN/NITRIC OXIDE SYSTEM PARTICIPATES IN HIPPOCAMPUS CA1 NEURONAL DEATH OF SHRSP FOLLOWING TRANSIENT FOREBRAIN ISCHAEMIA
Authors: Yamashita Kimihiro , Kataoka Yasufumi , Yamashita Yasuko S. , Himeno Akihiko , Tsutsumi Keisuke , Niwa Masami , Taniyama Kohtaro 
Published: June 2007

Summary1. When delayed neuronal death occurred in the hippocampus CA1 pyramidal cell layer of stroke‐prone spontaneously hypertensive rats (SHRSP) at 4 and 7 days after a 10 min bilateral carotid occlusion and reperfusion, intense endothelin‐1 (ET‐1)‐ and ET‐3‐like immunoreactivities became evident in astrocytes in the damaged hippocampus CA1 subfields.2. We also observed that microglia equipped with an ETb receptor aggregated within the CA1 pyramidal cell layer with neuronal death.3. There was a dramatic increase in nitric oxide synthase (NOS) activity in astrocytes and microglia in the damaged hippocampus CA1 subfields.4. Thus, the possibility that microglia with the ETb receptor are activated to produce NO, a neurotoxic factor, by astrocytic ET‐1 and ET‐3 produced in response to transient forebrain ischaemia would have to be considered.
TEMPORAL AND SPATIAL PROPERTIES OF SLOW WAVES IN THE ELECTROENCEPHALOGRAM OF SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Chichibu Shiko , Ohta Yoshio , Chikugo Taka‐aki , Suzuki Tsuneyuki 
Published: June 2007

Summary1. Electroencephalogram (EEG) of stroke‐prone spontaneously hypertensive rats (SHRSP) and M(malignant)‐SHRSP were analysed for excitability changes in the cerebral neuronal circuit using power spectral comparisons.2. EEG in hypertensive SHRSP and M‐SHRSP showed the emergence of slow wave bursts parallel to the development of hypertension.3. These bursts were composed of spikes and sharp waves, and became dominant in the later stages of hypertension.4. Bursts were interposed by a silent period indicating a strongly depressed state of neuronal activities. The ratio of the periods of the depressed to the burst increased with the progress of the hypertension.5. A shift of the major component toward a lower frequency band also indicated decreased cerebral activity.