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A 62-year-old woman with activity-dependent two-to-one atrioventricular block (2:1AVB) and a normal left ventricular ejection fraction was referred to our department for the evaluation of exclusively exercise-induced marked symptoms. The treadmill test helped establish a clear correlation between 2:1AVB and symptoms. The test results demonstrated that exercise-induced marked symptoms were attributed to abrupt transient hypotension combined with relative bradycardia, probably due to increased diastolic mitral and tricuspid regurgitation because of 2:1AVB during moderate-to-heavy exercise. After pacemaker implantation for 2:1AVB, the symptoms and transient hypotension disappeared, and her exercise capacity improved.

A 68-year-old man with sick sinus syndrome (SSS) was referred to our department for pacemaker implantation. After implantation of a pacemaker with rate-responsive dual chamber (DDDR) mode and minimized ventricular pacing (MVP) functions, paroxysmal atrial fibrillation (PAF) repeatedly developed. Pacemaker memory showed that the intrinsic atrioventricular (AV) (atrial pacing-ventricular sensing [Ap-Vs]) interval was paradoxically prolonged during rate-responsive atrial single-chamber (AAIR) mode rapid pacing because of MVP. Accordingly, to eliminate the paradoxical prolongation of the AV interval during rapid atrial pacing, we changed MVP to medium AV hysteresis and conducted DDDR mode pacing with rate-dependent AV delay. PAF then sharply decreased without antiarrhythmic drugs.

We examined whether central nitric oxide is involved in blood pressure (BP) regulation in deoxycorticosterone acetate (DOCA)-salt hypertension. DOCA-salt rats were intracerebroventricularly infused (ICV) NG-monomethyl L-arginine (L-NMMA) for 4 weeks at either low (0.08 mg/kg/d; n = 8) or high (0.16 mg/kg/d; n = 8) dose. Saline ICV (n = 9) and intraperitoneal infused L-NMMA (low, n = 6; high dose, n = 6) were served as controls. Also, L-NMMA ICV (low, n = 6; high dose, n = 6) was conducted in normal rats. At week 3 and after, DOCA-salt with low L-NMMA ICV showed a higher BP than saline ICV (at week 4: 167.4 +/- 3.6 vs. 150.3 +/- 3.9 mm Hg, P < 0.01); this difference of BP was cancelled after ganglionic block. High L-NMMA ICV did not affect the trend of BP; however, it caused a reduced amount of saline drinking and a less estimated sodium retention than saline or low L-NMMA ICV (for 3 wk; 47.5 +/- 1.1 vs. 66.0 +/- 3.7 and 61.7 +/- 2.5 mmol, P < 0.01). In normal rats, high, but not low, L-NMMA ICV elevated BP with no effect on drinking behavior. Intraperitoneal infused L-NMMA did not affect the development of hypertension and/or sodium balance. These data suggested that, in DOCA-salt, central nitric oxide is involved in BP regulation through the dual action on sympathetic nervous activity and sodium balance.

We have been investigating an integration of sensing and compression in an image sensor. A compression Sensor reduces the number of pixels in the image signal that have to be read out from the sensor, We present a real-time object tracking system by using a compression sensor that has 128×128 pixels and FPGA, By using this system. several moving objects can be extracted and tracked independently at 1200 frames/second. We also describe real-time depth estimation by using a binocular compression sensor. We show some results obtained by the system.

This study was conducted to examine if central amiloride-sensitive transport systems are involved in the development and/or maintenance of hypertension in spontaneously hypertensive rats (SHR). Either amiloride (75 microg/60 microl/day) or artificial cerebrospinal fluid (aCSF, 60 microl/day) was infused centrally (i.c.v.) for 4 weeks to development (4-5-weeks-old) and maintenance (10-12-weeks-old) phases of hypertension in SHR. In development phase, amiloride i.c.v. (n=14) blunted the elevation of blood pressure (BP) compared to aCSF i.c.v. (n=9) (amiloride vs. aCSF; after 3 weeks of i.c.v., 146+/-3 vs. 166+/-5 mmHg, P

Although the parathyroid hormone-related protein gene is widely expressed in the central nervous system, the role of this protein in blood pressure is unknown. This article examines whether parathyroid hormone-related protein is involved in the central regulation of blood pressure. An intraventricularly injected solution of parathyroid hormone-related protein elicited a dose-dependent increase of mean arterial pressure accompanied by a decrease of heart rate in conscious Sprague-Dawley rats. An anti-parathyroid hormone-related protein monoclonal antibody, given in an intraventricularly injected solution, blocked the pressor effect of parathyroid hormone-related protein. Furthermore, this pressor effect of parathyroid hormone-related protein was also abolished after pretreatment by intravenous administration of either hexamethonium bromide or doxazosin mesylate. These results suggest that central parathyroid hormone-related protein is implicated in the regulation of blood pressure, and that this effect may be mediated through sympathetic activation.

Baroreceptor reflex control of heart rate (HR) was examined before and 15 min after intracerebroventricular infusion (i.c.v.) of 10 microliters of high-Ca2+ solution (Ca2+, 16.3 mM) in conscious spontaneously hypertensive (SHR) and Wistar-Kyoto rats (WKY). The slope of the individual regression line of the relation between reflex HR changes (delta HR) and changes in mean arterial pressure (delta MAP) produced by bolus injections of phenylephrine or sodium nitroprusside (delta HR/delta MAP; beats/min/ mm Hg) for bradycardia was significantly less in SHR (-0.60 +/- 0.30; n = 10) than in WKY (-1.78 +/- 0.27; n = 10; p < 0.01) at baseline. The slope increased in SHR during administration of high Ca2+ to -1.39 +/- 0.17 (p < 0.01) but not in WKY: In contrast, no significant changes were observed for the reflex tachycardia both in SHR (n = 7) and WKY (n = 10). Further, we analyzed sigmoidal MAP-HR reflex curves in SHR with i.c.v. of either high Ca2+ (n = 6) or artificial cerebrospinal fluid (aCSF; n = 5). Administration of high Ca2+ reduced the bradycardic plateau and increased HR range without changes in average gain. Our results suggest a modulatory role for central Ca2+ in the baroreceptor reflex control of HR in SHR.

Parathyroid hormone-related protein (PTHrP) is one of the main factors from tumors causing malignancy associated hypercalcemia. It is also expressed in various kinds of normal tissues including vascular smooth muscle systems. Colocalization of the PTH/PTHrP receptor and locally produced PTHrP and its vasorelaxant activities suggest that PTHrP has a regulatory role in the modulation of blood pressure (BP). There have been many evidences that indicate the importance of circulating PTH and PTH/PTHrP receptors in the regulation of BP in various conditions. These data suggest that, under normal physiological conditions, locally produced PTHrP is a real factor that regulates these smooth musele systems in a paracrine or autocrine fashion. The central nervous system also has a very important role to regulate the BP. The evidence that PTHrP is expressed in the central nervous system and the presence of the PTHrP immunoreactivity in human cerebrospinal fluid lead to the possibility that PTHrP has some role in the central regulation of BP. We have found that intraventricularly administered PTHrP had a pressor effect on systemic BP which support the previous possibility.

To examine the role of serine proteases in the control of aldosterone (Ald) secretion, we studied the effects of nafamostat mesilate (Naf), a serine protease inhibitor, on in vivo Ald secretion and Ald content in the rat adrenal gland. Either Naf (2 mg/kg/h; n =10) or saline (2 ml/h; n =10) was administered intravenously for 30 min to anesthetized Wistar rats whose left adrenal vein was cannulated selectively via the inferior vena cava. Naf caused a significant decrease in Ald secretion rate compared to saline (1.99±0.32 vs. 3.42±0.56 ng/min, p

The depressor effect by oral calcium supplementation is known to be more pronounced in salt-dependent than in renin-dependent hypertension. This study was conducted to investigate the role of central calcium on two different pathophysiologic subtypes of experimental hypertension; (a) salt-dependent, deoxycorticosterone acetate-salt hypertensive rats (DOCA), and (b) renin-dependent, 2-kidney, 1 clip (2-K, 1C) hypertensive rats. In DOCA (n = 10), high-calcium solution (Ca+2, 65.2 mM, 10 microl) given centrally (i.c.v.) elicited a marked decrease in mean blood pressure (MBP; 170 +/- 4 to 138 +/- 5 mm Hg, p < 0.01) with a decrease in heart rate (HR; 390 +/- 18 to 344 +/- 17 beats/min, p < 0.05) lasting for 40 min. In 2-K, 1C (n = 10), high-Ca2+ i.c.v. showed a lesser decrease in MBP (178 +/- 4 to 171 +/- 5 mm Hg) and HR (419 +/- 10 to 395 +/- 12 beats/min) with shorter duration (for 20 min) than in DOCA. This significant depressor and bradycardic response to Ca2+ i.c.v. observed in DOCA was dose dependent at Ca2+ concentrations between 65.2 and 130.4 mM. In DOCA, high Ca2+ i.c.v. reduced the plasma noradrenaline (Nad) concentration significantly (479 +/- 81 to 319 +/- 62 pg/ml, p < 0.05). These results suggest that central Ca2+ plays a more important role in regulating sympathetic nerve activity and BP in salt-dependent than in renin-dependent experimental hypertension.

This study attempted to determine whether central magnesium (Mg) influences the regulation of blood pressure (BP). An intracerebroventricular (icv) injection of a high Mg2+ solution (190.0 mEq/L, 10 microL), made by adding MgC12 to artificial cerebrospinal fluid, increased the mean BP in both conscious spontaneously hypertensive rats (SHR; n = 17, p < 0.001) and Wistar Kyoto rats (WKY; n = 8, p < 0.005). Spontaneously hypertensive rats showed a greater pressor response than WKY (+11.7 +/- 0.9 mm Hg versus +3.5 +/- 1.1 mm Hg, p < 0.001). This pressor response to Mg2+ given icv was dose-dependent in the range of Mg2+ concentration between 47.5 and 190.0 mEq/L in SHR. A high Mg2+ solution (190.0 mEq/L), made by adding MgSO4 given icv, also increased the mean BP in SHR (n = 7, p < 0.001) and WKY (n = 6, p < 0.01), whereas the high osmolarity solution (340 mOsm/kg H2O) given icv did not change the mean BP in either SHR or WKY. Also administered was a high Mg2+ solution icv after either hexamethonium bromide (Hx; 50 mg/kg intravenously) or arginine vasopressin antagonist (aAVP, (CH2)5Tyr(Me)AVP, 30 micrograms/kg i.v.). The pressor response to the high Mg2+ solution was abolished by arginine vasopressin antagonist both in SHR and WKY, although it was not canceled by Hx. A high Mg2+ solution administered icv caused a 3.5-fold increase in plasma arginine vasopressin concentration in SHR (n = 5, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

The role of central Ca2+ in the regulation of blood pressure (BP) was investigated in conscious spontaneously hypertensive (SHR) and Wistar-Kyoto rats (WKY). Ten microliters of a high Ca2+ solution (Ca2+: 32.6 mM) administered intracerebroventricularly (i.c.v.) decreased the mean arterial pressure (MAP) for more than 20 min in SHR (n = 7, P0.005), while no change of MAP was observed in the WKY (n = 6). This depressor response to Ca2+ i.c.v. was dose-dependent at Ca2+ concentrations between 16.3 and 65.2 mM. We also investigated the effect of high Ca2+ i.c.v. in SHR after pretreatment with Ca2+ channel blockers, diltiazem (60 micrograms/10 microliters) or nisoldipine (4, 8, 16 and 32 micrograms/10 microliters), administered i.c.v., the autonomic ganglion blocker, hexamethonium (50 mg/kg), administered i.v. and alpha-methyl-p-tyrosine (100 and 400 micrograms/10 microliters) delivered i.c.v. Pretreatment with i.c.v. diltiazem (n = 8) or nisoldipine (n = 5 for 8 micrograms, n = 6 for 4, 16, 32 micrograms) abolished and/or blunted the decrease of MAP due to high Ca2+. Hexamethonium administered i.v. (n = 6) also canceled the depressor action of i.c.v. Ca2+. Pretreatment with 100 micrograms of i.c.v. alpha-methyl-p-tyrosine could not prevent the depressor action of i.c.v. Ca2+; however, 400 micrograms of alpha-methyl-p-tyrosine administered i.c.v. abolished the effect of i.c.v. Ca2+. Furthermore Ca2+ channel blockers administered i.c.v. in themselves increased MAP in SHR (P0.05). These results suggest that central Ca2+ is involved in the central regulation of BP in SHR. This effect may be mediated through changes in sympathetic activity.