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Biomedical subjects

H Muratani

Publications and source records attributed to H Muratani.

At least 55 records · Page 3Linked to original sources
PubMed1994

Neural effects on renal blood flow during acute hypotension vary with antihypertensive drugs.

To examine the neural effects of antihypertensive drugs on renal blood flow, we measured blood flow and renal sympathetic nerve activity simultaneously in conscious spontaneously hypertensive rats aged 13 to 15 weeks. One to two days after surgery, intravenous administration of manidipine (calcium antagonist, n = 10), doxazosin (alpha 1-adrenergic receptor antagonist, n = 9), and clonidine (n = 7) lowered mean arterial pressure by at least 20% from baseline levels. Manidipine initiated a reduction of renal blood flow when mean pressure decreased by 20 +/- 2 mm Hg. At the maximal decrease in renal blood flow (mean pressure, -33 +/- 2 mm Hg), percent decrease in flow (-27 +/- 2%) significantly correlated with percent increase in renal nerve activity (+205 +/- 40%, r = -.878). Doxazosin began to decrease renal blood flow at a level of arterial pressure similar to that in manidipine treatment, whereas the maximal decrease in flow (-19 +/- 2%; mean pressure, -33 +/- 2 mm Hg; nerve activity, +225 +/- 44%) was significantly less than that in manidipine treatment. Although clonidine decreased arterial pressure and renal nerve activity, renal blood flow did not decrease even at the maximal decrease in mean pressure of 29 +/- 1 mm Hg. The addition of clonidine to manidipine treatment suppressed reflexly enhanced renal nerve activity and restored blood flow to the pretreatment level despite pronounced hypotension. These results clearly demonstrate that antihypertensive drugs with blocking action on renal nerve activity are capable of maintaining renal blood flow and that those associated with reflex-induced enhancement of nerve activity exert deteriorating effects on renal blood flow. Furthermore, a decrease in renal blood flow induced by calcium antagonists is mainly attributed to reflexly enhanced renal nerve activity.

Animals↗
PubMed1994

Short-term effects of angiotensin II blockade on renal blood flow and sympathetic activity in awake rats.

To investigate the effects of an angiotensin II type 1 receptor antagonist (CV-11974) on renal blood flow and renal sympathetic nerve activity compared with a calcium antagonist (nicardipine), we measured both parameters in conscious spontaneously hypertensive rats aged 13 to 15 weeks. One to 2 days after surgery, CV-11974 (n = 9) and nicardipine (n = 8) were intravenously administered to decrease arterial pressure in a similar time course and degree of hypotension. CV-11974 increased renal blood flow by 23 +/- 4% at the maximal fall in mean arterial pressure (-32 +/- 1 mm Hg), and renal nerve activity increased by 70 +/- 7%. The maximal increase in renal blood flow (+27 +/- 4%) was observed when mean pressure was reduced by approximately 20 mm Hg. The maximal reduction of renal vascular resistance (-33 +/- 3%) correlated significantly with pretreatment levels of plasma renin concentration (r = -.792). In contrast, nicardipine produced a progressive reduction of renal blood flow and marked increases in heart rate and renal nerve activity. Increases in heart rate and nerve activity were greater than those with CV-11974 treatment (P < .001). At the maximal fall in mean pressure (-32 +/- 1 mm Hg), renal blood flow decreased by 23 +/- 4%, which was significantly correlated with percent changes in renal nerve activity (+150 +/- 11%, r = -.744). Renal denervation in another set of rats (n = 6) improved renal blood flow and renal vascular resistance responses to nicardipine.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin Receptor Antagonists↗
PubMed1994

[In vitro analysis of temperature-sensitivity of neurons in the rat dorsal motor nucleus of the vagal nerve].

Extracellular and intracellular recordings were made from neurons in the rat dorsal motor nucleus of the vagal nerve (DMV) in vitro to investigate the thermosensitivity of their firing rates and membrane properties. Out of 69 neurons which were extracellularly recorded, sixteen (23%) were warm-sensitive neurons and three (4%) were cold-sensitive neurons. The thermosensitivity of all the neurons tested was preserved during the synaptic blockade in a low Ca2+ (0.2 mM)/high Mg2+ (12 mM) solution. Intracellular recordings demonstrated that warm-sensitive neurons depolarized with a decrease in the input resistance (Rinput) during warming of the brain tissue. The responses of warm-sensitive neurons were completely abolished in the low Ca2+/high Mg2+ solution which contained TTX (5 microM). Cold-sensitive neurons showed a hyperpolarization with a decreased Rinput during warming, whose reversal potential was about-83 mV. Both the hyperpolarization and the reduced Rinput of cold-sensitive neurons during warming were partially suppressed by perfusion with 10 mM of TEA. Therefore, it is concluded that the depolarization of warm-sensitive neurons during warming is seemed to be caused, at least in part, by opening of the TTX-sensitive Na2+ channels, while the depolarization of cold-sensitive neurons during cooling is largely determined by closure of the K+ channels.

Animals↗
PubMed1993

Ventrolateral medulla in spontaneously hypertensive rats: role of angiotensin II.

We investigated whether angiotensin II (ANG II), endogenous to the ventrolateral medulla (VLM), contributes to cardiovascular regulation in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. The action of ANG II endogenous to the VLM was examined by microinjection of 100 pmol of [Sar1,Thr8]ANG II into either the rostral (R) or caudal (C) VLM. This ANG II antagonist caused depressor and bradycardic responses in the RVLM and pressor and tachycardic responses in the CVLM. The magnitude of the blood pressure responses was significantly greater (P < 0.01 in RVLM and P < 0.05 in CVLM) in SHRs (-27 +/- 3 mmHg in RVLM and 29 +/- 4 mmHg in CVLM) than in WKY rats (-17 +/- 1 and 17 +/- 2 mmHg, respectively). Suppression of tonic activity of RVLM neurons by bilateral injection of muscimol in the RVLM showed that the pressor response produced by ANG II antagonist injection in the CVLM required the integrity of rostral pressor neurons. The present data suggest that ANG II endogenous to RVLM and CVLM acts as a tonic excitatory agent on vasomotor neurons of the VLM. The contribution of ANG II in the RVLM and CVLM to the prevailing level of blood pressure was significantly (P < 0.01) larger in SHRs vs. WKY rats when the effect of ANG II blockade was measured as the change in blood pressure. Blockade of gamma-aminobutyric acid (GABA)A receptors in the RVLM showed that inhibitory GABAergic input to the RVLM was not diminished in this strain.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1993

Renin responses in patients with orthostatic hypotension: case reports.

In orthostatic hypotensive patients renin is reported to increase in response to head-up tilt unless the lesion involves postganglionic sympathetic efferent nerves. The authors examined responses of plasma renin activity (PRA) to acute blood pressure reduction in 4 patients with orthostatic hypotension. When the coexistence of normal plasma norepinephrine (PNE) and normal or high-normal pressor response to alpha stimulant is considered to be a sign of preserved function of postganglionic fibers, 2 of the patients had sympathetic lesions mainly confined to central and/or preganglionic fibers. They were diagnosed as having multiple system atrophy (MSA). The other 2 were diagnosed as having idiopathic orthostatic hypotension with possible postganglionic lesions. Although 1 MSA patient showed an increase in PRA from 2.0 to 4.7 ng/mL/hr in response to the tilt, the other MSA patient showed no PRA response to the tilt. The head-up tilt did not provoke an apparent PRA response in patients with idiopathic orthostatic hypotension. The authors infused sodium nitroprusside (SNP) in the 3 patients whose PRA did not respond to the head-up tilt. The infusion decreased blood pressure by 40 mmHg or more, but PRA responses were inappropriately small or suppressed. In all cases, PNE did not respond at all to the head-up tilt and to the infusion of SNP. These findings suggest that possible preservation of postganglionic fibers does not necessarily indicate an intact responsiveness of PRA. The PRA profiling may not be an accurate predictor for the site of the fiber degeneration in orthostatic hypotension.

Aged↗
PubMed1992

Effects of vasopressin and angiotensin II on neurones in the rat dorsal motor nucleus of the vagus, in vitro.

1. Extracellular recordings were made from 297 spontaneously firing neurones in the dorsal motor nucleus of the vagus (DMV) in slice preparations of rat medulla oblongata. Some of the neurones recorded were identified to be vagal motoneurones by antidromic stimulation. The cells fired with a slow irregular pattern at an average rate of 1.1 +/- 0.1 spikes/s (mean +/- S.E.M.). 2. Arginine vasopressin (AVP) was applied by perfusion in 196 of the 297 cells. Most of the neurones (190/196, 97%) were excited by 10(-6) M AVP with an increase in firing rate from the basal level of 1.1 +/- 0.1 to a maximum of 2.5 +/- 0.2 spikes/s. There was a dose-dependent relation between the concentration of AVP and the increased firing rate in all DMV neurones tested (n = 38). The threshold concentration of the peptide to produce changes in firing rate was assumed to be about 10(-10) M. The remaining six neurones were not affected by application of AVP. 3. Application of oxytocin (OXT, 10(-6) M) increased the firing rate of all thirty-eight neurones tested. The effects of AVP and OXT on all neurones examined (n = 20 and 4, respectively) still persisted after blocking the synaptic transmission in a low-Ca2+ or Ca(2+)-free-high-Mg2+ solution, indicating the direct action of both AVP and OXT on the postsynaptic membranes. 4. The AVP-induced excitatory responses were completely but reversibly blocked by the V1-type receptor antagonists, [1-(beta-mercapto-beta, beta-cyclopentamethylene-propionic acid), 2-(O-methyl)tyrosine]-arginine vasopressin (d(CH2)5Tyr(Me)AVP) (n = 5) and Phaa-D-Tyr(Et)Phe-Gln-Asn-Lys-Pro-Arg-NH2 (n = 6), whereas a selective and reversible OXT receptor antagonist, desGly-NH2d(CH2)5[Tyr-(Me)2Thr4]ornithine vasotocin, which suppressed the OXT-induced excitation, did not block the responses to AVP (n = 11). 5. Application of angiotensin II (AII, 10(-6) M) to 153 neurones increased the firing rates of 60 (39%) neurones. The firing rate was increased from the basal level of 1.0 +/- 0.1 to a maximum of 1.8 +/- 0.2 spikes/s (n = 60). The effect of AII was completely abolished by an AII receptor antagonist, [Sar1,Ile8]angiotensin II (n = 6). There was a dose dependence of the excitatory response on AII concentration in all of eleven neurones tested. The threshold concentration was assumed to be about 10(-9) M. The activity of 5 (3%) of 153 neurones was decreased, and the remaining 88 (58%) neurones were not affected by AII.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1992

Chronic hypovolemia associated with accelerated hypertension and orthostatic hypotension in a patient on continuous ambulatory peritoneal dialysis.

We report a patient with nondiabetic end-stage renal disease on continuous ambulatory peritoneal dialysis (CAPD) associated with chronic hypovolemia. Despite the administration of nilvadipine, the patient showed accelerated hypertension and concomitantly orthostatic hypotension. Plasma renin activity was markedly high, and blockade of angiotensin II action by captopril or an angiotension II antagonist decreased the supine blood pressure. This indicated that the enhanced activity of the renin-angiotensin system was the principal cause of the supine hypertension. The plasma concentration of norepinephrine was also very high. After correction of hypovolemia by blood transfusion, the enhancement of the renin-angiotensin system and high plasma norepinephrine level were reduced, and symptomatic orthostatic hypotension disappeared. The accelerated hypertension was easily controlled by the administration of low-dose captopril and nilvadipine. These findings suggest that chronic hypovolemia related to the intractable supine hypertension as well as orthostatic hypotension. Hypovolemia-induced enhancement of the renin-angiotensin system and sympathetic nerve activity may cause vasoconstrictive hypertension in patients on CAPD.

Blood Volume↗
PubMed1992

Isolated bilateral abducens nerve palsies caused by the rupture of a vertebral artery aneurysm.

We report two cases with isolated bilateral abducens nerve palsies due to the rupture of a vertebral aneurysm. Surgery revealed that the aneurysm did not directly compress the abducens nerve. Within a year after the subarachnoid hemorrhage, the patients gained full recovery from the bilateral abducens nerve palsies. In view of the clinical and operative findings, it may be regarded as a compression and/or stretching of the bilateral abducens nerves by a thick clot in the prepontine cistern, and not as a manifestation of the raised intracranial pressure. The mechanisms of the isolated abducens nerve palsy are discussed.

Abducens Nerve↗
PubMed1992

Effects of temperature and neuroactive substances on hypothalamic neurones in vitro: possible implications for the induction of fever.

This paper reviews some of our findings which have shown the usefulness of in vitro methods in the study of hypothalamic neurones. (1) Membrane current analyses of dispersed neurones of the rat preoptic and anterior hypothalamus (POA) during thermal stimulation have revealed that warm-sensitive neurones are endowed with a non-inactivating Na+ channel having a high Q10 in the hyperthermic range (35-41 degrees C). (2) A brain slice study has shown that neurones in the organum vasculosum lamina terminalis (OVLT) region have much higher sensitivity to PGE2 than POA neurones. This provides further evidence of a critical role of the OVLT in translation of blood-borne cytokine signals into brain signals for fever induction. (3) Local application of IL-1 beta and IFN alpha altered the activity of thermosensitive (TS) neurones and glucose responsive (GR) neurones in vitro in an appropriate way to produce fever and anorexia. While the responses to IL-1 beta required the local release of prostaglandins, the responses to IFN alpha were found to be mediated by opioid receptor mechanisms. (4) The responses of POA TS neurones and VMH GR neurones to IL-1 beta but not those to IFN alpha, were reversibly blocked by alpha MSH, an endogenous antipyretic peptide. Thus, immune cytokines and their related neuroactive substances may affect hypothalamic TS and GR neurones thereby producing elaborately regulated changes in homeostatic functions such as thermoregulation (fever) and feeding (anorexia), which are considered as host defence responses.

Animals↗
PubMed1992

Acute effects of manidipine on renal blood flow and sympathetic nerve activity in conscious, spontaneously hypertensive rats.

To examine acute effects of manidipine hydrochloride, a new calcium antagonist, on renal blood flow (RBF) in spontaneously hypertensive rats, we recorded changes in RBF as the Doppler shift and a neurogram of renal sympathetic nerve activity (RSNA) simultaneously in a conscious and unrestrained state. An intravenous infusion of manidipine did not decrease RBF until mean arterial pressure (MAP) fell by 20 +/- 1 mmHg and RSNA increased by 98 +/- 18%. At the nadir of RBF (-25 +/- 2%, MAP: -31 +/- 2 mmHg, RSNA: +154 +/- 25%), percent increase in RSNA significantly correlated with percent decrease in RBF (r = -0.802, p < 0.02). On the other hand, the infusion of sodium nitroprusside did not decrease RBF significantly even at a nadir of MAP (-35 +/- 2 mmHg). Air jet stress increased both MAP and RSNA associated with a decrease in RBF. Responses of MAP and RBF were blunted after manidipine infusion while the stress evoked a similar degree of enhancement of RSNA to that of the control trial. Although manidipine may be less effective than nitroprusside in maintaining RBF during abrupt reductions of MAP, the results of this study suggest that antihypertensive treatment with manidipine may be clinically beneficial in maintaining RBF both at rest and during psychologically stressful conditions.

Air Pressure↗
PubMed1992

Renal vascular responses in spontaneously hypertensive rats chronically treated with manidipine.

An enhanced renal vasoconstrictive response to emotional stress may be related to the pathogenesis of essential hypertension. We examined the effects of chronic manidipine treatment on renal blood flow (RBF) responses to air jet stress, angiotensin II (ANG II), and endothelin-3 (ET-3) in the conscious unrestrained spontaneously hypertensive rat (SHR). Male SHRs were placed on a control diet or one containing 0.05% of manidipine for 4 weeks. Age-matched Wistar-Kyoto (WKY) rats placed on a control diet served as normotensive controls. In comparison with control SHRs, manidipine reduced blood pressure (p < 0.01), increased urinary sodium excretion (p < 0.01), and reduced body weight (p < 0.01). Air jet stress elevated arterial pressure and increased RBF. The pressor response was enhanced more in the control SHRs than in the WKY rats (p < 0.01) and was not altered by manidipine. The percent fall in RBF in the manidipine-treated SHRs (-16%) was less than that in the control SHRs (-30%, p < 0.05) and similar to that in the WKY rats (-18%). In contrast, the pressor effect and the percent fall in RBF caused by ANG II (0.1 nmol/kg/min) were similar in the three groups. Intravenous ET-3 (1 nmol/kg) caused a transient fall, followed by a sustained increase in systemic blood pressure, both of which were associated with a decrease in RBF. The RBF response to ET-3 was blunted in SHRs compared to WKYs and was not altered by manidipine treatment. These results suggest that antihypertensive therapy with manidipine may be beneficial in maintaining RBF during emotional stress.

Air Pressure↗
PubMed1991

Effect of angiotensin II in ventrolateral medulla of spontaneously hypertensive rats.

The spontaneously hypertensive rat (SHR) exhibits an enhanced activity of the peripheral sympathetic and brain renin-angiotensin systems. In the present experiments, we evaluated the cardiovascular response of angiotensin II (ANG II) microinjected in the rostral (RVLM) and the caudal (CVLM) ventrolateral medulla of age-matched (14-16 wk old) SHR and Wistar-Kyoto (WKY) rats. Responses of mean arterial pressure (MAP) and heart rate (HR) to microinjection of ANG II (5, 20 and 100 pmol) into histologically verified sites of the RVLM and CVLM were compared with those obtained by injections of the excitatory agent L-glutamate (2 nmol) at the same site. In both strains, ANG II elicited dose-dependent pressor responses in the RVLM and depressor responses in the CVLM, both of which peaked at a dose of 20 pmol. The magnitude of the fall in MAP produced by injections of ANG II into the CVLM were significantly (P less than 0.01) greater in SHR than in WKY group. In contrast, peak pressor responses elicited by injection of ANG II into the RVLM were of similar magnitude in the two groups. When compared with the MAP response produced by L-glutamate injections, responses to ANG II microinjection were slower in onset, and the latency to the peak response was longer. Ganglionic blockade with hexamethonium bromide prevented the effect of ANG II injection in the RVLM. This study provides evidence that ANG II acts as an excitatory agent at sites within the ventrolateral medulla that determine the vasomotor control of blood pressure in both normotensive and hypertensive rats.

Angiotensin II↗
PubMed1991

Severe hypertension with segmental renal infarction following surgical removal of a retroperitoneal malignant hemangiopericytoma: a case report.

Severe hypertension developed in a fifty-five year-old woman after surgical removal of a retroperitoneal tumor, when the renal artery was injured. Renal arteriography after the surgery demonstrated a segmental infarction of the right kidney. A close relationship between activation of the renin-angiotensin system and the development of severe hypertension was observed. Satisfactory control of blood pressure concomitant with reduction of plasma renin activity was achieved by a combination of an angiotensin-converting anzyme inhibitor, beta-blocking agent, and calcium-entry blocker. The mechanism of activation of the renin-angiotensin system in renal infarction is discussed.

Female↗
PubMed1991

Usefulness of leg-crossing for maintaining blood pressure in a sitting position in patients with orthostatic hypotension--case reports.

The authors report a case with idiopathic orthostatic hypotension in which the patient prevents his blood pressure from falling to a symptomatic level by leg-crossing in a sitting position. Including 4 other patients with orthostatic hypotension and 5 normal subjects, their study found that the changes in blood pressure with leg-crossing inversely correlated with those induced by assuming seated posture from a supine position. Leg-crossing may, therefore, be one of the useful nonpharmacologic measures for maintaining blood pressure in a sitting position in patients with orthostatic hypotension.

Blood Pressure↗
PubMed1990

Chloride ion plays an important role in sodium induced volume expansion in normal humans.

Eight normal women took part in a randomized crossover study to investigate the effect of dietary supplementation with 105 mEq sodium chloride (NaCl) for 3 days or equimolar sodium citrate (NaCit) after salt depletion. NaCit supplement induced greater urinary sodium and potassium excretions than did the NaCl supplement (197 +/- 10 v 107 +/- 19 mEq/3 days for sodium, P less than .01, 130 +/- 7 v 96 +/- 6 mEq/3 days for potassium, P less than .01, respectively) and less body weight gain (+0.6 +/- 0.1 v +1.6 +/- 0.1 kg, P less than .01). Suppressions of plasma norepinephrine, renin activity and aldosterone concentration were significantly smaller with NaCit than with NaCl supplement. We conclude that the anionic component of sodium salts may have some effects on renal sodium handling and modulates volume expansion and humoral factors.

Adolescent↗
PubMed1990

Baroreceptor reflex in elderly essential hypertensives: effect of chronic inhibition of angiotensin converting enzyme.

Baroreflex function and plasma angiotensin II (Ang II) were examined in five elderly and five young or middle-aged essential hypertensive patients before and after enalapril treatment. Baroreflex sensitivity (BS) during blood pressure (BP) elevation by phenylephrine (PE) but not during BP reduction by sodium nitroprusside (SNP) was significantly attenuated in the elderly compared with the younger group, while plasma Ang II concentration was not different between the two groups. Enalapril treatment reduced BP without significant changes in heart rate and plasma norepinephrine in both groups, suggesting a leftward shift of barofunction curve. It also increased the BS in some cases in each group. However, plasma Ang II was not significantly reduced during enalapril treatment. The changes in BS did not correlate with changes in plasma Ang II. These results suggest that BS may be attenuated with increasing age independent of plasma Ang II and that ACE inhibitor influences the set point of the barofunction curve and BS by different mechanisms.

Adult↗
PubMed1989

Familial myopathy with scapulohumeral distribution, rigid spine, cardiopathy and mitochondrial abnormality.

A 37-year-old woman with scapulohumeral muscular atrophy, rigid spine and cardiopathy is reported. Muscle weakness, advanced atrioventricular block and contractures at the neck, elbows and ankles had occurred during her childhood. An autosomal dominant mode of inheritance was suggested because her mother, sister and brother had the same disorder. Pleomorphic mitochondria had accumulated in the subsarcolemmal space of the skeletal muscle. There was no evident enzyme defect in the mitochondrial electron transport system. Although the clinical features had some similarity with those of Emery-Dreifuss muscular dystrophy or rigid spine syndrome, the pattern of inheritance and the muscle pathology differed.

Adult↗