Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To examine the role of the sympathetic nervous system in hypertension, the in vitro activity of tyrosine hydroxylase was examined in one-kidney, one clip (1K1C) and two-kidney, one clip (2K1C) hypertensive rabbits and their respective controls 2 weeks after surgical procedures. The in vitro activity of tyrosine hydroxylase provides a measure of catecholamine synthesis and serves as a biochemical index of activity of noradrenergic neurons and the adrenal medulla. Mean atrial pressure rose from 91.5 +/- 1.0 to 128.5 +/- 5.6 mm Hg (p less than 0.01) in the 1K1C group and from 91.8 +/- 1.3 to 106.5 +/- 5.0 mm Hg (p less than 0.02) in the 2K1C group, whereas no change in blood pressure was found in their respective controls. Adrenal tyrosine hydroxylase activity was increased 85% in the 1K1C group, as compared with values in one-kidney controls (from 11.8 +/- 1.5 to 21.8 +/- 1.1 pmol CO2/min/mg; p less than 0.0002), and was increased 49% in the 2K1C group, as compared with values in two-kidney controls (from 8.01 +/- 1.2 to 11.9 +/- 1.1 pmol CO2/min/mg; p less than 0.02). In the 1K1C group, proximal mesenteric tyrosine hydroxylase activity was decreased 46% compared with values in one-kidney controls (from 23.5 +/- 5.0 to 12.8 +/- 2.5 pmol CO2/min/mg; p less than 0.03) and distal mesenteric tyrosine hydroxylase activity was decreased 42% (from 7.73 +/- 1.2 to 4.46 +/- 0.8 pmol CO2/min/mg; p less than 0.03). In the 2K1C group, neither proximal nor distal mesenteric tyrosine hydroxylase activity was altered. Tyrosine hydroxylase activity was not detectable in the femoral arteries, or in the thoracic and abdominal aorta.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1988 Oct
PMID:Adrenal and vascular tyrosine hydroxylase activity in Goldblatt hypertension. 290 8

Cerebral blood flow was measured and compared in 10 symmetrical brain regions following unilateral trigeminal ganglionectomy (n = 13), sham operation (n = 6), or trigeminal root section (rhizotomy) (n = 8) in cats. Multiple determinations were obtained in anesthetized and paralyzed animals using radiolabeled microspheres during (i) normocapnia-normotension, (ii) hypercapnia (5% CO2/95% room air), (iii) angiotensin-induced acute severe hypertension (190 greater than mean arterial blood pressure less than 210 mmHg), or (iv) bicuculline-induced seizures. Flow was symmetrical in all brain regions at rest and during increases induced by hypercapnia in the three groups. During severe hypertension or seizures, marked elevations developed bilaterally (approximately 93% and approximately 130%, respectively). In ganglionectomized animals, increases due to hypertension or seizures were attenuated by 28-32% on the denervated side within cortical gray matter regions corresponding to the anterior, middle, and posterior cerebral arteries. Flow was symmetrical within all brain regions in sham-operated animals and in the rhizotomy group, despite comparable increases in regional cerebral blood flow induced by angiotensin. Hence, the trigeminal nerve mediates blood flow adaptations during severe hypertension and seizures. Furthermore, since trigeminal cell bodies and peripheral axons are destroyed or degenerate following ganglionectomy but not following rhizotomy, local "axon reflex-like" mechanisms mediate these increases in cerebral blood flow.
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PMID:Trigeminovascular fibers increase blood flow in cortical gray matter by axon reflex-like mechanisms during acute severe hypertension or seizures. 291 86

Serotonin induces constrictor responses on smooth muscle tissues from several vascular regions mainly by its interaction with serotonin-S2 receptor sites. The individual sensitivity of various blood vessels to serotonin may vary considerably. Serotonin (e.g. released from aggregating platelets) also induces vascular contractions by amplifying the response to other vasoactive substances. The vascular reactivity to serotonin can be markedly augmented by acute hypoxia (95% N2, 5% CO2; canine coronary arteries) and by cooling from 37 degrees to 29 degrees C (rabbit tibial and canine saphenous arteries). Blood vessels become hyperreactive to the vasoconstrictor component of serotonin in a number of disease states. Isolated perfused kidneys from spontaneously hypertensive rats (SHR) exhibit direct and indirect (amplifying) vasoconstrictor responses to serotonin. The amplifying effect of serotonin is significantly more pronounced in 6-month-old than in 2-month-old SHRs. Both the direct and indirect vasoconstrictor responses to serotonin, whether or not augmented by acute or chronic conditions, are inhibited by the serotonin-S2 receptor antagonist, ketanserin (4 X 10(-10) to 4 X 10(-7) mol/l). Both the hypersensitivity of vascular tissue to serotonin and the amplifying effect of the amine may greatly contribute to hypertension and other cardiovascular disorders.
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PMID:Augmentation of vasoconstrictor responses to serotonin by acute and chronic factors: inhibition by ketanserin. 293 13

Blood flow in the feline thoracic spinal cord was measured, using a laser-Doppler flowmetry. Rhythmic changes in the spinal cord blood flow were repeatedly observed with a frequency of about three to eight cycles per minute, unrelated to the respiratory or cardiac cycles. These changes were unaffected by hypertension induced by angiotensin II, but disappeared when systemic blood pressure was lowered by trimethaphan or when hypercapnia was induced. CO2 responsiveness of the blood flow and postocclusive reactive hyperemia were also examined, in both the normal and injured spinal cord. CO2 responsiveness was lost 1 h after a 500 gm/cm injury without rhythmic changes, but was partially regained 2 days later, at which time rhythmic changes were frequently observed. Postocclusive hyperemia apparently diminished 1 h after a 500 gm/cm injury, but reappeared 2 days later. Vasomotion in the normal and injured spinal cord is discussed.
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PMID:Vasomotion in normal and injured spinal cord. 296 40

Mean hemispheric cerebral blood flow (CBF) was studied in 11 comatose brain-injured patients following intravenous administration of xenon-133. Repeated measurements were performed in order to evaluate cerebral vasoreactivity following a decrease in PaCO2. In addition, the effect of induced barbiturate coma was evaluated in patients with intracranial hypertension. The cerebral vasoreactivity and the CBF response following induction of barbiturate coma varied. In patients with normal CO2 reactivity, barbiturate treatment was accompanied by a considerable decrease in CBF as compared to patients with decreased or abolished CO2 response. During barbiturate treatment the intracranial pressure (ICP) became normal in three of four patients with preserved CO2 response, but reached normal levels in only one of five patients with impaired CO2 reactivity. Patients whose ICP became normal recovered. The data suggest a positive correlation between CO2 reactivity and the effect of barbiturate treatment. Furthermore, preserved cerebral vasoreactivity after severe head injury may be of prognostic value.
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PMID:Cerebral hemodynamics in patients with acute severe head trauma. 308 May 55

Two siblings, a 14.5-year-old boy and his 11.5-year-old sister, with congenital nemaline myopathy presented with severe respiratory failure and, in the case of the older patient, with cor pulmonale and systemic hypertension. The children were treated initially by continuous mechanical ventilation, but after a few weeks they only required ventilation at night. At the start of treatment, both were found to have a decreased ventilatory response to CO2 which apparently improved during 4 to 5 years of follow-up treatment. It has not been possible to wean them from nocturnal mechanical ventilation, but during the daytime they attend school and function almost normally. It is postulated that respiratory failure in nemaline myopathy may not be related to the severity of the muscle weakness but may result from a disturbance of the feedback required for normal control of breathing.
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PMID:Nemaline myopathy as a cause of sleep hypoventilation. 308 71

Regional cerebral blood flow (rCBF) during hypertension and hypercapnia was studied in 33 patients with putaminal hemorrhage, using a single photon emission CT by means of Xenon 133 inhalation method. The results obtained were as follows: 1) A significant relationship was obtained between the impairment of autoregulation, CO2 reactivity and the degree of cerebral ischemia, i. e., in most cases, these vascular responses were impaired in cases of ischemia showing the rCBF decrease over 30 to 40% of normal values. However, there were particular cases with cerebral ischemia of over 30 to 40% in which autoregulation seemed to be preserved in the acute stage, which was considered to be the similar phenomenon as so called "false autoregulation". 2) The cerebrovascular responses such as autoregulation and CO2 reactivity were preserved in cases of less than 50 ml of hematoma volume. In cases with 50 to 74 ml of hematoma volume however, autoregulation and CO2 reactivity were mostly impaired, especially in the affected hemisphere rather than the non-affected, in the period of 1 to 2 months from the onset. Furthermore, the impairment was also involved in both hemispheres if the hematoma was over 75 ml in volume. 3) The cerebrovascular responses were markedly impaired in the region of basal ganglia of the affected hemisphere which corresponded well to the hematoma site. 4) There was a close correlation between the cerebrovascular responses and the activity of daily life (ADL), i. e, the prognosis might be poor in cases with global impairment, but which seemed to be rather good in cases with local impairment. It might be concluded, from the results mentioned above, that the study of autoregulation and CO2 reactivity is probably significant in estimating the pathogenesis and the treatment of cerebral ischemia following hypertensive putaminal hemorrhage.
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PMID:[A study of cerebrovascular autoregulation and CO2 reactivity in putaminal hemorrhage]. 310 23

Dihydralazine is widely used for acute control of hypertension. In experimental studies it seems to dilate cerebral resistance vessels and increase intracranial pressure. However, the effect on cerebral blood flow (CBF) in man has been little studied. Measurements of CBF were performed with the i.v. xenon-133 technique in seven young, normotensive volunteers before and 15, 60 and 180 min after 6.25 mg i.v. dihydralazine, corresponding approximately to 0.1 mg kg-1 body weight. For comparison the CBF reactivity to inhalation of 5% CO2 in air was investigated. Dihydralazine increased CBF throughout the period of study, in median 16, 27 and 23% at the three periods of measurements, respectively. The arterial blood pressure remained unchanged, whereas heart rate increased significantly. During CO2 inhalation, CBF increased on average 29%. Thus, the cerebral vasodilation exerted by a small i.v. dose of dihydralazine was of the same order of magnitude as the effect of 5% CO2 inhalation. These results in normal subjects should be extrapolated to diseased persons only with extreme caution. Still, the very marked and long lasting vasodilation observed suggests that dihydralazine, from a theoretical point of view, in certain clinical situations may be harmful.
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PMID:Dihydralazine induces marked cerebral vasodilation in man. 311 65

The effects of postoperative external heat supply on shivering, oxygen uptake, carbon dioxide production, ventilatory requirements and haemodynamic variables were studied postoperatively after aortocoronary bypass surgery in 24 men with stable angina pectoris. After hypothermic cardiopulmonary bypass (CPB) at 25 degrees C, the patients were rewarmed to a nasopharyngeal temperature of at least 38 degrees C, resulting in a rectal temperature of about 34 degrees C before termination of CPB. Twelve patients, forming the control group, were given no other external heat supply. In another group (n = 12), the "radiant heat supply group", additional external heat was provided postoperatively, the main source of which was a thermal ceiling supplemented with heated, humidified respiratory gases. In this latter group the postoperative rewarming was accomplished earlier and was converted into a mainly passive process. Shivering, oxygen uptake, CO2 production and ventilation volumes were significantly reduced compared with the control group. Cardiac index and stroke index were higher and systemic oxygen extraction was lower in the radiant heat supply group. Postoperative hypertension and vasoconstriction were greatly decreased, suggesting that residual hypothermia is an important cause of the postoperative vasoconstriction.
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PMID:Postoperative ventilatory and circulatory effects of heating after aortocoronary bypass surgery. Postoperative external heat supply. 311 49

Cerebral blood flow was sequentially determined (every 2-3 min) with helium clearance in two "vulnerable" structures: the hippocampus and the frontoparietal cortex during bicuculline (n = 11) and kainic acid (n = 9)-induced seizures in unanaesthetized, spontaneously breathing rats. Tissue partial pressures of oxygen and carbon dioxide were continuously and simultaneously evaluated in the same brain areas. All these variables were measured by mass spectrometry with a single gas sampling cannula previously implanted in each structure. The systemic variables, arterial blood pressure, arterial partial pressures of oxygen and carbon dioxide, pH, and bicarbonate concentration were also determined. Arterial and venous catheters were chronically implanted several days prior to the definitive experiments. Bicuculline induced short (about 15 min), recurrent, generalized seizures, with an abrupt rise in arterial blood pressure, an arterial metabolic acidosis and comparable blood flow increases (4-fold) in the hippocampus and the neocortex. A marked increase in tissue partial pressure of oxygen was always preceded by an increase in tissue partial pressure of carbon dioxide. After the seizures, in the 5 rats that survived, cerebral blood flow was significantly lowered; tissue partial pressure of oxygen and partial pressure of carbon dioxide also decreased, but to a lesser extent. Histological examination revealed two types of lesions: predominantly selective chromatolysis but also ischaemic cell change. Kainic acid first induced a decrease in arterial pressure and then hypertension during status epilepticus, with a return of arterial pressure towards basal levels during the recovery period (4 h after the injection). Respiratory alkalosis occurred throughout the experiment. Cerebral blood flow increased progressively to become maximal during status epilepticus. This vasodilatation was greater in the hippocampus (x 8) than in the neocortex (x 4). During recovery, cerebral blood flow tended to decrease but remained significantly elevated. In both structures, tissue partial pressure of oxygen was first lowered while tissue partial pressure of carbon dioxide was elevated; with the occurrence of the wet dog shakes, tissue partial pressure of O2 increased and tissue partial pressure of CO2 decreased. The changes in tissue gases were maximal during status epilepticus and tended to return to their basal levels thereafter, but no decrease in tissue partial pressure of O2 was observed, even 4 h after kainic acid administration. Histological analysis demonstrated ischaemic cell changes, particularly in the limbic system.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Continuous determination of the cerebrovascular changes induced by bicuculline and kainic acid in unanaesthetized spontaneously breathing rats. 312 92


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