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)

The results of 8 to 12 weeks of treatment of the anemia of uremia with rHuEPO in patients with chronic renal failure and uremia are: a sustained increased hematocrit; increased RBC mass, and subsequent increased MAP; and increased TPRI. The observed trends of decreased LVEF, and echo Doppler evidence of a trend toward LV systolic and diastolic dysfunction, although not individually statistically significant, represent 3 separate evaluation techniques coupled with hypertension and TPRI increase during administration of rHuEPO to increase the hematocrit and packed red blood cell volume in patients with chronic renal failure and anemia. Increased TPRI and hypertension associated with correction of uremic anemia vasodilation and the increased blood viscosity have been noted in earlier investigations with transfusions. The hypertension and elevated TPRI demonstrated during rHuEPO therapy in patients with progressive chronic renal failure associated with increased hematocrit, and the trends toward systolic and diastolic cardiac dysfunction are noted herein. These changes were associated with the combined increase of packed RBC mass and plasma volume in this study. The natural progressive course of worsening of renal function exhibited by these patients could have limited their ability to regulate plasma volume, making them vulnerable to volume-dependent hypertension and a significant preload adding to potential cardiac dysfunction in addition to the increased TPRI.
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PMID:Cardiovascular hemodynamic effects of correction of anemia of chronic renal failure with recombinant-human erythropoietin. 205 68

Hypertension and renal mass reduction induce glomerular hypertension (GH), hyperfiltration (HF) and renal injury. GH may contribute to allograft loss in post-transplant hypertensive patients (PT x HT). HF and GH may be evaluated by renal response to acute protein intake (API). Since ACE inhibition may prevent GH, the effects of fosinopril (Fos) were evaluated in 10 PT X HT on azathioprine and prednisone. Patients received 5 to 40 mg/day of Fos during 12 months. Baseline MAP (111.1 +/- 2.9 mm Hg) was significantly reduced by 10 to 12 mm Hg, rising to 114.7 +/- 2.7 mm Hg after Fos was administered. GFR (63.7 +/- 5.9 ml/min) decreased after 4 (48.1 +/- 4.6, P less than 0.05) and 12 months (50.7 +/- 4.6, P less than 0.05), rising to 59.4 +/- 5.6 after Fos was given. There was no GFR response to API before and after one month of Fos, however, a clear response became apparent at 4 (+ 27% P less than 0.05), and 12 months (+ 18%, P less than 0.05), disappearing after Fos discontinuation. Proteinuria (918.8 +/- 710.6 mg/d) decreased after 4 (72.3 +/- 21.6 mg/d, P less than 0.05) and 12 months, rising to 297.8 +/- 172.3 mg/day after therapy. GFR response to API in 22 controls and 17 uninephrectomized donors was 13 and 11%, respectively. Lack of response to API in PT x HT suggests HF and GH. Reduction of GFR, restoration of response to API and reduction of proteinuria, indicate that ACE inhibition with fosinopril ameliorates HF and GH. This effect may be beneficial in preventing hemodynamic-mediated allograft injury.
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PMID:Fosinopril prevents hyperfiltration and decreases proteinuria in post-transplant hypertensives. 214 57

The pattern of dying from immersion hyperthermia was documented in 8 dogs, 9 rhesus monkeys and 12 pigtail monkeys. Under light general anesthesia and spontaneous breathing, the animals were immersed into water of 45 degrees C, which was subsequently adjusted to control brain (parietal epidural) temperature at 42 +/- 0.5 degrees C. Transient initial hypertension, tachycardia, tachypnea and hypocarbia were followed by progressive hypotension with decreasing central venous pressure and pulmonary artery occlusion pressures (measured in three dogs only), bradycardia and bradypnea. Cardiac arrest occurred in the dogs after immersion of 288 +/- 66 min and more rapidly (P less than 0.02) in the rhesus monkeys (at 137 +/- 75 min) and pigtail monkeys (at 178 +/- 26 min). EEG silence occurred in the monkeys at MAP 40 mmHg and in the dogs at MAP 25 mmHg. Cardiac arrest occurred in form of sudden ventricular fibrillation (2/5 dogs, 2/9 rhesus monkeys, 3/12 pigtail monkeys), or later in electromechanical dissociation leading to electric asystole (3/5 dogs, 7/9 rhesus monkeys, 9/12 pigtail monkeys). The mean blood glucose levels decreased to less than 30 mg/dl (P less than 0.002), whereas hematocrit, serum osmolality, lactate and potassium levels increased. Necropsies revealed macroscopic petechial hemorrhages in all extracerebral organs, but not in the brain. There was no gross evidence of cerebral edema. Death seemed to be the result of primary cardiovascular failure leading to secondary (ischemic) cerebral failure (EEG silence) and apnea, which coincided with pulselessness.
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PMID:Hyperthermia-induced cardiac arrest in dogs and monkeys. 217 84

The aim of the intensive care of the injured is the coupling of the availability and the requirement of the cerebral metabolic substates. The measurement of the cerebral blood flow is not currently available at the bedside and less direct monitoring is required. The cerebral perfusion can be estimated looking at the cerebral perfusion pressure (CPP), that can be easily measured using intracranial pressure (ICP) and the systemic arterial pressure (MAP) monitoring. Hundred-twenty-one consecutive head injured admitted to an Intensive Care Unit were studied assessing the severity of the neurological injury, the CT-Scan diagnosis of the intracranial lesion, the Trauma Score and the behavior of the ICP and MAP. The outcome was classified according to a modified version of the Glasgow Outcome Scale. More than 77% of the patients suffered raised intracranial pressure above 20 mmHg and 16 of them had a CPP less than 60 mmHg for more than 5 minutes. The outcome was directly related to the degree of intracranial hypertension and to the severity of insufficient CPP. The treatment of the severe head injured must be aimed at maintaining a good CPP, because of the close relationships between this value and the prognostic result. The monitoring of the ICP is a reliable and relatively safe procedure in this series, where the rate of infections complicating the intracranial recording is less than 3%.
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PMID:[Cerebral perfusion pressure in endocranial hypertension in comatose head-injured patients]. 221 79

Blood pressure (BP) becomes more sodium and body fluid sensitive as renal function deteriorates. Thus, hypertension in chronic renal failure is mostly of the sodium sensitive type. We studied whether the increased sodium sensitivity (SS) can be restored to normal on the maintenance phase of hemodialysis (HD) therapy. Body weight (BW) and BP (specifically, mean arterial pressure [MAP]) were measured after HD and before the next HD, and the body fluid sensitivity (BFS) was calculated as the ratio of changes in these factors on both introduction and maintenance phases in HD patients (n = 56) who were not taking any antihypertensive drugs (BFS = delta MAP/delta BW). In a preliminary study, the amount of interdialytic sodium intake (QNa+) was measured (n = 30), and SS was calculated as the ratio of the change in MAP to QNa+ (SS = delta MAP/QNa+). Interdialytic BW gain (3.1 +/- 0.1 kg) was correlated with the amount of sodium intake (136 +/- 17 mEq), resulting in a positive relationship between BFS and SS (r = 0.79, P less than .0001). Therefore, BFS was used as an index of SS. As a whole, BFS decreased from the introduction to the maintenance phase (6.5 +/- 1.0 to 3.5 +/- 0.6 mm Hg/L, P less than .01). This decrease was marked (6.2 +/- 1.1 to 2.9 +/- 0.6 mm Hg/L, P less than .01) in patients (n = 46) whose BP was normalized in the maintenance phase, while not significant (7.9 +/- 1.9 to 6.3 +/- 1.3 mm Hg/L) in patients (n = 10) whose BP was still high.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Normalization of increased sodium sensitivity by maintenance hemodialysis. 222 54

We evaluated the effect of acute unilateral renal denervation (DNX) on the tubuloglomerular feedback (TGF) mechanism in Inactin-anesthetized hydropenic male 8- to 10-wk-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). SHR had higher mean arterial pressure (MAP, 28%) and renal vascular resistance (RVR, 35%), whereas renal blood flow (RBF), glomerular filtration rate (GFR), urine flow, and sodium excretion were similar. DNX in SHR did not change MAP but decreased RVR (26%) and increased RBF (29%), GFR (16%), urine flow (52%), and sodium excretion (431%). DNX did not affect these in WKY. Loop of Henle perfusion with Ringer solution reduced early proximal flow rate (EPFR) in SHR more than in WKY; significantly different at a loop flow of 20 nl/min (9.8 +/- 0.7 vs. 6.5 +/- 0.7 nl/min). DNX in SHR increased the nonperfused EPFR from 25.6 +/- 1.1 to 31.7 +/- 1.3 nl/min and reduced TGF responses during perfusion at both 20 nl/min (9.8 +/- 0.7 vs. 4.4 +/- 0.7 nl/min) and 40 nl/min (14.2 +/- 1.1 vs. 10.4 +/- 0.7 nl/min). TGF sensitivity was attenuated by DNX, as indicated by reduced maximum reactivity (-0.89 +/- 0.14 to -0.36 +/- 0.07) and increased turning point (16.5 +/- 0.9 to 25.2 +/- 2.9 nl/min). TGF responses in WKY were not influenced by DNX. Sham denervation did not alter renal hemodynamics and TGF. These results indicate that renal nerves exert a tonic influence on the renal vasculature and the TGF system in SHR but not in WKY. Enhanced TGF responsiveness may be involved in volume retention and in the maintenance of hypertension in SHR.
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PMID:Attenuation of enhanced tubuloglomerular feedback activity in SHR by renal denervation. 233 Sep 89

The extent of cerebral injury and edema was determined in isoflurane-anesthetized rats (n = 32) after 180 min of middle cerebral artery occlusion (MCAO) and 120 min of reperfusion. One of the following was employed during the occlusion period only: 1) control, mean arterial pressure [MAP = 131 +/- 7 (SD) mmHg] and hematocrit (43 +/- 2%) were not manipulated; 2) hemodilution, the hematocrit was reduced to 30% with 5% albumin (MAP = 104 +/- 19 mmHg); 3) hemodilution-normotension, hemodilution was established, and MAP was maintained at 131 +/- 9 mmHg with phenylephrine; 4) hemodilution-hypertension, hemodilution was established, and MAP increased to 161 +/- 2 mmHg with phenylephrine. Brain injury was determined with 2,3,5-triphenyltetrazolium chloride, and cerebral edema was assessed by microgravimetry. Brain injury and cerebral edema were less in both phenylephrine groups, compared with the control and hemodilution groups (P less than 0.05). These results are consistent with the premise that if normotension is maintained, hemodilution reduces ischemic brain injury and edema. They also indicate that the addition of phenylephrine-induced hypertension to hemodilution therapy results in a further reduction of ischemic injury without exacerbating cerebral edema.
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PMID:Hypertension and hemodilution during cerebral ischemia reduce brain injury and edema. 237 8

The effect transcutaneous oestradiol for four months supplemented by medroxyprogesterone (Perlutex) from the 12th to 26th day of every month was assessed in an open uncontrolled prospective investigation in 34 women with menopausal symptoms and follicle stimulating hormone greater than 40 international units and luteinizing hormone greater than 25 international units. A marked effect was found on sweating and hot flushes and other menopausal complaints as expressed by Kupperman's menopausal index. Serum oestradiol increased during the first two months to follicular phase values and this was followed by an unexplained decrease after the fourth month which did not, however, result in aggravation of the symptoms. No alterations were found in steroid-hormone-binding globulin, lipids and body weight. Whether the patients placed the plasters in the hip or abdominal regions was found to be of no significance. Seventeen patients had no side effects of the treatment. Nine patients had transient skin symptoms which disappeared spontaneously. Five patients had mastalgia which disappeared after reduction of the Perlutex dose. One patient developed metrorrhagia. A total of three patients abandoned the treatment: one on account of skin symptoms, one on account of high blood pressure and a third on account of psychiatric symptoms which were unrelated to the treatment. A total of 28 patients wanted to continue treatment after the fourth month.
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PMID:[Transcutaneous estradiol treatment in the climacteric]. 240 44

Relationships between changes in levels of catechols and directly recorded sympathetic nerve activity were examined using simultaneous measurements of renal sympathetic nerve activity and arterial and renal venous concentrations of norepinephrine (NE), dihydroxyphenylalanine (dopa), and dihyroxyphenylglycol (DHPG) during reflexive alterations in renal sympathetic nerve activity in anesthetized, adrenal-demedullated rats. Nitroprusside infusion increased renal sympathetic nerve activity by 90%, arterial levels of dopa by 96%, NE by 326%, and DHPG by 141%. Phenylephrine infusion increased arterial DHPG levels by 81% and decreased renal sympathetic nerve activity by 37% and NE levels by 26%; arterial dopa levels were unchanged. Ganglionic blockade by chlorisondamine (with concomitant phenylephrine infusion to maintain MAP) decreased renal sympathetic nerve activity by 65% and NE concentrations by 37%; arterial dopa concentrations were unchanged, and DHPG concentrations increased by 60%. Proportionate responses of arterial levels of NE were strongly related to proportionate changes in renal sympathetic nerve activity. Clearance of DHPG from arterial plasma was prolonged by phenylephrine-induced hypertension and by nitroprusside-induced hypotension. The results suggest that changes in arterial NE levels reflect changes in sympathetic activity; changes in dopa levels reflect changes in catecholamine biosynthesis; and changes in DHPG levels depend on reuptake of released NE and on hemodynamic factors affecting DHPG clearance.
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PMID:Plasma levels of catechols during reflexive changes in sympathetic nerve activity. 250 66

Chronic hypertension causes the lower and upper limits of CBF autoregulation to reset to higher blood pressure levels. In the present study we examined whether the theophylline derivative P-23, which had lowered blood pressure in SHR, would influence CBF autoregulation. P-23 (10 mg/kg po) was administered once daily for 4 weeks and tail systolic pressure was measured weekly in this P-23 group and in a control group of SHR. At the end of the treatment period, CBF autoregulation was studied. CBF was determined using the intracarotid 133Xe injection method in halothane/nitrous oxide anesthetised animals. The lower and upper limits of autoregulation were studied in two subgroups of rats by, either raising blood pressure (MAP) stepwise with norepinephrine or lowering MAP stepwise by controlled bleeding and measuring CBF at MAP intervals of 10 mmHg. In the P-23-treated group, blood pressure fell significantly but in the control group, blood pressure increased slightly. The lower part of the autoregulation curve was shifted towards lower pressure in the treated group and the lower limit of autoregulation was significantly different from that in the control. The upper limit of autoregulation was above 180 mmHg in both groups. The beneficial effect of P-23 on CBF autoregulation should be taken into consideration during chronic administration in clinical studies in man.
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PMID:Cerebral blood flow (CBF) autoregulation in spontaneously hypertensive rats (SHR) during chronic administration of a theophylline derivative (P-23). 251 76


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