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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We recently demonstrated a direct relationship between autoregulation-related changes in renal vascular resistance (RVR) and renal interstitial ATP concentrations. To assess the possible role for extracellular ATP in the regulation of tubuloglomerular feedback (TGF)-mediated autoregulatory adjustments in RVR, renal interstitial ATP concentrations were measured with microdialysis probes in anesthetized dogs at different renal arterial pressures (RAPs) within the autoregulatory range during augmented and diminished activity of the TGF mechanism. Stepwise reductions in RAP from ambient pressure (129+/-3 mm Hg) to 102+/-2 mm Hg (step 1) and 75+/-1 mm Hg (step 2) resulted in significant decreases in ATP concentrations from 9.0+/-0.8 to 6.3+/-0.6 nmol/L in step 1 and to 4.2+/-0.5 nmol/L in step 2. Changes in RVR were highly correlated with changes in ATP concentrations (r=0.86, P<0.001, n=12). Acetazolamide (100 microgram. kg(-1). min(-1), n=6), which increases solute delivery to the macula densa, thus augmenting TGF activity, significantly decreased renal blood flow (RBF) by -16+/-2% and glomerular filtration rate (GFR) by -22+/-4% and increased ATP concentrations from 8.4+/-0.7 to 15.5+/-1.4 nmol/L. Although basal RBF and GFR levels were reduced by the acetazolamide infusion, autoregulation efficiency was maintained, and interstitial ATP concentrations were significantly decreased in response to reductions in RAP by -36+/-4% in step 1 and by -54+/-2% in step 2. The relationship between changes in RVR and interstitial ATP concentrations was preserved during acetazolamide treatment (r=0.80, P<0.01). Inhibition of the TGF mechanism by furosemide significantly increased RBF by 33+/-6% and GFR by 13+/-2% and decreased ATP concentrations from 8.9+/-1.4 to 5.0+/-0.8 nmol/L (n=6). Furosemide caused marked impairment of RBF and GFR autoregulatory efficiency (by -14+/-3% and -11+/-3% in step 1 and by -26+/-2% and -18+/-4% in step 2, respectively). In the furosemide-treated kidneys, interstitial ATP levels remained low and were not altered during reductions in RAP (4.7+/-0.7 nmol/L in step 1 and 4.7+/-0.8 nmol/L in step 2), and changes in RVR did not exhibit a correlation with changes in ATP concentrations (r=0.22, P=0.30). These data support the hypothesis that extracellular ATP contributes to autoregulatory adjustments in RVR that are mediated by changes in activity of the TGF mechanism.
Hypertension 2001 Feb
PMID:Renal interstitial atp responses to changes in arterial pressure during alterations in tubuloglomerular feedback activity. 1123 Mar 69

The present study was carried out to examine whether pentoxifylline administration to horses premedicated with frusemide would attenuate the exercise-induced pulmonary arterial, capillary and venous hypertension to a greater extent than frusemide alone, thereby affecting the occurrence of exercise-induced pulmonary haemorrhage (EIPH). Using established techniques, we determined right heart and pulmonary vascular pressures in 6 healthy, sound Thoroughbred horses at rest and during exercise performed at maximal heart rate at a workload of 14 m/s on 3.5% uphill grade in the control (no medications), frusemide (250 mg i.v., 4 h pre-exercise)-control, and the frusemide (250 mg i.v., 4 h pre-exercise) + pentoxifylline (8.5 mg/kg bwt i.v., 15 min preexercise) treatments. Sequence of the 3 treatments was randomised for every horse and 7 days were allowed between them. In the control study, galloping at 14 m/s on 3.5% uphill grade elicited significant right atrial as well as pulmonary arterial, capillary and venous hypertension and all horses experienced EIPH as detected by the presence of fresh blood in the trachea on endoscopic examination. Frusemide administration was not attended by changes in heart rate at rest or during exercise. Although in the frusemide-control experiments, a significant reduction in mean pulmonary arterial, capillary and wedge pressures was observed both at rest and during galloping at 14 m/s on 3.5% uphill grade, all horses still experienced EIPH. Pentoxifylline administration to standing horses premedicated with frusemide caused nervousness, muscular fasciculations, sweating and tachycardia. Although these symptoms had largely abated within 15 min, there were no significant changes in the right atrial or pulmonary vascular pressures. Exercise in the frusemide + pentoxifylline experiments also caused significant right atrial as well as pulmonary arterial, capillary and venous hypertension, but these data were not found to be significantly different from the frusemide-control experiments. All horses in the frusemide + pentoxifylline experiments also experienced EIPH. In conclusion, our data indicate that pentoxifylline (8.5 mg/kg bwt i.v., 15 min pre-exercise) is ineffective in modifying the pulmonary haemodynamic effects of frusemide in exercising horses. It should be noted, however, that we did not examine whether erythrocyte plasticity was altered by the administration of pentoxifylline. Since the intravascular force exerted onto the blood-gas barrier of exercising horses premedicated with frusemide remained unaffected by pentoxifylline administration, it is concluded that concomitant pentoxifylline administration is unlikely to offer additional benefit to horses experiencing EIPH.
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PMID:Intravenous pentoxifylline does not enhance the pulmonary haemodynamic efficacy of frusemide in strenuously exercising thoroughbred horses. 1146 67

Reported causes of pancreatitis in pregnancy include: gallstone disease, hyperlipidemia, alcohol ingestion, viral, and idiopathic. Few reports associate pancreatitis with pregnancy-induced hypertension. A 35-year-old women with pregnancy-induced hypertension and spontaneous rupture of membranes was admitted for induction of labor. Her postpartum course was complicated by acute renal failure that responded well to treatment with Lasix and Albumin. Subsequently, the patient developed acute pancreatitis and recovered following conservative treatment. It is possible that the pancreatic ischemia due to generalized vasoconstriction of preeclampsia and loop diuretics in the setting of oliguria with renal failure, had a synergistic effect on the pancreas. Therefore, we suggest that in postpartum women with pregnancy-induced hypertension and acute renal failure, diuretics should be cautiously used because they may increase the risk of pancreatitis.
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PMID:Pregnancy-induced hypertension complicated by postpartum renal failure and pancreatitis: a case report. 1201 78

This study was carried out to assess whether with a similar degree of blood pressure reduction, Lisinopril compares favorably or otherwise with lacidipine in respect of effects on urinary albumin excretion and renal function as assessed by creatinine clearance, plasma creatinine, urea and electrolytes. Thirty hypertensive diabetic nephropathy patients with moderate hypertension were studied. After a 2-week washout period, they were allocated into two groups matched at baseline for age, sex, weight, blood pressure, and urinary albumin excretion rate as well as creatinine clearance. There were 8 males and 7 females in each group. One group received lisinopril (with furosemide if needed to control BP) and the other group received lacidipine. Staged increases in doses of antihypertensives were used until BP was controlled or maximum dose of 40 mg/day lisinopril or 8 mg/day lacidipine was reached. Furosemide was added to lisinopril if BP was not controlled at 40 mg/day. These medications were given for 12 weeks at the end of which measurements done at baseline were repeated. Comparison of baseline and end of study values of these parameters within the groups and between the two groups were made. Lisinopril group and lacidipine group achieved similar and highly significant reduction in blood pressure levels P < 0.001. There was reduction in urinary albumin excretion rate in both groups but this only reached statistical significance in the lisinopril group [480] [269] mg/day vs. 315 [202] mg/day P < 0.05] while for the lacidipine group it was not significant [491] [257] mg/day vs. 335 [182] mg/day P > 0.05]. However, comparison of albumin excretion rate between both groups at baseline and at end of the study did not show any significant difference, P > 0.1. With both drugs there is a tendency for creatinine clearance to increase and plasma creatinine to drop while plasma potassium tended to rise more with lisinopril than lacidipine but differences within and between both groups, did not reach statistical significance P > 0.05. In conclusion, blood pressure reduction was comparable in both drugs; both drugs reduced albuminuria but lisinopril appeared superior. Treatment with both drugs tended to increase creatinine clearance but both had no significant effects on blood sugar.
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PMID:Comparative effect of lisinopril and lacidipine on urinary albumin excretion in patients with type 11 diabetic nephropathy. 1251 31

The goal of this study was to determine the in vivo pulmonary arterial buffering function (BF) during acute and moderate pulmonary hypertension achieved by phenylephrine-induced smooth muscle activation. Pulmonary pressure (Konigsberg P7) and diameter (sonomicrometry) were measured in nine anesthetized sheep. Transit pulmonary arterial hypertension was induced by mechanical occlusion of the pulmonary artery (HP) and by phenylephrine infusion (5 microg/kg/min) (PHE). A viscoelastic Kelvin-Voigt model was used. By increasing the values of the viscous modulus, the pressure-diameter hysteresis area was reduced to a minimum in order to obtain the purely elastic pressure-diameter relationship. The elastic index (E) was calculated as the first derivative of the exponential model of the purely elastic pressure-diameter relationship at the mean pressure point. Systolic, diastolic, mean and pulse pressures were similar during HP and PHE, but significantly higher with regard to control steady state. In HP, E and arterial diameter (both its minimum and maximum values) increased significantly. In contrast, when pulmonary hypertension was induced by VSM activation, E was maintained concomitantly with pulmonary artery vasoconstriction. Pulmonary hypertension produced by occlusion of the pulmonary artery increases elasticity. Smooth muscle activation may offset the deleterious effect of pulmonary hypertension on arterial wall elasticity by reducing E and impeding arterial dilatation and collagen recruitment, maintaining BF during pulmonary hypertension.
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PMID:Improved pulmonary artery buffering function during phenylephrine-induced pulmonary hypertension. 1284 38

The frusemide dose-response for attenuation of exercise-induced pulmonary capillary hypertension was studied in 7 healthy, exercise-conditioned Thoroughbred horses using previously described haemodynamic procedures. Four different doses of frusemide were tested: 250 mg regardless of bodyweight (amounting to 0.56 +/- 0.03 mg/kg bwt), 1.0 mg/kg bwt, 1.5 mg/kg bwt and 2.0 mg/kg bwt. Frusemide was administered i.v., 4 h before exercise. Haemodynamic data were obtained at rest and during treadmill exercise performed at 14.2 m/s on a 3.5% uphill grade; this workload elicited maximal heart rate of horses. Airway endoscopy was performed post exercise to detect exercise-induced pulmonary haemorrhage (EIPH). In standing horses, frusemide administration resulted in a significant (P<0.05) decrease in mean pulmonary arterial, pulmonary capillary and pulmonary artery wedge pressures, but significant differences among the various frusemide doses were not observed. In the control experiments, exercise caused significant increments in the right atrial as well as pulmonary arterial, wedge, and capillary pressures, and all horses experienced EIPH. Following frusemide administration, the exercise-induced rise in right atrial and pulmonary vascular pressures was significantly attenuated, but significant differences between the frusemide doses of 250 mg, 1.0 mg/kg, and 1.5 mg/kg were not discerned and all horses remained positive for EIPH. Although a further significant (P<0.05) attenuation of the exercise-induced rise in pulmonary capillary blood pressure occurred when frusemide dose increased from 250 mg to 2.0 mg/kg bwt, all horses still experienced EIPH. It is concluded that a linear response to increasing frusemide dosage in terms of attenuation of the pulmonary capillary hypertension does not exist in strenuously exercising Thoroughbred horses.
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PMID:Pulmonary vascular pressures of strenuously exercising Thoroughbreds after administration of varying doses of frusemide. 1533 11

We described a case of systemic lupus erythematosus (SLE) complicated with multiple intracerebral hemorrhage. A 52-year-old female with no history of hypertension had been treated with steroid hormone therapy for more than 15 years. Four days before admission, she experienced acute onset of headache and nausea. On the day of admission, the patient suffered from headache and nausea again followed by a deteriorated level of consciousness. The computed tomographic scan revealed two subcortical hematomas in the right frontal and left temporo-occipital area with atypical findings compared to those of the usual intracerebral hemorrhage. Cerebral angiography demonstrated that cortical arteries around the hematomas were markedly stretched and displaced. Multiple segmental stenosis and irregular lumen of the internal carotid artery and bilateral cortical arteries were possibly representative of vasculopathy. Transit time of blood flow was severely delayed with no apparent obstruction of the cerebral arteries, veins and dural sinuses. These findings suggested the existence of severely increased intracranial pressure. Emergent surgical evacuation of the hematomas was successfully performed with a favorable outcome for the patient. Intraoperatively, the brain was congested even after the evacuation of the hematomas. Surgical manipulation was able easily to cause bleeding from the cavity of the hematomas, which was hard to control. It is supposed that vasculopathy including fibrinoid degeneration and vasculitis may have affected the susceptibility of small arteries and veins to rupture in the present case. Subsequent increase of intracranial pressure might cause another hematomas by adding of hemodynamic stress to small vessels apart from those at the site of the first hemorrhage.
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PMID:[A case of systemic Lupus erythematosus complicated with multiple subcortical hemorrhage]. 1591 70

We have identified 2 relatively young patients with significant hypertension, an elongated single aberrant renal artery supplying blood to a renal segment, and evidence for localization of the elevated plasma renin activity to the side and vein draining the affected kidney. Furosemide-induced diuresis and acute oral captopril stimulated the renal vein/contralateral renin ratios to 4.3:1 and 6.5:1 in patients 1 and 2, respectively. These renal vein ratios are significantly higher than normal (>3:1 under similar conditions). Partial resection of the portion of the kidney affected by the aberrant tortuous artery led to a marked reduction in blood pressure in patient 1. Patient 2, not an operative candidate, responded satisfactorily to use of a converting enzyme inhibitor, which helped to confirm the dependency of the blood pressure on the abnormal flow relationship existing within that aberrant artery and the kidney. We believe these 2 patients are representative of a small but distinct subgroup within the larger number of patients with elongated single or multiple renal aberrant arteries. Each aberrant artery had no focal stenosis, although a decrease in flow relative to the tissue perfusion demands was apparent from the marked activation of the renin-angiotensin system in the venous system draining that artery. The increased length of such vessels may contribute to their decreased flow, although their average diameter may reside just above such a critical value for a normal length vessel. This new syndrome, involving more than one component of the flow/resistance relationship, has been overlooked when renin-dependent forms of hypertension are considered.
Hypertension 2005 Aug
PMID:Renin-dependent hypertension caused by nonfocal stenotic aberrant renal arteries: proof of a new syndrome. 1596 71

A 46-year-old male with long-term treatment-resistant hypertension and past history of cerebral hemorrhage was found to have suppressed plasma renin activity (PRA) and normal plasma aldosterone concentration (PAC) with aldosterone/renin ratio of 25.3. Furosemide plus upright test did not stimulate PRA, but computed tomography scan of the abdomen revealed no abnormal lesions in either adrenal gland. Selective adrenal venous sampling (SAVS) showed that PAC in the left and the right adrenal vein were 1000 ng/dl and 230 ng/dl, respectively, which increased to 1500 ng/dl and 620 ng/dl, respectively, after ACTH stimulation. Diagnosis of primary aldosteronism due to hypersecretion of aldosterone from the left adrenal gland was made, and laparoscopic left adrenalectomy was performed. Pathological examination of the 'apparently normal' adrenal tissue resected revealed the presence of poorly encapsulated multiple adrenocortical micronodules which showed positive immunoreactivity for 3beta-hydroxysteroid dehydrogenase by immunohistochemical study, but negative immunoreactivity in the hyperplastic zona glomerulosa consistent with paradoxical hyperplasia associated with primary aldosteronism. Postoperatively, PRA was normalized and his high blood pressure was well controlled with lower doses of antihypertensive drugs than those used before surgery. The clinicopathological features of our case are consistent with the diagnosis of unilateral multiple adrenocortical micronodules (UMN), a new subset of primary aldosteronism, in which SAVS proved to be a useful diagnostic tool for its localization.
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PMID:A case with primary aldosteronism due to unilateral multiple adrenocortical micronodules. 1612 11

Superoxide (O(2)(-)) regulates renal function and is implicated in hypertension. O(2)(-) production increases in response to increased ion delivery in thick ascending limbs (TALs) and macula densa and mechanical strain in other cell types. Tubular flow in the kidney acutely varies causing changes in ion delivery and mechanical stress. We hypothesized that increasing luminal flow stimulates O(2)(-) production by NADPH oxidase in TALs via activation of Na-K-2Cl cotransport. We measured intracellular O(2)(-) in isolated rat TALs using dihydroethidium in the presence and absence of luminal flow and inhibitors of NADPH oxidase, Na-K-2Cl cotransport, and Na/H exchange. In the absence of flow, the rate of O(2)(-) production was 5.8 +/- 1.4 AU/s. After flow was initiated, it increased to 29.7 +/- 4.3 AU/s (P < 0.001). O(2)(-) production was linearly related to flow. Tempol alone and apocynin alone blocked the flow-induced increase in O(2)(-) production (3.5 +/- 1.7 vs. 4.5 +/- 2.8 AU/s and 8.2 +/- 2.1 vs. 10.6 +/- 2.8 AU/s, respectively). Furosemide decreased flow-induced O(2)(-) production by 55% (37.3 +/- 5.2 to 16.8 +/- 2.8 AU/s; P < 0.002); however, dimethylamiloride had no effect. Finally, we examined whether changes in mechanical forces are involved in flow-induced O(2)(-) production by using a Na-free solution to perfuse TALs. In the absence of NaCl, luminal flow enhanced O(2)(-) production (1.5 +/- 0.5 to 13.5 +/- 1.1 AU/s; P < 0.001), approximately 50% less stimulation than when flow was increased in the presence of luminal NaCl. We conclude that flow stimulates O(2)(-) production in TALs via activation of NADPH oxidase and that NaCl absorption due to Na-K-2Cl cotransport and flow-associated mechanical factors contribute equally to this process.
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PMID:Flow increases superoxide production by NADPH oxidase via activation of Na-K-2Cl cotransport and mechanical stress in thick ascending limbs. 1713 67


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