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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Splanchnic blood flow (SBF) was measured simultaneously with cardiac output (dye dilution) and intrarterial blood pressure by constant infusion of indocyanine green in 11 control subjects, 13 patients with essential hypertension (EH) and seven hypertensive patients with renal artery stenosis (RAS). The cardiac index (CI) was lower (P less than 0.05) in patients with EH (3.17 plus or minus 0.07 L/min/m-2) (mean plus or minus SEM) than in control subjects (3.43 plus or minus 0.09). Associated with the lower CI was a significantly (P less than 0.01) lower SBF (0.797 plus or minus 0.02 L/min/m-2 vs 0.889 plus or minus 0.04). Patients with RAS presented with higher (P less than 0.01 vs EH, nonsignificant vs control subjects) cardiac index (3.66 plus or minus 0.17) and even lower SBF (0.749 PLUS OR MINUS 0.02). Furthermore, there was a negative correlation (r = - 0.652) between the mean arterial pressure and the SBF when results for all patients were considered. The correlation remained (r = - 0.568) in the EH group and the slope of regression line was not different from that for all subjects. The CI and SBF were weakly correlated (r = 0.423) in control subjects and patients with EH, whereas in patients with RAS, a negative correlation was found (r = - 0.778). This study indicates that the SBF, although significantly decreased in patients with EH, remains proportional to the CI in control subjects and in essential hypertensive patients. No redistribution of CI in regard to the splanchnic circulation occurs in EH. In contrast, in patients with RAS a dissociation of CI and SBF occurs and the fraction of the CI which passes through the splanchnic vascular bed is markedly reduced. The close correlation between mean arterial pressure and SBF suggests that both parameters are influenced by a common pathophysiological factor.
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PMID:Splanchnic blood flow in essential hypertension and in hypertensive patients with renal artery stenosis. 12 33

Renal para-aminohippurate (PAH) clearances were predicted in 16 kidneys of eight hypertensive patients with renal artery stenosis, pyelonephritis, or obstructive nephropathy, without individual ureteral catheterization. Predictions of left or right kidney clearance (CL or CR) were based on roentgenographic renal frontal areas (A), on total PAH clearances (CT), and on individual PAH extractions (E) measured at renal vein catheterization according to the formula (formula: see text). When these patients underwent ureteral catheterization for diagnostic reasons, individual PAH clearances were measured and ranged from 22 to 286 cm3/min. After correction for differences in total PAH clearance on the two occasions, predicted and individually measured values corresponded closely along a line of identity. The 95% confidence limit (+/- 2 SEM) for predictions of individual PAH clearance was approximately +/- 38 cm3/min and for percet of total PAH clearance distributed to left or right kidney, +/- 6%. Individual renal PAH clearances can therefore be predicted at renal vein catheterization with acceptable error. Thus, the substantially invasive procedure of ureteral catheterization is not required to ascertain left and right kidney PAH clearance in patients already at risk from renal disease.
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PMID:Individual renal clearances determined at renal vein catheterization. 84 70

Renin activities were determined in plasma and in single, microdissected juxtaglomerular apparatus in 19 patients with unilateral renal artery stenosis. The mean juxtaglomerular apparatus renin concentration in the stenosed kidneys was 5.5 +/- 1.2 (SEM) mug.l-1.h-1 which is about ten times that of the suppressed renin concentration in the contralateral kidneys (0.6 +/- 0.05 mug.l-1.h-1). On the affected side a positive correlation was found between intrarenal and renal venous renin concentration (r = 0.93; p less than 0.001). Both intrarenal and renal venous renin concentrations of the stenosed kindeys were positively correlated to renin secretion rates, as calculated from renin analysis in plasma from the vena cava and renal veins. No relationship could be demonstrated between intrarenal or renal venous renin concentration and the degree of blood pressure elevation or transstenotic pressure gradient. However, a positive correlation was evident between peripheral plasma renin activity and diastolic blood pressure (r = 0.88; p less than 0.001). Comparative enzyme kinetic analyses of renin from the juxtaglomerular apparatus and renal venous plasma were performed using sheep substrate. The lowest apparent Km-values of renin were found in renal venous plasma from the stenosed kidneys (198 +/- 13 mug/l) compared with the contralateral side (301 +/- 20 mug/l; p less than 0.001). Mean apparent Km-values of juxtaglomerular apparatus renin in the stenosed (270 +/- 36 mug/l) and contralateral (292 +/- 37 mug/l) kidneys did not differ. No significant differences were found between mean apparent Km-values for renin in peripheral plasma of renovascular hypertensive patients and control subjects using either homologous human or heterologous sheep renin substrate. The results suggest that, in addition to the renin concentration other factors are relevant to chronic high blood pressure in renovascular hypertension.
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PMID:Kidney and plasma renin in human renovascular hypertension. 100 43

This study consisted of five different experiments with conscious rabbits. In experiment 1, the angiotensin II (ANG II) antagonist [Sar1-Ala8]ANG II infused iv into one-kidney rabbits with renal artery stenosis (RAS) of 3 days' duration, at a dose that blocked pressor responses to ANG II, did not decrease the exaggerated pressor responses to norepinephrine (NE). In experiment 2, captopril infused iv into one-kidney, 3-day, RAS rabbits blocked pressor hyperresponsiveness to NE, and the concurrent infusion of [Sar1-Ala8]ANG II did not reestablish pressor hyperresponsiveness, indicating that this ANG II analogue had no agonistic action to promote hyperresponsiveness to NE. In experiment 3, infusion of ANG II at a subpressor dose (6.7 pmol . min-1 . kg body wt-1) into normal rabbits resulted in pressor hyperresponsiveness to NE, which was blocked by [Sar1-Ala8]ANG II. Experiment 4 involved infusing [Sar1-Ala8]ANG II or [Sar1-Ile8]ANG II at various doses into 3-day RAS rabbits, to determine their abilities to attenuate the pressor responses to ANG II (100 ng/kg) and the pressor hyper-responses to NE (800 ng . min-1 . kg-1). [Sar1-Ile8]ANG II decreased the ANG II pressor responses at an ID50 dose of 64 +/- 5 (SEM) pmol . min-1 . kg-1 and attenuated the NE pressor hyper-response at an ID50 dose of 65 +/- 5 pmol . min-1 . kg-1; [Sar1-Ala8]ANG II diminished the ANG II pressor response at an ID50 dose of 757 +/- 247 and the NE pressor hyper-response at an ID50 dose of 10,061 +/- 944 pmol . min-1 . kg-1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Angiotensin receptors and pressor hyperresponsiveness in renal prehypertensive rabbits. 301 4

The spontaneously hypertensive rat (SHR) and the stroke-prone substrain (sp-SHR) have been reported to have several abnormalities in levels of peptides both in tissue and in plasma (beta-endorphin, prolactin, thyroid stimulating hormone and vasopressin) when compared to the Wistar Kyoto (WKY) normotensive control rat. As the secretion of these peptides is under dopaminergic control and the abnormalities consistently suggest under-activity of the dopaminergic control system in the brain, injections of dopamine (0.4 mg/kg) were given i.c.v. to 10 SHR, 10 renal artery stenosis hypertensive rats (LRAS) and 10 genetically hypertensive rats of the New Zealand strain (GHR). Mean blood pressure fell from 205 +/- 6 (SEM) mmHg to 128 +/- 8 mmHg in the SHR (p less than 0.001), from 184 +/- 7 mmHg to 176 +/- 7 mmHg in the LRAS (p greater 0.05) and from 157 +/- 5 mmHg to 138 +/- 6 mmHg in he GHR (p less than 0.02). These effects were unlikely to be due to leakage of dopamine out into the periphery as i.v. dopamine (0.4 mg/kg) increased blood pressure in these animals.
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PMID:Neuropeptide abnormalities suggest a dopaminergic basis for high blood pressure in the spontaneously hypertensive rat. 609 77

Microvascular responses in the cremaster muscle were compared with changes in mean arterial pressure and hindquarters vascular resistance during the development (initial 3 hours) of two-kidney one-clip renal hypertension in rats, to examine the possibility that an autoregulatory mechanism may contribute to the development of hypertension. Rats were anesthetized with urethane and chloralose and implanted with Doppler flow probes on the renal artery and abdominal aorta. Acute hypertension was produced by inflation of a balloon occluder on the renal artery to reduce renal flow by 50%. The cremaster muscle was isolated with intact innervation and circulation for measurement of microvessel diameters. To determine whether increased pressure contributed to the changes in hindquarters vascular resistance or in microvascular diameters during acute hypertension, arterial pressure was prevented from increasing in the hindquarters region after renal artery stenosis by servo-controlled inflation of a balloon occluder around the sacral aorta to maintain hindquarters pressure at normotensive levels. In hypertensive rats with unprotected hindquarters, mean arterial pressure and hindquarters vascular resistance increased 26% and 20%, respectively, after renal artery stenosis. In comparison, hypertensive rats with protected hindquarters exhibited a similar increase in mean arterial pressure, but hindquarters vascular resistance was significantly reduced compared to that in hypertensive rats with unprotected hindquarters. In the cremaster microcirculation, vasoconstriction was observed only in the small third- (mean +/- SEM: 29 +/- 4 micron) and fourth- (12 +/- 2 micron) order arterioles in rats with unprotected hindquarters. In general, microvessel diameters in rats with protected hindquarters that had lower hindquarters vascular resistance than those with unprotected hindquarters were larger for the second- (82 +/- 5 micron), third-, and fourth-order arterioles, suggesting less vasoconstrictor tone. Our data indicate that the increase in hindquarters resistance during the development of renal hypertension is, in part, dependent on the presence of a pressure-dependent autoregulatory process.
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PMID:Hemodynamic and microvascular responses in the hindquarters during the development of renal hypertension in rats. Evidence for the involvement of an autoregulatory component. 648 83

The effects of captopril 450 mg/day for 4 weeks on blood pressure, heart rate, cardiac output and extracellular fluid volume were compared in severe, often drug-resistant hypertension (n = 23), mild to moderate hypertension associated with renal artery stenosis (n = 10) and mild to moderate essential hypertension (n = 20). Plasma renin in the three groups was 52 +/- 19, 58 +/- 17 and 20 +/- 4 microU/ml (mean +/- SEM), respectively. Blood pressure fell by 18 +/- 4%, 21 +/- 2% and 18 +/- 1%. The pressure drop was mainly due to a fall in peripheral vascular resistance. Addition of the diuretic hydrochlorothiazide (25-100 mg/day) caused a further fall in resistance. Despite the vasodilator effect of captopril, reflex cardiostimulation and reactive fluid retention were not observed. In severe hypertension, captopril alone was more effective in lowering blood pressure than combined diuretic-betablocker-vasodilator therapy. Moreover, cardiac output in these patients was higher and resistance was lower after captopril than during combined treatment. Thus, captopril was capable of normalising the abnormal haemodynamic state in patients with essential hypertension, and in hypertension associated with renal artery stenosis. Despite marked differences in pre-treatment plasma renin, the effects of captopril on systemic haemodynamics were similar in all the patients.
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PMID:Haemodynamic profile of captopril treatment in various forms of hypertension. 702 56

Hypertension was induced in rats by either renal artery stenosis or a fructose-enriched diet, and the consequent changes in plasma glucose, insulin, and triglyceride (TG) concentrations, and the steady-state plasma insulin (SSPI) and glucose (SSPG) concentrations in response to a 180-min continuous infusion of glucose and insulin in these two groups of hypertensive rats, were compared to values in a sham-operated group with normal blood pressure. Mean (+/- SEM) blood pressure was significantly higher than the control values (121 +/- 3 mm Hg) at the end of the study in rats with renal artery stenosis (178 +/- 13 mm Hg) and fructose-fed rats (151 +/- 5 mm Hg), whereas left ventricular weight was only significantly (P < .01) higher in rats with renal artery stenosis. Plasma glucose concentration was the same in all three groups, but fructose-fed rats had significantly higher plasma insulin (59 +/- 7 microU/mL) and TG (317 +/- 48 mg/dL) concentration than either sham-operated rats (30 +/- 4 microU/mL and 121 mg/dL) or rats with renal artery stenosis (34 +/- 5 microU/mL and 124 +/- 14 mg/dL). Although SSPI concentrations were similar (approximately 250 microU/mL) in all three groups of rats, SSPG concentrations were significantly higher (P < .01) in the fructose-fed rats (187 +/- 10 mg/dL) than in either sham-operated normotensive rats (120 +/- 6 mg/dL) or hypertensive rats with renal artery stenosis (133 +/- 4 mg/dL). Thus, insulin resistance, hyperinsulinemia, and hypertriglyceridemia developed in rats with fructose-induced hypertension, whereas none of these changes were seen in rats with renal artery stenosis.
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PMID:Comparison of the metabolic changes in rats with hypertension secondary to fructose feeding or renal artery stenosis. 766 31

Comparison of survival data among centers may be used to assess performance, but may be influenced by the number of patients who die during the first 90 days of renal replacement therapy (RRT). Data published by registries in Europe do not detail these deaths, and US data generally exclude them from analysis for financial reasons. To study factors influencing such deaths we compared 42 patients who died within 90 days of first commencing RRT in one Scottish renal unit (group A) between 1971 and 1992 with 42 age- and sex-matched controls who started RRT over the same period and survived longer (group B). Patients who died within 90 days of RRT ranged in age from 25.3 to 83.7 years and had a mean age of 65.2 (SEM, 1.6; 95% confidence interval, 61.9 to 68.4). The proportion of patients who died during the first 90 days of RRT increased from 2% of all patients treated before 1981 to 12% in subsequent years. Thirty-three patients in group A received emergency dialysis via temporary venous access compared with only nine in group B (P < 0.055). There were more patients in group A with a diagnosis of arteriosclerotic renal artery stenosis (14 v 1) and with a history of smoking (15 v 2) than in group B (P < 0.0005). Median renal or nonrenal follow-up before RRT was 1.1 month in group A and 10.6 months in group B (P < 0.0001). Fewer patients in group A had no coexisting disease (1 v 17; P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Death during the first 90 days of dialysis: a case control study. 784 55

The inability to separate irreversible lesions of tubular epithelia from reversible tubular atrophy constitutes a major problem in histopathology and in decisions for revascularization of shrunken kidneys with renal artery stenosis. In order to characterize reversible tubular atrophy ('kidney hibernation') we studied the physiological and biochemical parameters and morphology including histochemistry in rat kidneys made atrophic by renal artery stenosis and treatment with the angiotensin-converting enzyme inhibitor, enalapril. Renal artery stenosis was induced by a 0.2-mm clip around the left renal artery. Following 7 weeks of clipping and 2 concomitant weeks of enalapril treatment, the kidney length decreased from 17.8 +/- 0.3 to 13.7 +/- 0.7 mm (mean +/- SEM). Renal blood flow and glomerular filtration rate decreased to 39 +/- 3% and to approximately 3% of control values, respectively. The activities of the intracellular proteolytic enzymes cathepsin B and L and of Na-K-ATPase in microdissected proximal tubular segments decreased to values below 50 and 10%, respectively. All changes were significant (p < 0.05). Histochemical staining for ATPase activity in the distal tubule segments remained unchanged. Tubular cells were atrophic but not necrotic. Histochemical staining of alkaline phosphatase in the tubular brush border and of acid phosphatase and peroxidase in lysosomes was greatly reduced. All observed changes were reversible within 2-3 weeks following removal of the clip and withdrawal of enalapril either with or without contralateral nephrectomy. Thus, a form of kidney hibernation with readily reversible tubular atrophy has been described. Based on this description it may be possible in consecutive experiments to differentiate between reversible and irreversible tubular atrophy.
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PMID:Characteristics of renal tubular atrophy in experimental renovascular hypertension: a model of kidney hibernation. 868 34


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