Function In Essential Hypertension Research Articles

Effect of Carvedilol on Ambulatory Blood Pressure, Renal Hemodynamics, and Cardiac Function in Essential Hypertension

A randomized, double-blind, placebo-controlled study was set up to study the effects of acute and chronic administration of carvedilol, a vasodilatory beta-blocker in essential hypertension. Acute administration of a single dose of 50 mg of carvedilol reduced systolic and diastolic blood pressure, without inducing reflex tachycardia. Renal blood flow was preserved; accordingly renal vascular resistance was significantly reduced. A significant reduction of glomerular filtration rate and filtration fraction was observed. Plasma renin activity (PRA) and plasma aldosterone were not changed. Chronic carvedilol treatment produced a significant fall in systolic and diastolic office and ambulatory blood pressure, heart rate, cardiac output, PRA and plasma aldosterone. Blood pressure variability was not changed. Renal blood flow, glomerular filtration rate and filtration fraction also remained unchanged; renal vascular resistance decreased significantly. It is concluded that carvedilol possesses definite antihypertensive and renal vasodilating properties, both acutely and after chronic treatment.

Effect of Carvedilol on Ambulatory Blood Pressure, Renal Hemodynamics, and Cardiac Function in Essential Hypertension

Effect of Carvedilol on Ambulatory Blood Pressure, Renal Hemodynamics, and Cardiac Function in Essential Hypertension

Effect of Carvedilol on Ambulatory Blood Pressure, Renal Hemodynamics, and Cardiac Function in Essential Hypertension

Summary A randomized, double-blind, placebo-controlled study was set up to study the effects of acute and chronic administration of carvedilol, a vasodilatory β-blocker in essential hypertension. Acute administration of a single dose of 50 mg of carvedilol reduced systolic and diastolic blood pressure, without inducing reflex tachycardia. Renal blood flow was preserved; accordingly renal vascular resistance was significantly reduced. A significant reduction of glomerular filtration rate and filtration fraction was observed. Plasma renin activity (PRA) and plasma aldosterone were not changed. Chronic carvedilol treatment produced a significant fall in systolic and diastolic office and ambulatory blood pressure, heart rate, cardiac output, PRA and plasma aldosterone. Blood pressure variability was not changed. Renal blood flow, glomerular filtration rate and filtration fraction also remained unchanged; renal vascular resistance decreased significantly. It is concluded that carvedilol possesses definite antihypertensive and renal vasodilating properties, both acutely and after chronic treatment.

Effect of long term felodipine treatment on renal vascular tone, glomerular filtration rate and renal tubular function in essential hypertension.

The effect of long term felodipine i treatment on renal vascular tone, glomerular flltration rate and renal tubular function was explored in 10 male patients with essential hypertension on a standardised daily intake of Na+ (150 nmol), K+ (75 nmol) and water (2500ml). The results of felodipine given IOmg bid for 8 weeks were compared with placebo intake (table I). Renal plasma flow and glomerular flltration rate (GFR) were measured as l3lhippurateand slCr-EDTAclearance using single injection technique. 24-hour renal clearance of creatinine (C-Q), electrolytes and urate were measured by routine methods. Fractional excretion was taken as the ratio of clearance electrolytes and urate! creatinine clearance. Mean blood pressure (MBP), renal blood flow (RBF), renal vascular resistance (RVR) and flltration fraction (FF) were calculated and the results are presented as median (M) and upper (UQ) and lower (LQ) quartiles. There was a positive correlation between glomerular flltration rate and creatinine clearance after placebo as well as after felodipine (0.83; p < 0.01 and 0.69; p < 0.05, respectively).

本態性高血圧症における血小板機能とプロスタノイドに関する研究

To evaluate platelet function in essential hypertension, we studied the plasma levels of β-thromboglobulin (β-TG), platelet factor 4 (PF4),6-keto-prostaglandin F1α (6KPGF; a stable metabolite of PGI2) and thromboxane Bc (TXB2; a stable metabolite of TXA2), and platelet aggregation in 51 patients with uncomplicated hypertension and 44 age-matched normotensive controls. The plasma levels of β-TG and PF4 were significantly greater than normal. After administration of antihypertensive drugs,3-TG and PF4 levels were decreased, but the difference reached statistical significance for PF4 only. The plasma levels of 6KPGF were similar in the two groups, whereas TXB2 levels were higher in hypertensives than in normotensives. Consequently, the ratio TXB2/6KPGF was elevated in hypertensives.The results of platelet aggregation revealed no difference in the two groups. After control of blood pressure with single or several combinations of anti-hypertensive drugs, the values remained unchanged.β-TG correlated positively with systolic blood pressure, and 6KPGE correlated negatively with mean and diastolic blood pressure.β-TG and PF4 showed age-related elevations. These data suggest that platelet fun ction was enhanced in essential hypertension. PGI2 may be importantly involved in blood pressure regulation.The imbalanced production of prostagland ins might contribute to the pathogenesis of essential hypertension. Antihypertensive therapy may be useful to protect patients with hypertension from life-threatening thromboembolism by suppressing enhanced platelet function.

Preliminary observations on abnormalities of membrane structure and function in essential hypertension.

To test the hypothesis that structural abnormalities exist in the cell membrane in persons with essential hypertension and that these abnormalities affect membrane-related cellular functions, we examined several membrane-dependent phenomena and membrane lipid composition in the blood cells of subjects with essential hypertension. We analyzed platelet aggregability, membrane fluidity, membrane fatty acid composition, and erythrocyte deformability in four normolipidemic subjects with untreated essential hypertension and in five age-matched normotensive controls. As compared with the controls, the subjects with essential hypertension had platelets that aggregated at lower concentrations of adenosine 5'-diphosphate, platelet membranes that were less fluid, and erythrocytes that were more deformable. Lipid analysis of the membranes of platelets from the two study groups showed that although the cholesterol content was identical, the membranes from the essential hypertension group contained significantly less linoleic acid (18:2) than did those from the normotensive controls. Given the known effects of cis-unsaturated fatty acyl composition on membrane fluidity and membrane-related cellular functions, these data suggest that one factor contributing to essential hypertension is an inherent structural membrane abnormality that alters the physical and functional properties of the cell membrane.

Hemodynamic and renal function in essential hypertension during treatment with enalapril

Enalapril (at a mean dose of 25 mg), a potent, long-acting angiotensin converting enzyme inhibitor, was prescribed in combination with hydrochlorothiazide (at a mean dose of 64 mg) for 96 weeks in 11 patients with essential hypertension who had pretreatment (placebo) glomerular filtration rates of less than 80 ml/minute/1.73 m 2. Blood pressure was well controlled. After 56 weeks of therapy, glomerular filtration rate (assessed by inulin clearance) increased 55 percent and effective renal plasma flow (assessed by para-aminohippurate clearance) increased by 32 percent; these increases were sustained through the 96 weeks of therapy. Furthermore, gains in renal function were sustained without adversely affecting 24-hour urinary protein excretion, sodium excretion, or body fluid composition. These results suggest that enalapril, in combination with hydrochlorothiazide, has the pharmacologic capability to favorably modify a primary pathophysiologic characteristic of essential hypertension by decreasing renal vascular and mesangial tone.

Cardiovascular, Humoral, and Renal Effects of Phenoxybenzamine in Hypertension

We examined the effects of alpha adrenergic receptor blockade with phenoxybenzamine on various parameters related to blood pressure regulation in 10 normotensive and 12 essential hypertensive subjects. The responses were observed before and after phenoxybenzamine treatment during standardized maneuvers of volume expansion with saline infusion and volume contraction with a diuretic. Alpha adrenergic blockade produced a significantly greater (P less than 0.02) reduction in blood pressure in the hypertensive group than in the normotensive subjects. The baroreceptor response, evaluated by comparing the change in plasma norepinephrine concentration in relation to the change in blood pressure, was significantly reduced (P less than 0.05) in hypertensives compared to normal subjects. Plasma and urinary norepinephrine concentration, which were similar in the two groups, increased in both during phenoxybenzamine treatment. There was no significant change in the mean levels of plasma renin activity or plasma aldosterone concentration in either group after phenoxybenzamine treatment. However, the relationship between plasma renin activity and plasma aldosterone levels, as judged by linear regression analysis, was significantly altered (P less than 0.05) by phenoxybenzamine therapy in both groups. The latter may reflect an effect of phenoxybenzamine on the metabolism or secretion of aldosterone. These results, utilizing an alpha adrenergic antagonist, confirm the enhanced vascular reactivity and diminished baroreceptor function in essential hypertension; no evidence for an alpha adrenergic effect on plasma renin activity could be demonstrated in normotensive or hypertensive subjects.

Effect of Atenolol on Left Ventricular Function in Essential Hypertension

Effect of Atenolol on Left Ventricular Function in Essential Hypertension

Responses of plasma catecholamine and plasma renin activity after glucagon stimulation in essential hypertension.

Abstract. To investigate the roles of the sympatheticoadrenomedullary system and the renin-angiotensin system in the pathogenesis of essential hypertension, the levels of plasma catecholamine and plasma renin activity (PRA) after glucagon-stimulation were evaluated. In 9 patients with essential hypertension whose levels of PRA were either normal or high (NHREH), iv bolus injection of 1 mg glucagon caused a rapid and significant increase in plasma epinephrine concentration from the basal values of 170 ± 25 pg/ml, mean ± sem to 314 ± 30 pg/ml (P &lt; 0.05) at 5 min after the injection, reaching the mean peak values of 358 ± 87 pg/ml (P &lt; 0.05). Plasma norepinephrine also rose from the basal values of 357 ± 50 pg/ml to the peak values of 1065 ± 231 pg/ml (P &lt; 0.02) while increase in PRA was detected in 4 of 9 patients. In 7 patients with low renin essential hypertension (LREH), plasma epinephrine failed to increase after glucagon stimulation whereas plasma norepinephrine increased significantly from the basal values of 391 ± 77 pg/ml, reaching 1212 ± 274 pg/ml at their peak values (P &lt; 0.01). There was no discernible response of PRA to glucagon. These results suggest that both epinephrine secretion from adrenal medulla and renin release from juxtaglomerular (JG) cells after glucagon injection are impaired in LREH in contrast to their significant responses observed in NHREH. It also indicates that glucagon load may be useful for the simultaneous assessment of the reserve of both renin secretion and sympatheticoadrenomedullary function in essential hypertension.

Norepinephrine kinetics in essential hypertension. Defective neuronal uptake of norepinephrine in some patients.

To assess sympathetic nervous system function in essential hypertension, we measured the rates of release to and removal from plasma of the sympathetic neurotransmitter, norepinephrine. In normal subjects, disappearance of tritiated l-norepinephrine from plasma, after infusion to steady state, was biexponential, with t1 1/2 = 2.0 +/- 0.4 minutes (mean +/- standard deviation) and t2 1/2 = 33 +/- 15 minutes. The rapid component of removal seemed to represent neuronal uptake of norepinephrine: the t1 1/2 was lengthened by the selective inhibitor of neuronal norepinephrine uptake, desipramine; it was not changed by the extraneuronal uptake blocker, cortisol; and it was prolonged in patients with peripheral sympathetic nerve dysfunction (idiopathic autonomic insufficiency). In eight of 37 hypertensive patients, the t1 1/2 was greater than 2.8 minutes (range, 3.3-6.0 min), longer than in any normal subject; this appears to be presumptive evidence of the existence of defective neuronal norepinephrine uptake. In these patients the rate of spillover of norepinephrine to plasma, of transmitter escaping uptake after release, was 0.73 +/- 0.39 micrograms/m2/min (4.3 +/- 2.3 nmoles/m2/min), higher than in normal subjects, 0.36 +/- 0.14 micrograms/m2/min (2.1 +/- 0.8 nmoles/m2/min) (p less than 0.01). A defect in neuronal uptake of norepinephrine, by exposing adrenergic receptors to high local norepinephrine concentration, may be important in the pathogenesis of blood pressure elevation in some patients with essential hypertension.

Influence of hospitalization and placebo therapy on blood pressure and sympathetic function in essential hypertension.

The decline in blood pressure (BP) in essential hypertensives following hospitalization may result from: 1) regression toward the mean; 2) reduction of anxiety as patients habituate to a new environment; 3) the placebo effect of medication; and 4) an independent effect of hospitalization itself. A randomized crossover study of 12 essential hypertensives demonstrated a fall in supine blood pressure from 165.0/97.9 +/- 2.3/1.1 mm Hg to 154.3/89.6 +/- 2.7/1.1 mm Hg (p less than 0.005) due to hospitalization. A similar reduction in BP from 164.9/99.5 +/- 8.4/4.1 mm Hg to 151.9/93.4 +/- 4.5/1.9 mm Hg (p less than 0.005) resulted from regression toward the mean and habituation during the study period. Urinary catecholamines fell from 68.7 +/- 5.0 to 55.1 +/- 4.3 micrograms/g creatinine/24 hours (p less than 0.05) due to hospitalization and from 56.1 +/- 5.4 to 49.7 +/- 4.3 micrograms/g creatinine/24 hours (p less than 0.05) with time. Although placebo therapy tended to reduce BP, it failed to do so significantly. When expressed as a percentage of the individual's overall mean, urinary catecholamine excretion fell from 110.5% +/- 3.7% to 89.5% +/- 3.7% (p less than 0.001) during hospitalization and from 105.8% +/- 3.9% to 94.2% +/- 3.9% (p less than 0.05) during the outpatient period. Blood pressure and sympathetic activity rapidly returned to prehospitalization values on discharge. These factors may confound the analysis of drug effects on BP and sympathetic activity in essential hypertensives following admission to hospital.

Changes in renal function in essential hypertension : Reubi FC, Weidmann P, Hodler J, Cottier PT: Am J Med 64: 556–563, 1978

Changes in renal function in essential hypertension : Reubi FC, Weidmann P, Hodler J, Cottier PT: Am J Med 64: 556–563, 1978

Changes in renal function in essential hypertension

Studies of renal hemodynamics, plasma renin activity (PRA), plasma aldosterone, and water and sodium excretion were performed in 171 patients with essential hypertension and 61 normotensive subjects. The para-amino hippurate clearance (C PAH) was usually normal or moderately reduced in those with benign hypertension and markedly depressed in those with malignant hypertension. The PAH extraction ratio was normal or slightly reduced in the patients with benign hypertension and moderately impaired in those with low C PAH indicating that a disproportionate decrease in cortical flow occurred only in the latter. The c pah did not correlate Inversely with the mean blood pressure in the patients with benign hypotension. Reexamination of untreated patients after an average of 28 1 2 months revealed a decrease in renal plasma flow but no further increase in blood pressure. These findings suggest that in uncomplicated hypertension the increase in blood pressure is not caused by renal circulatory disturbances. PRA was unrelated to renal hemodynamics in benign hypertension. In malignant hypertension, it was inversely correlated with the renal plasma flow. Under mild loading with isotonic saline solution, the fractional water excretion correlated with the blood pressure. Sodium excretion was neither related to the blood pressure nor to the estimated peritubular oncotic pressure, but correlated inversely with plasma aldosterone. These observations provide no support for the causative role of a primary disturbance in sodium excretion in essential hypertension.

Elevated plasma dopamine beta hydroxylase activity in rats with neurogenic hypertension

Increased plasma dopamine beta hydroxylase, DBH, activity has been cited as evidence of increased sympathetic function in essential hypertension. Here-to-fore, experimental hypertension in animals has been associated with normal plasma DBH activity. This study shows that rats with neurogenic hypertension, induced by sinoaortic denervation, SAD, have elevated DBH activity; the mean increase in plasma DBH measured 3 days to 11 weeks after operation was 74% higher in the SAD group than in the sham-operated, control group. DBH activity showed a positive correlation with arterial pressure. Mesentery DBH activity was inversely related to plasma enzyme activity in SAD rats, indicating sympathetic nerve terminals in mesentery are a source of plasma DBH. We conclude that plasma DBH activity is an index of increased sympathetic function since it is consistently elevated in rats with neurogenic hypertension resulting from sustained central activation of the sympathetic nervous system.

Effects of parathyroid hormone on renal tubular reabsorption of calcium, sodium, and phosphate.

Effects of parathyroid hormone on renal tubular reabsorption of calcium, sodium, and phosphate.

Calcium deprivation and renal handling of calcium during repeated saline infusions.

ARTICLESCalcium deprivation and renal handling of calcium during repeated saline infusionsAS Brickman, SG Massry, and JW CoburnAS Brickman, SG Massry, and JW CoburnPublished Online:01 Jan 1971https://doi.org/10.1152/ajplegacy.1971.220.1.44MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByUrine calcium and urine sodium concentrations are not related, after adjustment for urine magnesium24 December 2001 | Clinical Endocrinology, Vol. 53, No. 2The importance of calcium in the control of salt intakeNeuroscience & Biobehavioral Reviews, Vol. 20, No. 1Renal Excretion of CalciumParathyroid hormone in sodium-dependent hypertensionLife Sciences, Vol. 41, No. 11Renal Handling of CalciumEnhanced parathyroid function in essential hypertension: a homeostatic response to a urinary calcium leak.Hypertension, Vol. 2, No. 2Renal action of cholera toxin: I. Effects on urinary excretion of electrolytes and cyclic AMPKidney International, Vol. 7, No. 2BIBLIOGRAPHY More from this issue > Volume 220Issue 1January 1971Pages 44-48 Copyright & PermissionsCopyright © 1971 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1971.220.1.44PubMed5538670History Published online 1 January 1971 Published in print 1 January 1971 Metrics

Effect of hypercalcemia on renal tubular sodium handling in the rat.

ARTICLESEffect of hypercalcemia on renal tubular sodium handling in the ratGF DiBonaGF DiBonaPublished Online:01 Jan 1971https://doi.org/10.1152/ajplegacy.1971.220.1.49MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByDiuretics and Disorders of Calcium HomeostasisSeminars in Nephrology, Vol. 31, No. 6Calcium Inhibits Paracellular Sodium Conductance through Claudin-2 by Competitive BindingJournal of Biological Chemistry, Vol. 285, No. 47Increased endothelin-1 expression in the kidney in hypercalcemic ratsKidney International, Vol. 63, No. 3The importance of calcium in the control of salt intakeNeuroscience & Biobehavioral Reviews, Vol. 20, No. 1Hypercalcemia and the KidneyCalcium and hypoxic injury in the renal medulla of the perfused rat kidneyKidney International, Vol. 34, No. 2Renal Excretion of CalciumRole of the loop segment in the urinary concentrating defect of hypercalcemiaKidney International, Vol. 29, No. 5Formation of calcium complexes by borogluconate in vitro and during calcium borogluconate infusion in sheepResearch in Veterinary Science, Vol. 39, No. 1FAMILIAL HYPOCALCIURIC HYPERCALCAEMIA I: RENAL HANDLING OF CALCIUM, MAGNESIUM AND PHOSPHATEClinical Endocrinology, Vol. 22, No. 1Inhibition of transcellular NaCI reabsorption in dog kidneys during hypercalcemiaActa Physiologica Scandinavica, Vol. 120, No. 4Effect of Serum Calcium on Phosphate TransportPathophysiology of human proximal tubular transport defectsKlinische Wochenschrift, Vol. 60, No. 19Effect of calcium and phosphate on bicarbonate and fluid transport by proximal tubules in vitroKidney International, Vol. 21, No. 3Renal Handling of CalciumThe Kidney in Systemic DiseaseEnhanced parathyroid function in essential hypertension: a homeostatic response to a urinary calcium leak.Hypertension, Vol. 2, No. 2Influence of Calcium on Renal Handling of PhosphateRenal Handling of Phosphate: Update22 June 2013Effects of hypercalcemia on water and sodium excretion by the isolated dog kidneyPfl�gers Archiv European Journal of Physiology, Vol. 363, No. 1Simultaneous Mg, Ca, P, K, Na and Cl analysis in rat tubular fluidPflügers Archiv, Vol. 346, No. 3Hyposthenuria in hypercalcemiaPfl�gers Archiv European Journal of Physiology, Vol. 350, No. 1 More from this issue > Volume 220Issue 1January 1971Pages 49-53 Copyright & PermissionsCopyright © 1971 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1971.220.1.49PubMed5538671History Published online 1 January 1971 Published in print 1 January 1971 Metrics

The effect of chlorothiazide on separate kidney function in essential hypertension

The effect of chlorothiazide on separate kidney function in essential hypertension

PATHOPHYSIOLOGICAL STUDY OF RETINAL CIRCULATION AND DIAGNOSIS OF RETINAL BLOOD VESSEL FUNCTION IN HYPERTENSION AND CEREBRAL ARTERIOSCLEROSIS. 2. STUDY ON RETINAL CIRCULATION DURING HYPOXEMIA

Eye ground findings recorded by the criteria of Keith-Wagener or Scheie in essential hypertension and cerebral arteriosclerosis, have proven to be of much value clinically. However, these observation are mostly morphological and do not express were hemodynamic changes. Studies in our department have been centered around the vessel reaction of verious organs caused by induced hypoxemia and the findings concerning the coronary, cerebral, hepatic, and renal circulations have been reported previously. Recently, the determination of retinal blood flow has been established by ophthalmologists and this prompts us to study the hemodynamics of the retinal circulation during the resting state and during induced hypoxemia with the purpose of investigating the pathophysiology of the retinal circulation and the possibility of advancing a step towards the diagnosis of retinal vessel function. Methods and Materials A) Methods used : Values concerning retinal hemodynamics during the resting state were calculated by measuring the brachial and retinal blood pressures and eye ground photography. Immediately after those Procedures a mixture of 10% O2 and 90% N2 was administered for 20 minutes and the above procedures were repeated to determine the retinal hemodynamics during the induced hypoxemia. B) Calculations i) Retinal blood flow was calculation by the Hagen-Poiseuille law. ii) Comparison of central retinal artery and brachial artery blood pressures. iii) Systolic blood pressure ratio iv) Diastolic blood pressure ratio v) Pulse pressure ratio vi) Further relative differential pressure ratio