The Pressure—Volume Relationship in Normotensive and Permanent Essential Hypertensive Patients

1976 ◽  
Vol 50 (3) ◽  
pp. 207-212 ◽  
Author(s):  
M. E. Safar ◽  
N. PH. Chau ◽  
Y. A. Weiss ◽  
G. M. London ◽  
A. CH. Simon ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Blood Volume ◽  
Normal Subjects ◽  
Sodium Balance ◽  
Total Blood ◽  
Hypertensive Patients ◽  
Volume Relationship ◽  
Pressure Volume Relationship

1. Blood pressure, blood volume and renal blood flow were determined in 101 men; forty-three were normal subjects and fifty-eight were untreated permanent essential hypertensive patients with normal renal function and equilibrated sodium balance. 2. A significant negative pressure—volume relationship was observed overall. The relationship could be expressed as a hyperbola whose slope expressed the reduction in blood volume per unit rise in pressure: the higher the blood pressure, the lower the slope. Thus essential hypertensive subjects have a smaller decrement in blood volume per unit rise in pressure than normal subjects. 3. The relation between change in blood volume and change in pressure was confirmed in each individual by defining for each a ratio ΔV/ΔP, statistically identical with the hyperbolic slope dV/dP. The ΔV/ΔP ratio was found to be well correlated with the renal blood flow and the creatinine clearance. No correlation existed between the total blood volume and these two renal parameters. 4. It is concluded that the present study demonstrates a blood volume regulation disturbance in essential hypertension and provides evidence from human studies that a renal defect accompanies high blood pressure.

Renal Denervation in Combination With Angiotensin Receptor Blockade Prolongs Blood Pressure Trough During Hemorrhage

Hypertension ◽  
2021 ◽  
Author(s):  
Reetu R. Singh ◽  
Zoe McArdle ◽  
Lindsea C. Booth ◽  
Clive N. May ◽  
Geoff A. Head ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Blood Loss ◽  
Renal Blood Flow ◽  
Blood Volume ◽  
Antihypertensive Medication ◽  
Renal Denervation ◽  
Organ Damage ◽  
Antihypertensive Medications ◽  
Hemodynamic Responses

Majority of patients with hypertension and chronic kidney disease (CKD) undergoing renal denervation (RDN) are maintained on antihypertensive medication. However, RDN may impair compensatory responses to hypotension induced by blood loss. Therefore, continuation of antihypertensive medications in denervated patients may exacerbate hypotensive episodes. This study examined whether antihypertensive medication compromised hemodynamic responses to blood loss in normotensive (control) sheep and in sheep with hypertensive CKD at 30 months after RDN (control-RDN, CKD-RDN) or sham (control-intact, CKD-intact) procedure. CKD-RDN sheep had lower basal blood pressure (BP; ≈9 mm Hg) and higher basal renal blood flow (≈38%) than CKD-intact. Candesartan lowered BP and increased renal blood flow in all groups. 10% loss of blood volume alone caused a modest fall in BP (≈6–8 mm Hg) in all groups but did not affect the recovery of BP. 10% loss of blood volume in the presence of candesartan prolonged the time at trough BP by 9 minutes and attenuated the fall in renal blood flow in the CKD-RDN group compared with CKD-intact. Candesartan in combination with RDN prolonged trough BP and attenuated renal hemodynamic responses to blood loss. To minimize the risk of hypotension-mediated organ damage, patients with RDN maintained on antihypertensive medications may require closer monitoring when undergoing surgery or experiencing traumatic blood loss.

scholarly journals Endothelin-A Receptor Antagonism Reduces Blood Pressure and Increases Renal Blood Flow in Hypertensive Patients With Chronic Renal Failure

Circulation ◽  
2004 ◽  
Vol 109 (9) ◽  
pp. 1186-1193 ◽  
Author(s):  
Jane Goddard ◽  
Neil R. Johnston ◽  
Malcolm F. Hand ◽  
Allan D. Cumming ◽  
Ton J. Rabelink ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Failure ◽  
Blood Flow ◽  
Chronic Renal Failure ◽  
Renal Blood Flow ◽  
Hypertensive Patients ◽  
Receptor Antagonism ◽  
Endothelin A Receptor ◽  
Endothelin A

Observations on Cardiac Output and ”Pulmonary Blood Volume” in Normal Man by External Recording of the Intracardiac Flow of 131I Labelled Albumin

1961 ◽  
Vol 1 (04) ◽  
pp. 353-379
Author(s):  
Jacques Lammerant ◽  
Norman Veall ◽  
Michel De Visscher
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Normal Subjects ◽  
Published Data ◽  
Total Blood Volume ◽  
Total Blood ◽  
Pulmonary Blood Volume ◽  
Intracardiac Flow ◽  
Normal Man ◽  
Mean Circulation

Summary1. The technique for the measurement of cardiac output by external recording of the intracardiac flow of 131I labelled human serum albumin has been extended to provide a measure of the mean circulation time from right to left heart and hence a new approach to the estimation of the pulmonary blood volume.2. Values for the basal cardiac output in normal subjects and its variations with age are in good agreement with the previously published data of other workers.3. The pulmonary blood volume in normal man in the basal state was found to be 28.2 ± 0.6% of the total blood volume.4. There was no correlation between cardiac output and pulmonary blood volume in a series of normal subjects in the basal state.5. The increase in cardiac output during digestion was associated with a decrease in pulmonary blood volume equal to 6.3 ± 1.2% of the total blood volume, that is, about 280 ml.6. The increase in cardiac output during exercise was associated with a decrease in pulmonary blood volume equal to 4.5 ± 1.0% of the total blood volume, that is, about 200 ml.7. The increase in cardiac output attributed to alarm is not associated with a decrease in pulmonary blood volume, the latter may in fact be increased.8. The total blood volume is advocated as a standard of reference for studies of this type in normal subjects in preference to body weight or surface area.9. The significance of these results and the validity of the method are discussed.

Hypothalamic paraventricular nucleus is critical for renal vasoconstriction elicited by elevations in body temperature

2008 ◽  
Vol 294 (2) ◽  
pp. F309-F315 ◽  
Author(s):  
Joo Lee Cham ◽  
Emilio Badoer
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Core Temperature ◽  
Paraventricular Nucleus ◽  
Hypothalamic Paraventricular Nucleus ◽  
Body Core Temperature ◽  
Control Group ◽  
Body Core

Redistribution of blood from the viscera to the peripheral vasculature is the major cardiovascular response designed to restore thermoregulatory homeostasis after an elevation in body core temperature. In this study, we investigated the role of the hypothalamic paraventricular nucleus (PVN) in the reflex decrease in renal blood flow that is induced by hyperthermia, as this brain region is known to play a key role in renal function and may contribute to the central pathways underlying thermoregulatory responses. In anesthetized rats, blood pressure, heart rate, renal blood flow, and tail skin temperature were recorded in response to elevating body core temperature. In the control group, saline was microinjected bilaterally into the PVN; in the second group, muscimol (1 nmol in 100 nl per side) was microinjected to inhibit neuronal activity in the PVN; and in a third group, muscimol was microinjected outside the PVN. Compared with control, microinjection of muscimol into the PVN did not significantly affect the blood pressure or heart rate responses. However, the normal reflex reduction in renal blood flow observed in response to hyperthermia in the control group (∼70% from a resting level of 11.5 ml/min) was abolished by the microinjection of muscimol into the PVN (maximum reduction of 8% from a resting of 9.1 ml/min). This effect was specific to the PVN since microinjection of muscimol outside the PVN did not prevent the normal renal blood flow response. The data suggest that the PVN plays an essential role in the reflex decrease in renal blood flow elicited by hyperthermia.

The relationship of blood flow velocity fluctuations to intracranial pressure B waves

1992 ◽  
Vol 76 (3) ◽  
pp. 415-421 ◽  
Author(s):  
David W. Newell ◽  
Rune Aaslid ◽  
Renate Stooss ◽  
Hans J. Reulen
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Intracranial Pressure ◽  
Arterial Blood Pressure ◽  
Wave Amplitude ◽  
Transcranial Doppler Ultrasound ◽  
Normal Subjects ◽  
Content Type ◽  
Arterial Blood ◽  
Flow Fluctuations

✓ Intracranial pressure (ICP) and continuous transcranial Doppler ultrasound signals were monitored in 20 head-injured patients and simultaneous synchronous fluctuations of middle cerebral artery (MCA) velocity and B waves of the ICP were observed. Continuous simultaneous monitoring of MCA velocity, ICP, arterial blood pressure, and expired CO2 revealed that both velocity waves and B waves occurred despite a constant CO2 concentration in ventilated patients and were usually not accompanied by fluctuations in the arterial blood pressure. Additional recordings from the extracranial carotid artery during the ICP B waves revealed similar synchronous fluctuations in the velocity of this artery, strongly supporting the hypothesis that blood flow fluctuations produce the velocity waves. The ratio between ICP wave amplitude and velocity wave amplitude was highly correlated to the ICP (r = 0.81, p < 0.001). Velocity waves of similar characteristics and frequency, but usually of shorter duration, were observed in seven of 10 normal subjects in whom MCA velocity was recorded for 1 hour. The findings in this report strongly suggest that B waves in the ICP are a secondary effect of vasomotor waves, producing cerebral blood flow fluctuations that become amplified in the ICP tracing, in states of reduced intracranial compliance.

scholarly journals Effects of Relative Blood Volume???Controlled Hemodialysis on Blood Pressure and Volume Status in Hypertensive Patients

ASAIO Journal ◽  
2007 ◽  
Vol 53 (3) ◽  
pp. 357-364 ◽  
Author(s):  
Judith J. Dasselaar ◽  
Roel M. Huisman ◽  
Paul E. de Jong ◽  
Johannes G. M. Burgerhof ◽  
Casper F. M. Franssen
Keyword(s):  
Blood Pressure ◽  
Blood Volume ◽  
Volume Status ◽  
Hypertensive Patients ◽  
Relative Blood Volume ◽  
Volume Controlled

Abstract 101: Tissue-specific Deletion of Collectrin in the Proximal Tubular Epithelium Increases Arterial Pressure and Augments Salt-sensitivity

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Sylvia Cechova ◽  
Pei-Lun Chu ◽  
Joseph C Gigliotti ◽  
Fan Chan ◽  
Thu H Le
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Collecting Duct ◽  
Critical Role ◽  
Specific Effect ◽  
Salt Sensitivity ◽  
Kidney Cortex ◽  
Mrna Levels ◽  
Proximal Tubular

Background: Collectrin ( Tmem27 ) is a key regulator of blood pressure (BP) and modulator of the bioavailability of nitric oxide (NO) and superoxide. It is highly expressed in the kidney in the proximal tubule (PT), collecting duct, and throughout the vascular endothelium. We reported that collectrin plays a critical role as a chaperone for the reabsorption of all amino acids (AAs) in the PT, and for the uptake of the cationic AA L-arginine (L-Arg) in endothelial cells. Global collectrin knockout ( Tmem27 Y/- ) mice display baseline hypertension (HTN), augmented salt-sensitive hypertension (SSH), and decreased renal blood flow. Objective and Methods: To determine the PT-specific effect of collectrin on BP homeostasis and salt sensitivity, we used the Cre -loxP approach and PEPCK-Cre to generate a mouse line lacking collectrin specifically in the PT-- PEPCK-Cre + Tmem27 Y/Flox mice. PEPCK-Cre - Tmem27 Y/Flox mice were used as control. Radiotelemetry was used to measure BP for 2 weeks at baseline and 2 weeks on high salt diet (HSD). Renal blood flow at baseline and on HSD was measured using contrast enhanced ultrasound in the same mice. Results: Successful deletion of collectrin in the PT was confirmed by assessing mRNA levels using real-time RT-PCR, immunohistochemistry staining of renal tissues using anti-collectrin antibody, and quantitation of protein from kidney cortex by Western analysis. Compared to control PEPCK-Cre - Tmem27 Y/Flox mice (n=6), PEPCK-Cre + Tmem27 Y/Flox mice (n=6) displayed significantly higher systolic BP (SBP) at baseline (120.0 ± 2.5 vs 131.6 ± 2.9 mm Hg; p = 0.014) and after HSD (135.3 ± 2.6 vs 151.5 ± 5.2 mm Hg; p = 0.019). Renal blood flow was not different between groups, at baseline nor after HSD. Conclusion: Collectrin in the PT plays an important role in blood pressure homeostasis and response to sodium intake, independent of renal blood flow. Increasing proximal tubular collectrin activity may be a novel therapeutic strategy for the treatment of hypertension and salt-sensitivity.

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