Changes In Body Fluid Volume Research Articles

Bioelectrical Impedance Analysis (BIA) detects body resistance increase in dogs undergoing blood donation.

Using raw parameters of bioelectrical impedance analysis (BIA) and derived Phase Angle (PhA) has emerged as an alternative to conventional predictive BIA for body fluid volumes and body composition estimation in human patients, offering an approach independent of predictive equations. Classic predictive equation-based BIA remains unsuitable for veterinary clinical practice due to the high morphological variability within the canine species. This study aimed to validate the feasibility of BIA in dogs and assess its utility in detecting changes in body fluid volumes, particularly in blood donation. Sixty healthy blood donor dogs and ten controls were longitudinally assessed using BIA raw parameters with a portable analyzer at a 50kHz frequency. Measurements were performed before and after blood donation in donor dogs, whereas in controls, they were carried out at two time points, approximating the timing of a donation. Significant increases in raw bioelectrical parameters were observed after blood donation in the donor group, while differences were not statistically significant in controls. Hematocrit values did not significantly differ between the two time points in both groups. These findings suggest the feasibility of using BIA to detect changes in body fluid volumes in dogs undergoing blood donation, highlighting its potential application in veterinary medicine. Further research should explore the applicability of BIA in spontaneous pathological conditions involving fluid loss or retention and investigate the potential utility of PhA as a prognostic or monitoring tool in veterinary clinical practice. This study provides valuable insights into using BIA in canine medicine, paving the way for enhanced diagnostic and monitoring strategies in clinical practice.

Intradialytic parenteral nutrition using a standard amino acid solution not for renal failure in maintenance hemodialysis patients with malnutrition: a multicenter pilot study

BackgroundStandard amino acid solutions have recently been removed from the contraindications for use in dialysis patients in Japan. However, the details of their safety and efficacy in these patients are still not known. In this study, we investigated the safety and efficacy of intradialytic parenteral nutrition (IDPN) using ENEFLUID® injection containing standard amino acids, glucose, electrolytes, fats, and water-soluble vitamins in maintenance hemodialysis patients with malnutrition.MethodsThis clinical trial was designed as a multicenter, prospective, non-randomized, open-label, single-arm, observational pilot study. The participants were patients on maintenance hemodialysis who were in the nutritional high-risk group according to the Nutritional Risk Index for Japanese Hemodialysis Patients. One bag of ENEFLUID® injection was administered during every hemodialysis session for 12 weeks. The primary endpoint was change in serum transthyretin levels between before and after the 12-week period. As safety endpoints, we evaluated changes in body fluid volume and blood biochemical tests, including blood urea nitrogen and electrolytes, as well as blood glucose variability using flash glucose monitoring (FGM).ResultsThe mean age and body mass index of the 13 participants were 79.0 ± 10.7 years and 18.0 ± 1.7 kg/m2, respectively. No significant changes were observed in nutritional parameters, including serum transthyretin, between before and after the start of the study. After IDPN initiation, there was no obvious fluid overload or significant changes in blood biochemical tests, including electrolytes, and the treatment could be safely continued for 12 weeks. In the FGM analysis, asymptomatic hypoglycemia during hemodialysis was observed at the beginning of the study, but there was a trend toward improvement after 12 weeks (area over the curve < 70 mg/dl per dialysis session: 747.5 ± 1333.9 to 21.6 ± 54.3, P = 0.09).ConclusionsIDPN using ENEFLUID® injection can be safely continued, although it does not significantly improve markers of nutritional status. It also showed the potential to ameliorate asymptomatic hypoglycemia during hemodialysis sessions. More detailed studies of the improvement in nutritional indicators are needed.Trial registration: This study was registered with the University Hospital Medical Information Network-Clinical Trials Registry (UMIN-CTR) on May 9, 2021 (registration ID, UMIN000044051).

Expression levels and activities of energy-yielding ATPases in the oligohaline neritid snail Theodoxus fluviatilis under changing environmental salinities.

ABSTRACTThe aquatic gastropod Theodoxus fluviatilis occurs in Europe and adjacent areas of Asia. The snail species has formed two genetically closely related subgroups, the freshwater ecotype (FW) and the brackish water ecotype (BW). Other than individuals of the FW ecotype, those of the BW ecotype survive in salinities of up to 28‰. Coastal aquatic ecosystems may be affected by climate change due to salinization. Thus, we investigated how the two Theodoxus ecotypes adjust to changes in environmental salinity, focusing on the question whether Na+/K+-ATPase or V-ATPase are regulated on the transcriptional, the translational or at the activity level under changing external salinities. Animals were gradually adjusted to extreme salinities in containers under long-day conditions and constant temperature. Whole body RNA- or protein extracts were prepared. Semi-quantitative PCR- and western blot-analyses did not reveal major changes in transcript or protein abundances for the two transporters under low or high salinity conditions. No significant changes in ATPase activities in whole body extracts of animals adjusted to high or low salinity conditions were detected. We conclude that constitutive expression of ATPases is sufficient to support osmotic and ion regulation in this species under changing salinities given the high level of tolerance with respect to changes in body fluid volume.

3092 Measuring Fluid Compartments Before and After Rapid Saline Infusion

OBJECTIVES/SPECIFIC AIMS: To evaluate the ability of various techniques to track changes in body fluid volumes before and after a rapid infusion of saline. METHODS/STUDY POPULATION: Eight healthy participants (5M; 3F) completed baseline measurements of 1) total body water using ethanol dilution and bioelectrical impedance analysis (BIA) and 2) blood volume, plasma volume and red blood cell (RBC) volume using carbon monoxide rebreathe technique and I-131 albumin dilution. Subsequently, 30mL saline/kg body weight was administered intravenously over 20 minutes after which BIA and ethanol dilution were repeated. RESULTS/ANTICIPATED RESULTS: On average, 2.29±0.35 L saline was infused with an average increase in net fluid input-output (I/O) of 1.56±0.29 L. BIA underestimated measured I/O by −3.4±7.9%, while ethanol dilution did not demonstrate a measurable change in total body water. Carbon monoxide rebreathe differed from I-131 albumin dilution measurements of blood, plasma and RBC volumes by +0.6±2.8%, −5.4±3.6%, and +11.0±4.7%, respectively. DISCUSSION/SIGNIFICANCE OF IMPACT: BIA is capable of tracking modest changes in total body water. Carbon monoxide rebreathe appears to be a viable alternative for the I-131 albumin dilution technique to determine blood volume. Together, these two techniques may be useful in monitoring fluid status in patients with impaired fluid regulation.

Regulation of Neuronal Activity in Hypothalamic Vasopressin Neurons.

Vasopressin is a peptide hormone secreted from the posterior pituitary gland in response to various physiological and/or pathological stimuli, including changes in body fluid volume and osmolality and stress exposure. Vasopressin secretion is controlled by the electrical activity of the vasopressinergic magnocellular neurosecretory cells located in the hypothalamic supraoptic nucleus and paraventricular nucleus. Vasopressin release can occur somatodendritically in the hypothalamus or at the level of pituitary axon terminals. The electrical activity of the vasopressin neurons assumes specific patterns of electrical discharge that are under the control of several factors, including the intrinsic properties of the neuronal membrane and synaptic and hormonal inputs. It is increasingly clear that glial cells perform critical signaling functions that contribute to signal transmission in neural circuits. Astrocytes contribute to neuronal signaling by regulating synaptic and extrasynaptic neurotransmission, as well as by mediating bidirectional neuronal-glial transmission. We recently discovered a novel form of neuronal-glial signaling that exploits the full spatial domain of astrocytes to transmit dendritic retrograde signals from vasopressin neurons to distal upstream neuronal targets. This retrograde trans-neuronal-glial transmission allows the vasopressin neurons to regulate their synaptic inputs by controlling upstream presynaptic neuron firing, thus providing a powerful means of controlling hormonal output.

The inextricable role of the kidney in hypertension.

An essential link between the kidney and blood pressure control has long been known. Here, we review evidence supporting the premise that an impaired capacity of the kidney to excrete sodium in response to elevated blood pressure is a major contributor to hypertension, irrespective of the initiating cause. In this regard, recent work suggests that novel pathways controlling key sodium transporters in kidney epithelia have a critical impact on hypertension pathogenesis, supporting a model in which impaired renal sodium excretion is a final common pathway through which vascular, neural, and inflammatory responses raise blood pressure. We also address recent findings calling into question long-standing notions regarding the relationship between sodium intake and changes in body fluid volume. Expanded understanding of the role of the kidney as both a cause and target of hypertension highlights key aspects of pathophysiology and may lead to identification of new strategies for prevention and treatment.

Oral Rehydration or Intravenous Drip? - A Volume Kinetic Study of Glucose Solutions to Young and Old

Background: The aim of this study was to use a volume kinetic model to compare oral versus intravenous fluid administration of glucose solutions in young and elderly healthy volunteers. We investigated differences in the absorption, distribution and elimination of the administered fluid. Methods: The study had a randomized, crossover design and all experiments were performed when subjects had been fasting overnight indicating a state of dehydration. Twenty-four healthy volunteers received an isotonic 2.5% glucose solution, 7 ml/kg during 15 minutes, both orally and intravenously at separate occasions. Repetitive blood tests over 120 minutes showed changes in body fluid volumes using volume kinetic principles. Results: There were significant different lag times of absorption between oral and intravenous administration of fluid. In the young, a plasma volume decrease was shown in the beginning of the oral rehydration experiments but they retained fluid at the end of the experiment. The elderly had a consistent slow elimination of glucose and retained water after oral rehydration. The two administration routes showed different patterns for the elderly’s fluid volume expansion with steeper slopes for intravenous rehydration.

A comprehensive, computer-model-based approach for diagnosis and treatment of complex acid–base disorders in critically-ill patients

We have developed a computer-model-based approach to quantitatively diagnose the causes of metabolic acid-base disorders in critically-ill patients. We use an interstitial-plasma-erythrocyte (IPE) model that is sufficiently detailed to accurately calculate steady-state changes from normal in fluid volumes and electrolyte concentrations in a given patient due to a number of causes of acid-base disorders. Normal fluid volumes for each patient are determined from their sex, height and weight using regression equations derived from measured data in humans. The model inputs (electrolyte masses and volumes) are altered to simulate the laboratory chemistry of each critically-ill patient. In this process, the model calculates changes in body-fluid volumes, osmolality and yields the individual values of IPE base excess (BE(IPE)) attributed to changes due to: (1) fluid dilution/contraction, (2) gain or loss of Cl(-), (3) hyper- or hypoalbuminemia, (4) presence of unmeasured ions, (5) gain of lactate, (6) gain or loss of phosphate, (7) gain or loss of calcium and magnesium, (8) gain or loss of potassium and (9) gain or loss of sodium. We use critically-ill patient data to show how our new approach is more informative and much simpler to interpret as compared to the approaches of Siggaard-Andersen or Stewart. We demonstrate how the model can be used at the bedside to diagnose acid-base disorders and suggest appropriate treatment. Hence, this new approach gives clinicians a new tool for diagnosing disorders and specifying fluid-therapy options for critically-ill patients.

LAMPREYS FEEL THE PRESSURE

It's a tough life for a river lamprey. Not only do these primitive fish have to swim upstream from the sea to the freshwater streams where they spawn and then die, they also have to cope with changes in water composition along the way. Because they are immersed in water, any change in the environment's saltiness affects lampreys' body fluid volume. In salty surroundings the fish lose water by osmosis, while splashing in a freshwater stream has the opposite effect. Now a study by Anne Brown has shed light on how lampreys achieve this tricky balance (p. 223).Most fish cope with changes in the environment's saltiness using the renin-angiotensin system, a protein network that regulates body fluid volume in virtually all vertebrates. When blood volume drops, renin triggers production of the active form of angiotensin. Angiotensin counteracts body fluid decreases by constricting blood vessels and encouraging the animal to drink. Until recently, lamprey osmotic regulation was a mystery, as they did not appear to have a renin-angiotensin system. When the system was finally discovered in lampreys, Brown was determined to find out how it responds to changes in body fluid volume and osmotic pressure.Studying river lampreys in the UK is problematic as they are a protected species, but the Ringkøbing Fjord in Denmark provided an excellent source of experimental creatures. To see how the animals responded to changes in body fluid volume, Brown removed up to 40% of the lampreys' blood. She found that the renin-angiotensin system became activated, and circulating active angiotensin levels rapidly doubled. When she injected lampreys with extra blood-like fluid, angiotensin levels dropped. Intriguingly, she found that salty fluid injections did not affect angiotensin levels. This suggests that the effects of increased body fluid volume are counteracted to some extent by increased saltiness.Brown also tested the effects of changing the environment's saltiness. Since the fjord's saltiness lies between freshwater and seawater, Brown could see how these migrating lampreys respond to osmotic pressure changes simply by moving the lampreys from saltwater to freshwater and vice versa. When she moved fish from freshwater to seawater, their angiotensin levels increased,but the reverse move caused angiotensin to drop. So the lamprey's renin-angiotensin system responds to both changes in volume and osmotic pressure, similar to the systems in bony fish like trout.Brown suspects that volume detectors within the fish may regulate the lamprey renin-angiotensin system, and that osmotic receptors (detecting saltiness) modulate the volume detectors' effects. But while most vertebrates have a kidney-based renin supply, renin-releasing cells have not yet been found in the lamprey kidney. The location of the lamprey's renin-producing cells remains a mystery for now.Since lampreys are primitive animals, Brown's results show that the renin-angiotensin system is an ancient and highly conserved blood volume regulation mechanism. After her adventures with lampreys in Danish fjords,Brown plans to study the renin-angiotensin system in the even more primitive hagfish. `Studying the hagfish would give us deeper insights into the origin of this system,' suggests Brown, `by taking us one step further back in evolutionary history.'

Natriuresis induced by mild hypernatremia in humans

The hypothesis that increases in plasma sodium induce natriuresis independently of changes in body fluid volume was tested in six slightly dehydrated seated subjects on controlled sodium intake (150 mmol/day). NaCl (3.85 mmol/kg) was infused intravenously over 90 min as isotonic (Iso) or as hypertonic saline (Hyper, 855 mmol/l). After Hyper, plasma sodium increased by 3% (142.0 +/- 0.6 to 146.2 +/- 0.5 mmol/l). During Iso a small decrease occurred (142.3 +/- 0.6 to 140.3 +/- 0.7 mmol/l). Iso increased estimates of plasma volume significantly more than Hyper. However, renal sodium excretion increased significantly more with Hyper (291 +/- 25 vs. 199 +/- 24 micromol/min). This excess was not mediated by arterial pressure, which actually decreased slightly. Creatinine clearance did not change measurably. Plasma renin activity, ANG II, and aldosterone decreased very similarly in Iso and Hyper. Plasma atrial natriuretic peptide remained unchanged, whereas plasma vasopressin increased with Hyper (1.4 +/- 0.4 to 3.1 +/- 0.5 pg/ml) and decreased (1.3 +/- 0.4 to 0.6 +/- 0.1 pg/ml) after Iso. In conclusion, the natriuretic response to Hyper was 50% larger than to Iso, indicating that renal sodium excretion may be determined partly by plasma sodium concentration. The mechanism is uncertain but appears independent of changes in blood pressure, glomerular filtration rate, the renin system, and atrial natriuretic peptide.

Accuracy of bioelectrical impedance spectroscopy in measuring changes in body composition during severe weight loss.

Bioelectrical impedance spectroscopy (BIS) is an attractive method for measuring body composition because it is noninvasive, simple, and cheap. The effect of obesity on the accuracy of impedance measurements has been recognized for some time, but no conclusive explanations or ways to correct the measurement errors have been published. We studied the effect of the composition of weight loss on the accuracy of BIS to measure changes in body fluid volumes during severe weight loss. Within subjects the effect of variable losses of fat mass was studied. In 10 morbidly obese female subjects who underwent gastric reduction surgery, changes in total body water (TBW) and extracellular water (ECW) were monitored for 1 year by deuterium (Deu) and bromide (Br) dilution and by BIS. Measurements were performed before the operation and after 2 weeks, 3 months, and 1 year. Extrapolated resistance values of extracellular (Recw) and intracellular water (Ricw) were used in mixture equations for calculating the corresponding fluid volumes. After 1 year, weight decreased by 53 kg, TBW (Deu) loss was 8.7 L, and ECW (Br) loss was 4.3 L. Comparison of BIS with reference methods for measuring all possible changes over 6 time-intervals revealed a mean overestimation of TBW (2.4 L, SD = 2.9) and ECW (0.74 L, SD = 2.6) losses by BIS. Overestimation increased significantly with increasing fat losses, expressed as percentage fat of the weight loss and as change in triceps skinfolds. Measured changes in Recw and Ricw were less than expected for an ideal agreement between dilution methods and mixture equations. BIS with the use of mixture equations overestimates fluid losses during weight loss. The error is associated with the amount of fat loss. The large contribution of the factor weight in the mixture equations is likely to be responsible. The assumptions of mixture theory are not valid in obesity.

TIME COURSE OF CARDIORESPIRATORY DECONDITIONING WITH 17 DAYS OF 6?? HEAD DOWN TILT BEDREST 866

The purpose of this project was to assess the time course of exercise cardiorespiratory changes in response to 17 days of 6° head down tilt bedrest. Seven males (age, 42.3 ±8.7 yr.; height, 181.4 ±6.5 cm; weight, 79.8 ±10.6) completed a continuous exercise test to volitional exhaustion on a supine cycling ergometer prior to bedrest (CON), on days 2 or 3 of bedrest (BR1), 8 or 9 (BR2), and 13 or 14 (BR3), as well as on days 3 or 4 of recovery (R1), and 7 or 8 (R2) to determine the submaximal (150 W) and maximal cardiorespiratory responses to exercise. Submaximal oxygen consumption(VO2) and minute ventilation (VE) did not change from CON during bedrest or recovery. Heart rate (HR: b·min-1) was significantly elevated (p<0.05) from CON (124±4) during BR2 (134±4), BR3(138±4), and R1 (135±2), but had returned to CON levels by R2(128±3). VO2max (L·min-1) was decreased(p<0.05) from CON (3.24±0.20) during BR1 (2.99±0.17; -7.3%), BR2 (3.00±0.17; -7.1%), BR3 (2.92±0.20; -9.0%), and R1(3.02±0.20; -6.6%), but was not different (p > 0.05) than CON by R2(3.13±0.19; -3.3%). HRmax did not change from CON during bedrest or recovery. Initial changes in VO2max (BR1) were significantly correlated with urine balance during bedrest day 1 (r=0.91, p < 0.05). These results suggest that the time course for changes in the cardiorespiratory responses to exercise are not linear and are related to the initial changes in body fluid volumes during 6° head down tilt bedrest.

Role of atrial natriuretic peptide in long-term volume homeostasis.

1. Long-term volume homeostasis is linked very closely to long-term arterial pressure control through the renal-body fluid feedback mechanism. A key feature of this control system is the ability of the kidneys to respond to changes in arterial pressure by altering renal excretion of salt and water, often referred to as renal-pressure natriuresis. 2. Quantitative studies indicate that ANP secretion is relatively sensitive to changes in atrial pressure and that the rate of hormonal secretion does not adapt to continuous long-term stimulation. 3. Under normal conditions, the renal-body fluid feedback mechanism for arterial pressure control is very efficient in minimizing changes in body fluid volumes during alterations in sodium intake. Therefore, only small changes in atrial pressure and ANP secretion occur. Alterations in plasma ANP concentration within physiological levels have little effect on renal-pressure natriuresis and, therefore, have little impact on volume homeostasis. 4. When the renal-body fluid feedback mechanism for arterial pressure control is impaired and body fluid volumes are elevated, such as in heart failure, large increases in atrial pressure and ANP secretion occur. The resultant pathophysiological plasma levels of ANP exert sustained natriuretic effects and chronically shift renal-pressure natriuresis to lower arterial pressures. In the absence of this chronic effect of ANP on renal-pressure natriuresis, reduced arterial pressure in compensated heart failure would result in protracted retention of salt and water and additional increments in body fluid volumes.

A novel computer-driven, servo-controlled fluid replacement technique and its application to renal function studies in conscious rats.

1. A new rat model has been developed allowing body fluid status to be accurately controlled and maintained throughout experimentation by computer-driven, servo-controlled replacement of spontaneous urinary fluid losses. 2. Experiments in vitro were performed to test the accuracy of the servo system, and experiments in vivo were carried out to re-assess basic renal function in servo-controlled vasopressin-replete Long Evans and vasopressin-deficient Brattleboro rats. The model was further evaluated in water-diuretic Wistar rats with or without administration of a vasopressin V2-receptor agonist, 1-desamino-8-D-arginine vasopressin. 3. The data gained from the present study indicate the suitability of the servo-controlled replacement system for conscious renal function studies in three different rat strains. Haemodynamic and renal function variables measured were demonstrated to be stable throughout a 5 h experimental procedure and reproducible between repeated experimental occasions over a 14 day post-operative period. 4. Using the servo-control technique, the expected action of 1-desamino-8-D-arginine vasopressin on renal water handling was demonstrated, but the natriuretic effect reported by some workers was not evident. 5. Since the servo-controlled fluid replacement technique maintains many of the inherent differences between vasopressin-replete Long Evans and vasopressin-deficient Brattleboro rats and eliminates the changes in body fluid volume during transition from a diuretic to an antidiuretic state, the model confers an advantage over previously employed constant infusion protocols.

Central alpha 2-adrenoceptor-mediated pressor response to clonidine in conscious, spontaneously hypertensive rats.

Pressor responses to intracerebroventricular (i.c.v.) injection of clonidine were investigated in conscious spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). Clonidine (1-10 micrograms, i.c.v.) caused a dose-dependent pressor response and decrease in heart rate in both SHR and WKY. In SHR, low doses (1, 2.5 micrograms) but not high doses (5, 10 micrograms) of i.c.v.-clonidine induced a depressor response following the pressor response. Both pressor and depressor responses to i.c.v.-clonidine were significantly greater in SHR than in WKY. In both SHR and WKY, pressor responses to i.c.v.-clonidine were abolished by pentobarbital anesthesia, pretreatment with i.v.-furosemide (5 mg/kg), 24-hr water deprivation and pretreatment with i.c.v.-yohimbine (100 micrograms), but not by pretreatment with i.v.-yohimbine (100 micrograms) and i.c.v.-prazosin (10 micrograms). On the 1st day after surgery for arterial catheter implantation, SHR reduced their water intake, and i.c.v.-clonidine (5 micrograms) caused a slight pressor response, whereas the same dose of clonidine on the 7th day after surgery resulted in a marked pressor response. These results suggest that clonidine caused a central alpha 2-adrenoceptor-mediated pressor response, which is greater in SHR than in WKY and is sensitive to body fluid volume changes and anesthesia.

Central α2-Adrenoceptor-Mediated Pressor Response to Clonidine in Conscious, Spontaneously Hypertensive Rats

Pressor responses to intracerebroventricular (i.c.v.) injection of clonidine were investigated in conscious spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). Clonidine (1–10 μg, i.c.v.) caused a dose-dependent pressor response and decrease in heart rate in both SHR and WKY. In SHR, low doses (1, 2.5 μg) but not high doses (5, 10 μg) of i.c.v.-clonidine induced a depressor response following the pressor response. Both pressor and depressor responses to i.c.v.-clonidine were significantly greater in SHR than in WKY. In both SHR and WKY, pressor re-' sponses to i.c.v.-clonidine were abolished by pentobarbital anesthesia, pretreatment with i.v.-furosemide (5 mg/kg), 24-hr water deprivation and pretreatment with i.c.v.-yohimbine (100jug), but not by pretreatment with i.v.-yohimbine (100 jug) and i.c.v.-prazosin (10 μg). On the 1st day after surgery for arterial catheter implantation, SHR reduced their water intake, and i.c.v.-clonidine (5 μg) caused a slight pressor response, whereas the same dose of clonidine on the 7th day after surgery resulted in a marked pressor response. These results suggest that clonidine caused a central α2-adrenoceptor-mediated pressor response, which is greater in SHR than in WKY and is sensitive to body fluid volume changes and anesthesia.

PATHWAYS LINKING RENAL EXCRETION AND ARTERIAL PRESSURE WITH VASCULAR STRUCTURE AND FUNCTION

1. A brief review is presented which summarizes the role of the kidney in the long-term regulation of arterial pressure and the mechanism whereby changes in body fluid volume can influence the function and structure of the systemic vasculature. 2. Studies indicate that the kidney detects changes of arterial pressure via changes of medullary blood flow which in the volume expanded state is poorly autoregulated. Elevations of renal arterial pressure raise vasa recta capillary pressure and renal interstitial fluid pressure, which in turn reduces tubular reabsorption of sodium and water. 3. The sensitivity of the pressure-diuresis relationship is controlled by renal sympathetic nerve activity and a variety of hormone and autocrine systems. 4. Evidence is also reviewed which shows that small changes of blood volume (5%) resulting from reduced renal excretion can acutely and chronically result in 25% increases of total peripheral resistance and arterial pressure. 5. Short-term increases of vascular resistance are predicted by regional autoregulatory responses while long-term elevations of vascular resistance appear to result from the structural changes of large vessel hypertrophy and microvascular rarefaction within skeletal muscle.

Circulatory disturbances in the postresuscitation period of myocardial infarction and the role of body fluid volume changes in their development

Circulatory disturbances in the postresuscitation period of myocardial infarction and the role of body fluid volume changes in their development

Hormones and hypertension.

SummaryIt seems clear that hypertension may be a common feature of growth hormone excess, but precise frequency figures cannot be derived from current data due to bias and inadequate epidemiological study techniques. The mechanism of increased blood pressure is also unclear. There is clear evidence of gross sodium retention and hypertrophy of the heart and blood vessels but these occur in both normotensive and hypertensive acromegaly. This is also true of changes in body fluid volumes. Studies of changes in the levels of, and blood pressure sensitivity to, hormones such as ANF, angiotensin II and catecholamines are frequently contradictory and also difficult to interpret at present. The interrelationships between growth hormone, renal function and blood pressure require further careful study.

Understanding the mechanism of adrenocortical steroid hypertension

Studies of the mechanism of ACTH induced hypertension in sheep have led to the hypothesis that adrenocortical steroids may raise blood pressure by a “hypertensinogenic” action which can be distinguished from effects mediated by occupancy of classical mineralocorticoid or glucocorticoid receptors. This concept is supported by recent structure-activity studies using synthetic and naturally occurring steroids. Development of steroid hypertension is rapid (4–6 h) and although associated with an increase in cardiac output, changes in total peripheral resistance are important. Many different mechanisms have been proposed to explain how steroids raise blood pressure. In sheep it has been shown that the autonomic nervous system and vasoactive prostanoids appear to buffer, rather than cause, the rise in blood pressure. The renin-angiotensin system, AVP and serotonin are also unlikely to be involved. Further, the effects of steroids on blood pressure are not simply related to effects on Na status and changes in body fluid volumes. A direct involvement of the central nervous system remains to be established. In understanding how ACTH raises blood pressure, studies in sheep have shown that it is important to try and dissociate the effects of steroids involved in development of hypertension from the many other actions of steroids.