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PubMed2002

Estrogen effects on osmotic regulation of AVP and fluid balance.

To determine estrogen effects on osmotic regulation of arginine vasopressin (AVP) and body fluids, we suppressed endogenous estrogen and progesterone using the gonadotropin-releasing hormone (GnRH) analog leuprolide acetate (GnRHa). Subjects were assigned to one of two groups: 1) GnRHa alone, then GnRHa + estrogen (E, n = 9, 25 +/- 1 yr); 2) GnRHa alone, then GnRHa + estrogen with progesterone (E/P, n = 6, 26 +/- 3). During GnRHa alone and with hormone treatment, we compared AVP and body fluid regulatory responses to 3% NaCl infusion (HSI, 120 min, 0.1 ml. min(-1). kg body wt(-1)), drinking (30 min, 15 ml/kg body wt), and recovery (60 min of seated rest). Plasma [E(2)] increased from 23.9 to 275.3 pg/ml with hormone treatments. Plasma [P(4)] increased from 0.6 to 5.7 ng/ml during E/P and was unchanged (0.4 to 0.6 ng/ml) during E. Compared with GnRHa alone, E reduced osmotic AVP release threshold (275 +/- 4 to 271 +/- 4 mosmol/kg, P < 0.05), and E/P reduced the AVP increase in response during HSI (6.0 +/- 1.3 to 4.2 +/- 0.6 pg/ml at the end of HSI), but free water clearance was unaffected in either group. Relative to GnRHa, pre-HSI plasma renin activity (PRA) was greater during E (0.8 +/- 0.1 vs. 1.2 +/- 0.2 ng ANG I. ml(-1). h(-1)) but not after HSI or recovery. PRA was greater than GnRHa during E/P at baseline (1.1 +/- 0.2 vs. 2.5 +/- 0.6) and after HSI (0.6 +/- 0.1 vs. 1.1 +/- 1.1) and recovery (0.5 +/- 0.1 vs. 1.3 +/- 0.2 ng ANG I. ml(-1). h(-1)). Baseline fractional excretion of sodium was unaffected by E or E/P but was attenuated by the end of recovery for both E (3.3 +/- 0.6 vs. 2.4 +/- 0.4%) and E/P (2.8 +/- 0.4 vs 1.7 +/- 0.4%, GnRHa alone and with hormone treatment, respectively). Fluid retention increased with both hormone treatments. Renal sensitivity to AVP may be lower during E due to intrarenal effects on water and sodium excretion. E/P increased sodium retention and renin-angiotensin-aldosterone stimulation.

Adult↗
PubMed1993

Effect of intrauterine growth retardation on postnatal weight change in preterm infants.

To investigate the cause or causes of early postnatal weight change, we measured total body water and fluid and energy balances in 14 preterm infants who were appropriate in size for gestational age (AGA) and in 5 weight-matched, preterm, small-for-gestational-age (SGA) infants. On the first day of life, AGA and SGA infants had the same weight and total body water content. At 6 +/- 2 days (mean +/- SD), AGA infants had had significant weight loss (94 +/- 45 gm) and body water loss (67 +/- 80 ml), whereas weight and total body water content in the SGA infants at the same age (5 +/- 1 days) did not differ from the values at birth. Loss of weight and total body water in AGA infants was accompanied by a greater diuresis than in SGA infants at the same amount of fluid intake. At the end of week 1, AGA and SGA infants had the same total energy expenditure (184 +/- 33 vs 171 +/- 17 kJ.kg-1 x day-1); energy intake, which had exceeded total energy expenditure from the third day of life and beyond, already provided 188 +/- 46 (AGA) or 209 +/- 109 kJ.kg-1 x day-1 (SGA), respectively, for energy storage. Nitrogen balance was positive. Subsequent weight gain occurred at the same rate in AGA and SGA infants; both total body water and solids increased. Energy intake, total energy expenditure, and the amount of energy stored (measured during stable weight gain on a regimen of full enteral feedings) had significantly increased compared with week 1, but both groups maintained similar energy storage.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Composition↗
PubMedDate not supplied

Forebrain contributions to one-kidney renal hypertension in the rabbit.

Electrolytic lesions were placed along the anteroventral wall of the third cerebral ventricle (AV3V region) in 10 albino rabbits (AV3V-X), and sham lesions were produced in 10 additional rabbits (SHAM). Two to 3 weeks later, all rabbits underwent unilateral nephrectomy and renal artery stenosis (clip I.D. = 0.508 mm). During a 1-week control period, and for 4 weeks after renal artery stenosis, measurements were made of mean arterial pressure (MAP), heart rate, body fluid compartment volumes, plasma electrolytes, and daily sodium, potassium, and water balances. Four weeks after renal artery stenosis (RAS), cardiovascular responses to norepinephrine (NE), angiotensin II (AII), saralasin, and autonomic blockade were obtained in the conscious animals. In SHAM rabbits, MAP rose from 77 to 117 mm Hg 4 weeks after RAS. In AV3V-X rabbits, MAP rose from 77 to only 92 mm Hg 4 weeks after RAS. Body fluid compartment volumes, plasma electrolytes, and fluid, sodium, and potassium balances showed similar modest changes in both groups of rabbits. Neither saralasin infusion nor autonomic blockade caused significantly different changes in MAP between SHAM and AV3V-X rabbits 4 weeks after RAS. However, pressor responses to both NE and AII were significantly less in AV3V-X rabbits at this time. It is concluded that one-kidney, one clip renal hypertension involves activation of neurohormonal pressor mechanisms originating in the forebrain, and that the expression of these pressor mechanisms in part includes an increase in cardiovascular reactivity.

Angiotensin II↗
PubMed2004

The ergogenics of fluid and electrolyte balance.

Fluid and electrolyte balance within a fairly narrow range is a requirement for human life. Athletes, particularly endurance athletes, routinely stress their bodies to the point of altering fluid and electrolyte levels. In some cases, significant fluctuations can lead to deterioration in performance and even the athlete's health. The body's physiologic response to such fluctuations of fluid and electrolyte levels is complex and not completely understood. This article examines how the body copes with changes in fluid and electrolyte balance and how these changes may be minimized via replacement to sustain athletic performance.

Body Temperature Regulation↗
PubMedDate not supplied

A description of the changing body composition of the growing premature infant.

Data from studies of two similar groups of premature infants were used to describe the changing body composition (BC) of a "typical" premature infant, 3 to 4 weeks old, gaining weight from 1,200 to 2,000 g and being fed its mother's expressed breast milk at a metabolizable energy intake of 93.6 kcal/kg/day. Serial measurements had been made of total body water (TBW), the extracellular fluid space (ECF), nitrogen balance, and gross energy balance in one group of premature (n = 17) infants and of total body potassium (TBK) in another group (n = 23); all infants studied weighed between 900 and 2,300 g. Equations relating TBW, ECF, and TBK to body weight were derived for estimating the content of these substances at body weights between 1,200 and 2,000 g. Protein content at 1,200 g body weight was estimated from measured TBK and N:K ratio (determined from the reference fetus) at this weight. Subsequent protein content was determined from average N accretion, determined from data of N balance, and carbohydrate and ash content were estimated from reference data. The remainder of the body weight was assumed to be fat. At 1,200 g, the proposed BC of the premature infant is 72.1% water, 10.7% protein, 14.9% fat, 1.9% ash, and 0.4% carbohydrate. At 2,000 g comparable figures are 67.8% water, 11.6% protein, 18.2% fat, 1.9% ash, and 0.5% carbohydrate. The description also provides estimates of the body cell mass (BCM) and intracellular fluid (ICF), the relationship of K to the BCM and ICF, and the energy balance of the growing premature infant.

Body Composition↗