Mechanism of attenuated thirst in aging: role of central volume receptors

1997 ◽  
Vol 272 (1) ◽  
pp. R148-R157 ◽  
Author(s):  
N. S. Stachenfeld ◽  
L. DiPietro ◽  
E. R. Nadel ◽  
G. W. Mack
Keyword(s):  
Older People ◽  
Blood Volume ◽  
Volume Expansion ◽  
Water Immersion ◽  
Inhibitory Influence ◽  
Central Blood Volume ◽  
Arterial Blood ◽  
Blood Volume Expansion ◽  
Central Volume ◽  
Older Subjects

To test the hypothesis that the inhibitory action of central blood volume expansion on thirst and renal fluid regulation is attenuated with aging, we monitored the drinking and renal responses of dehydrated older (70 +/- 2 yr, n = 6) and younger (24 +/- 1 yr, n = 6) subjects during 195 min of head-out water immersion (HOI), which shifts blood centrally and increases plasma volume (PV). Subjects dehydrated by exercising for 2 h at 36 degrees C in the evening and refraining from fluids overnight before HOI in 34 degrees C water or a seated control in water perfusion suit [time control (TC)] the next morning. Ad libitum water intake was allowed after 15 min of HOI. Dehydration decreased PV by 10.6 +/- 1 and 7.3 +/- 1.8% (P < 0.05) and increased plasma osmolality by 6 +/- 2 and 7 +/- 1 mosmol/kg H2O (P < 0.05) in older and younger subjects, respectively. Thirst ratings increased in both groups, but pre-HOI thirst perception on a line rating scale was lower in older (69 +/- 8 mm) than younger (94 +/- 6 mm, P < 0.05) subjects. Fifteen minutes of HOI restored PV by 7.8 +/- 1.0 and 5.7 +/- 1.0% in older and younger subjects, respectively, but suppressed thirst rating in younger subjects only (P < 0.05). Fluid intake was reduced in HOI compared with TC in younger (6.3 +/- 0.5 vs. 14.3 +/- 2.2 ml/kg, P < 0.05) but not in older (6.7 +/- 2.1 vs. 8.4 +/- 3.3 ml/kg) subjects. During HOI, older subjects had smaller suppression of plasma renin activity and aldosterone concentration but a greater increase in the plasma atrial natriuretic peptide concentration (P[ANP], P < 0.05). HOI increased fractional sodium excretion in both groups, but mean arterial pressure increased only in the older subjects (P < 0.05). We conclude that the inhibitory influence of central volume expansion on thirst and drinking behavior is diminished with aging. Furthermore, in contrast to younger people, HOI natriuresis is associated with exaggerated increases in P[ANP] and arterial blood pressure in older people, suggesting arterial baroreceptors may be involved in the fluid regulatory response to central blood volume expansion in older people.

Contribution of abdomen and legs to central blood volume expansion in humans during immersion

1997 ◽  
Vol 83 (3) ◽  
pp. 695-699 ◽  
Author(s):  
Lars Bo Johansen ◽  
Thomas Ulrik Skram Jensen ◽  
Bettina Pump ◽  
Peter Norsk
Keyword(s):  
Blood Volume ◽  
Volume Expansion ◽  
Protein Concentration ◽  
Water Immersion ◽  
Venous Pressure ◽  
Cuff Inflation ◽  
Central Blood Volume ◽  
Central Venous ◽  
Plasma Protein Concentration ◽  
Blood Volume Expansion

Johansen, Lars Bo, Thomas Ulrik Skram Jensen, Bettina Pump, and Peter Norsk. Contribution of abdomen and legs to central blood volume expansion in humans during immersion. J. Appl. Physiol. 83(3): 695–699, 1997.—The hypothesis was tested that the abdominal area constitutes an important reservoir for central blood volume expansion (CBVE) during water immersion in humans. Six men underwent 1) water immersion for 30 min (WI), 2) water immersion for 30 min with thigh cuff inflation (250 mmHg) during initial 15 min to exclude legs from contributing to CBVE (WI+Occl), and 3) a seated nonimmersed control with 15 min of thigh cuff inflation (Occl). Plasma protein concentration and hematocrit decreased from 68 ± 1 to 64 ± 1 g/l and from 46.7 ± 0.3 to 45.5 ± 0.4% ( P < 0.05), respectively, during WI but were unchanged during WI+Occl. Left atrial diameter increased from 27 ± 2 to 36 ± 1 mm ( P < 0.05) during WI and increased similarly during WI+Occl from 27 ± 2 to 35 ± 1 mm ( P < 0.05). Central venous pressure increased from −3.7 ± 1.0 to 10.4 ± 0.8 mmHg during WI ( P < 0.05) but only increased to 7.0 ± 0.8 mmHg during WI+Occl ( P < 0.05). In conclusion, the dilution of blood induced by WI to the neck is caused by fluid from the legs, whereas the CBVE is caused mainly by blood from the abdomen.

Cardiovascular and neuroendocrine responses to water immersion in compensated heart failure

2000 ◽  
Vol 279 (4) ◽  
pp. H1931-H1940 ◽  
Author(s):  
Anders Gabrielsen ◽  
Vibeke B. Sørensen ◽  
Bettina Pump ◽  
Søren Galatius ◽  
Regitze Videbæk ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Ejection Fraction ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Volume Expansion ◽  
Water Immersion ◽  
Central Blood Volume ◽  
Blood Volume Expansion ◽  
Neuroendocrine Responses

The hypothesis was tested that cardiovascular and neuroendocrine (norepinephrine, renin, and vasopressin) responses to central blood volume expansion are blunted in compensated heart failure (HF). Nine HF patients [New York Heart Association class II–III, ejection fraction = 0.28 ± 0.02 (SE)] and 10 age-matched controls (ejection fraction = 0.68 ± 0.03) underwent 30 min of thermoneutral (34.7 ± 0.02°C) water immersion (WI) to the xiphoid process. WI increased ( P < 0.05) central venous pressure by 3.7 ± 0.6 and 3.2 ± 0.4 mmHg and stroke volume index by 12.2 ± 2.1 and 7.2 ± 2.1 ml · beat−1 · m−2 in controls and HF patients, respectively. During WI, systemic vascular resistance decreased ( P < 0.05) similarly by 365 ± 66 and 582 ± 227 dyn · s · cm−5 in controls and HF patients, respectively. Forearm subcutaneous vascular resistance decreased by 19 ± 7% ( P < 0.05) in controls but did not change in HF patients. Heart rate decreased less during WI in HF patients, whereas release of norepinephrine, renin, and vasopressin was suppressed similarly in the two groups. We suggest that reflex control of forearm vascular beds and heart rate is blunted in compensated HF but that baroreflex-mediated systemic vasodilatation and neuroendocrine responses to central blood volume expansion are preserved.

Exaggerated ANF response to exercise in middle-aged vs. young runners

1990 ◽  
Vol 69 (5) ◽  
pp. 1607-1614 ◽  
Author(s):  
B. J. Freund ◽  
J. R. Claybaugh ◽  
G. M. Hashiro ◽  
M. Buono ◽  
S. Chrisney
Keyword(s):  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Central Blood Volume ◽  
Middle Aged ◽  
Blood Volume Expansion ◽  
Older Subjects ◽  
Response To Exercise ◽  
Renal Responses

Hormonal, electrolyte, and renal responses were measured before, during, and after a marathon (42.2 km) in 14 runners: 8 young (Y) (mean age 27.8 yr) and 6 middle aged (MA) (mean aged 46.7 yr). No differences between groups in prerun values for heart rate (HR), plasma osmolality (OSM), antidiuretic hormone (ADH), aldosterone (ALDO), atrial natriuretic factor (ANF), or plasma renin activity (PRA) were found. Renal and urinary measurements were also similar between groups before the marathon. After 10 km of running, both groups had significant increases in HR, ALDO, ANF, and PRA, while OSM, Na+, and ADH remained unchanged from prerun values. The increase in plasma ANF concentrations at this point was significantly greater in the MA subjects compared with the Y (mean increase 104.1 vs. 42.8 pg/ml, respectively; P less than 0.01). Immediate postmarathon values for OSM, ADH, and Na+ were significantly higher than initial values in both groups, while HR, PRA, and ALDO continued to increase above the elevated levels found at 10 km. ANF values immediately postmarathon remained higher than prerun concentrations but were significantly reduced from those obtained at 10 km. In contrast, HR continued to rise until the completion of the run. These data are consistent with recent reports of an exaggerated ANF response in older subjects in response to central blood volume expansion.

Control of right atrial pressure at constant cardiac output suppresses volume natriuresis in anesthetized rats

1984 ◽  
Vol 62 (7) ◽  
pp. 798-801 ◽  
Author(s):  
U. Ackermann ◽  
J. R. Rudolph
Keyword(s):  
Blood Volume ◽  
Volume Expansion ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Control Value ◽  
Volume Load ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Blood Volume Expansion

The blood volume of anesthetized rats was expanded acutely by 33% with donor blood while a caval snare was gradually tightened so that right atrial pressure (RAP) was prevented from rising (n = 6). In control experiments (n = 5) an aortic snare was used to hold mean arterial blood pressure near the values found in the experimental series. However, RAP was allowed to change freely and increased by 1.6 ± 0.4 mmHg (1 mmHg = 133.322 Pa) during volume expansion. When the two groups were compared, there were no significant differences between their mean arterial blood pressures (near 110 mmHg) or in their cardiac outputs (near 0.25 mL∙min−1∙g body weight−1). There were, however, significant differences between their renal responses to the volume load. When RAP was free to change, the rate of volume excretion [Formula: see text] increased to 30 ± 15 (SEM) μL∙min−1∙g kidney weight−1 (KW) from its control value of 3.49 ± 0.31 and the rate of sodium excretion [Formula: see text] increased to 3.59 ± 0.20 μequiv.∙min−1∙g KW−1 from its preinfusion value of 0.42 ± 0.10. When RAP was not allowed to increase during volume loading, [Formula: see text] and [Formula: see text] did not change from their respective preinfusion values (2.99 ± 0.46 μL∙min−1∙g KW−1 and 0.35 ± 0.10 μequiv.∙min−1∙g KW−1). The results imply that during acute blood volume expansion increased central vascular pressure is a prerequisite for the homeostasis of body water and salt.

Blood volume changes and high and low pressoreceptor activity in cats

1984 ◽  
Vol 247 (5) ◽  
pp. R833-R836 ◽  
Author(s):  
E. Tomomatsu ◽  
J. P. Gilmore
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Blood Volume ◽  
Mean Arterial Blood Pressure ◽  
Volume Expansion ◽  
Carotid Sinus ◽  
Nerve Activity ◽  
Arterial Blood ◽  
Blood Volume Expansion ◽  
Aortic Baroreceptors

Studies were undertaken in the cat to determine if moderate hemorrhage or volume expansion significantly altered carotid sinus and aortic baroreceptor activity. In addition, the experimental design provided the opportunity to compare gain of the two sets of receptors. A 20% blood volume expansion increased mean arterial blood pressure 5.2% and carotid sinus nerve activity 14.7%, whereas a 20% hemorrhage decreased mean arterial blood pressure 10.8% and carotid sinus nerve activity 32.3%. For the aortic baroreceptors, a 20% blood volume expansion increased mean arterial blood pressure 5.9% and nerve activity 10.5%, and a 20% hemorrhage decreased mean arterial blood pressure 8.9% and nerve activity 21.0%. The blood pressure-discharge curves for the carotid sinus and aortic baroreceptors were not different. The well-known high sensitivity of atrial receptors was also documented. We conclude that both high- and low-pressure receptors apprise the central nervous system of the status of intravascular volume and pressure.

Kidney function in ANF-transgenic mice: effect of blood volume expansion

1991 ◽  
Vol 260 (1) ◽  
pp. R1-R5 ◽  
Author(s):  
L. J. Field ◽  
A. T. Veress ◽  
M. E. Steinhelper ◽  
K. Cochrane ◽  
H. Sonnenberg
Keyword(s):  
Transgenic Mice ◽  
Kidney Function ◽  
Blood Volume ◽  
Volume Expansion ◽  
Fusion Gene ◽  
Transgenic Animals ◽  
Renal Perfusion ◽  
Arterial Blood ◽  
Blood Volume Expansion ◽  
Before And After

Transgenic mice, created from inbred C3HeB/FeJ embryos, were used to overexpress selectively in the liver a fusion gene comprising mouse transthyretin (TTR) regulatory and atrial natriuretic factor (ANF) structural sequences. Animals were anesthetized, and kidney function was studied before and after blood volume expansion. Baseline urine volumes and electrolyte excretions were not significantly different from those of non-transgenic littermates, despite a markedly lower arterial blood pressure in the experimental group. A slightly lower glomerular filtration rate (GFR) in transgenics was not different statistically. Plasma ANF levels measured by radioimmunoassay were approximately 10-fold higher in the transgenic animals, compared with their nontransgenic siblings. After acute blood volume expansion, the diuretic, natriuretic, kaliuretic, and chloruretic responses were markedly enhanced in the transgenic group. Arterial pressure was increased as a result of hypervolemia, although it remained relatively depressed relative to the controls. GFR again was not different. We conclude that transgenic mice overexpressing ANF can maintain normal excretion of salt and water, possibly via ANF-induced reduction of renal perfusion pressure. After acute blood volume expansion, an increase in pressure may allow full renal expression of the chronically elevated ANF levels.

Resonance in a mathematical model of baroreflex control: arterial blood pressure waves accompanying postural stress

2005 ◽  
Vol 288 (6) ◽  
pp. R1637-R1648 ◽  
Author(s):  
Peter E. Hammer ◽  
J. Philip Saul
Keyword(s):  
Blood Pressure ◽  
Mathematical Model ◽  
Blood Volume ◽  
Low Frequency ◽  
Pressure Waves ◽  
Central Blood Volume ◽  
Arterial Baroreflex ◽  
Arterial Blood ◽  
Gain Margin ◽  
The Stability

A mathematical model of the arterial baroreflex was developed and used to assess the stability of the reflex and its potential role in producing the low-frequency arterial blood pressure oscillations called Mayer waves that are commonly seen in humans and animals in response to decreased central blood volume. The model consists of an arrangement of discrete-time filters derived from published physiological studies, which is reduced to a numerical expression for the baroreflex open-loop frequency response. Model stability was assessed for two states: normal and decreased central blood volume. The state of decreased central blood volume was simulated by decreasing baroreflex parasympathetic heart rate gain and by increasing baroreflex sympathetic vaso/venomotor gains as occurs with the unloading of cardiopulmonary baroreceptors. For the normal state, the feedback system was stable by the Nyquist criterion (gain margin = 0.6), but in the hypovolemic state, the gain margin was small (0.07), and the closed-loop frequency response exhibited a sharp peak (gain of 11) at 0.07 Hz, the same frequency as that observed for arterial pressure fluctuations in a group of healthy standing subjects. These findings support the theory that stresses affecting central blood volume, including upright posture, can reduce the stability of the normally stable arterial baroreflex feedback, leading to resonance and low-frequency blood pressure waves.

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