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Biomedical subjects

J E Greenleaf

Publications and source records attributed to J E Greenleaf.

At least 109 records · Page 6Linked to original sources
PubMed1983

Hypervolemia and plasma vasopressin response during water immersion in men.

To investigate changes in plasma volume (PV) and osmolality as stimuli for plasma vasopressin (PVP) suppression and diuresis, seven normal healthy men (22-48 yr) were immersed to the neck for 4 h in a sitting position in tap water (34.5 degrees C) after overnight food and fluid restriction. Mean +/- SE urine volume was 823 +/- 123 ml/4 h; fluid intake was 400 ml/4 h, and mean negative water balance was 944 ml/4 h. Urinary sodium excretion increased from 0.77 to 1.25 mosmol/min (P less than 0.05) and UNaV from 0.14 to 0.37 meq/min (P less than 0.05). During immersion, PV (T-1824) increased by 8.8% (P less than 0.05) during the first 30 min and declined linearly thereafter. Mean +/- SD serum osmolality (294 +/- 1.2 mosmol/kg H2O) and sodium (143.2 +/- 0.4 meq/l) were constant throughout immersion; PVP (2.3 +/- 0.5 pg/ml) and plasma renin activity [0.3 +/- 0.2 ng ANG I/(ml X h]) were not significantly changed. Thus, the composition of the fluid entering the vascular space maintained constant serum osmolality and PVP throughout immersion. These findings do not support the hypothesis that acute expansion of central volume and PV cause suppression of PVP. The results suggest a mechanism other than or in addition to PVP suppression as a contributory cause of the immersion diuresis.

Adult↗
PubMed1982

Bethanechol-induced water intake in rats: possible mechanisms of induction.

Acute administration of the parasympathomimetic agent, bethanechol, at 2, 4, 8 and 12 mg/kg body wt, IP, induced drinking and increased urine output of rats in a dose-dependent fashion. The first significant increases in both water intake and urine output above that of controls occurred when 4 mg/kg was administered. The drinking and increased urine output in response to administration of 8 mg bethanechol/kg was inhibited by atropine sulfate (3 and 6 mg/kg, IP). In addition, the beta-adrenergic antagonist, propranolol (6 mg/kg, IP, administered 30 min prior to treatment with bethanechol), inhibited bethanechol (8 mg/kg, IP)-induced drinking. Urine output, however, was unaffected by propranolol. Further, the angiotensin I converting enzyme inhibitor, captopril, inhibited significantly the drinking response, but not the increased urine output, accompanying administration of bethanechol (8 mg/kg). The effect of bethanechol and the beta-adrenergic agonist, isoproterenol (25 micrograms/kg) separately and in combination, on water intake was also studied. Both compounds increased water intake but they exerted no interactive effect when administered simultaneously. Administration of bethanechol (8 mg/kg) to conscious rats was also accompanied by a significant reduction in both mean blood pressure and heart rate that reached minimal levels within 10 min after treatment. Both responses had returned to control level by one hr after treatment. These results suggest that bethanechol induces drinking in rats by way of the renin-angiotensin system.

Animals↗
PubMed1982

Reduction in peak oxygen uptake after prolonged bed rest.

The purpose was to test the hypothesis that the magnitude of the reduction in peak oxygen uptake (VO2) after bed rest is directly proportional to the level of pre-bed rest peak VO2. Complete pre- and post-bed rest working capacity and body weight data were available from three studies involving 24 men (19-24 yr; peak VO2, 2.39-4.80 l . min-1) and 8 women (23-34 yr; peak VO2 1.47-2.58 l . min-1), who underwent bed rest for 14-20 d with no remedial treatments. Regression analysis of percent change in post-bed rest peak VO2 on pre-bed rest peak VO2 with 32 subjects resulted in correlation coefficients (r) of--0.03 (NS) for data expressed in l . min-1 and -0.17 (NS) for data expressed in ml . min-1 . kg-1. Significant correlations were found that supported the hypothesis only when peak VO2 data were analyzed separately from studies that utilized the cycle ergometer, particularly with subjects in the supine position, as opposed to data obtained from treadmill peak VO2 tests. We conclude that orthostatic factors, associated with the upright body position and relatively high levels of physical fitness from endurance training, appear to increase variability of pre- and particularly post-bed rest peak VO2 data, which would lead to rejection of the hypothesis.

Adult↗
PubMed1982

Dehydration-induced drinking in humans.

Mechanisms of drinking have been studied extensively in laboratory mammals, but comparatively little information is available on human consumption of fluids. The assumption that osmotic disequilibrium between extra- and intracellular fluid can be rectified within seconds may not be true for plasma and red blood cell (RBC) fluid in humans inasmuch as stress-induced hyperosmotemia to +13 mosmol/kg does not cause a significant change in mean RBC corpuscular volume. Unlike some mammals, humans have a delay in rehydration (involuntary dehydration) after fluid loss. Two factors unique to humans that probably contribute to involuntary dehydration are 1) upright posture and 2) extracellular fluid and electrolyte loss by sweating from exercise and heat exposure. If drinking is influenced by upright postural changes, it may be related to increased plasma renin activity (PRA) but not to increases in plasma osmolality or arginine vasopressin concentration. Under combined stresses of heat, exercise, and prior dehydration, exercise is the greatest inhibiting factor and heat exposure has the least inhibitory effect on voluntary water intake. The rate of drinking during exercise in heat has a high correlation with sweat rate but is essentially unrelated to the well-established dipsogenic factors of plasma volume, osmolality, and PRA. However, it is likely that some or all of these dipsogenic factors act to initiate drinking in humans.

Arginine Vasopressin↗
PubMed1981

Peripheral conversion of L-5-hydroxytryptophan to serotonin induces drinking in rats.

Female rats administered serotonin (0.25 to 4.0 mg/kg, s.c.) showed a dose-dependent increase in water intake. The dipsogenic response was nearly maximal when 2 mg/lg was administered s.c. and plateaued by 2 hr after treatment. l-5-Hydroxytryptophan (5-HTP), the precursor of serotonin, is also a potent dipsogen which induces drinking by way of the renin-angiotensin system. The possibility that the dipsogenic activity of 5-HTP is dependent on decarboxylation to serotonin was the objective of these studies. Either benserazide (30 mg/kg. s.c.), a central and peripheral decarboxylase inhibitor, or carbidopa (6.5 mg/kg, s.c.), a peripheral decarboxylase inhibitor, was administered 15 min prior to the dipsogen. Both decarboxylase inhibitors attenuated the dipsogenic response to 5-HTP (25 mg/kg, s.c.) but not to serotonin (2 mg/kg, s.c.). The peripheral serotonergic receptor antagonist, methysergide (3 mg/kg, i.p.), blocked the dipsogenic responses to both 5-HTP (25 mg/kg, s.c.) and serotonin (2 mg/kg, s.c.). There was no interaction between 5-HTP (18 mg/kg, s.c.) and serotonin (1 mg/kg, s.c.) when administered simultaneously with respect to their dipsogenic effects. Thus, the drinking response accompanying administration of 5-HTP occurs following peripheral conversion to serotonin which, in turn, activates peripheral serotonergic receptors. The mechanisms(s) by which activation of peripheral serotonergic receptors increases water intake is not known, but appears to involve release of renin from the kidney.

5-Hydroxytryptophan↗
PubMed1981

Antidipsogenic effect of clonidine on angiotensin II-, hypertonic saline-, pilocarpine- and dehydration-induced water intakes.

The dipsogenic responses of female rats to administration of angiotensin II (150 micrograms/kg b.w., IP), pilocarpine (3 mg/kg IP), hypertonic saline (1 M NaCl solution, 1% b.w.), and a 24 hour dehydration were attenuated by acute IP administration of graded doses of the central and peripheral alpha 2-adrenergic agonist, clonidine. For all treatments except dehydration, clonidine inhibited significantly the dipsogenic response at the lowest dose used (6 micrograms/kg, IP). The first significant effect on dehydration-induced drinking required approximately a 4 fold higher dose (25 micrograms/kg, IP). Attenuation of the response to these dipsogenic stimuli by clonidine, suggests that its ability to stimulate alpha-adrenergic receptors centrally may play an important role in its dipsogenic inhibitory activity.

Angiotensin II↗
PubMed1981

Plasma volume, osmolality, vasopressin, and renin activity during graded exercise in man.

Plasma volume (PV), renin activity (PRA), and osmotic (Osm), sodium (Na+), and arginine vasopressin (AVP) concentrations were measured in venous blood samples taken before and after three levels of cycle ergometer exercise (100, 175, and 225 W) in 15 young male volunteers. Plasma volume and solute concentrations changed significantly (P less than 0.05, denoted by *) with work intensity. The % delta PV was -3.7%* at 100 W, -8.8%* at 175 W, and -12.4%* at 225 W. Plasma Na+ concentration, Osm, and AVP increase were curvilinear with graded exercise and were significant only when work intensity exceeded 40% VO2max. PRA increase was linear and significant at all work levels. The % delta PV was significantly correlated with delta Osm (r = 0.99*) and delta Na+ (r = 0.89*) but had low correlations with delta AVP (r = 0.22, NS) and delta PRA (r = 0.12, NS). However, delta AVP was significantly correlated with delta Na+ (r = 0.86*) and delta Osm (r = 0.83*), whereas delta PRA had low correlations with delta Na+ (r = 0.33, NS), delta Osm (r = 0.29, NS), and delta AVP (r = 0.43, NS). The data support the hypothesis that a) with exercise, AVP release is a primary factor for fluid and electrolyte regulation as it is highly correlated with the plasma hyperosmolality produced by a net hypotonic plasma efflux; b) an exercise intensity greater than 40% VO2max is required to change plasma osmolality and, thus, stimulate significant AVP release; and c) the stimulation of the renin-angiotensin system is a more general stress response, which responds to increasing sympathetic nervous activity.

Adult↗
PubMed1981

Exercise training hypotension: implications for plasma volume, renin, and vasopressin.

To determine the function of changes in plasma volume (PV), plasma renin activity (PRA), and arginine vasopressin (AVP) in the mechanism of the reduction of resting blood pressure during exercise training, resting supine, sitting, and standing systolic (SBP) and 5th-phase diastolic (DBP) blood pressures were measured in 10 men (19-24 yr) before and after an 8-day (2 h/day) training period on a cycle ergometer. The control group (5 men) exercised at 1.4 1/min [44% peak O2 uptake (VO2 max)] at 23.8 degrees C Tdb and 50% rh, and the acclimation group at 1.5 1/min (46% VO2 max) at 39.8 degrees C Tdb and 50% rh. After acclimation, resting supine and sitting DPB decreased (P less than 0.05) by 6 and 9 mmHg, respectively. There were no significant changes in DBP in the controls or in SBP in either group. After training, PV increased by 12.2% in controls and by 17.6% after acclimation. The resting hypotension could not be attributed to changes in resting levels of PV, AVP, or PRA. However, large decreases in PV and large increases in AVP and especially PRA during acclimation exposures suggest these responses may play a role in the chronic hypotensive response.

Acclimatization↗
PubMed1981

Hemodilution, vasopressin suppression, and diuresis during water immersion in man.

We hypothesize that hemodilution in the early stages of water immersion plays an important role in vasopressin (AVP) suppression and subsequent diuresis. Ten men (19-24 years) were immersed to the neck in a semireclining position for 8 h in 34.6 degree C tap water. After 8 h of immersion there were decreases (p less than 0.05) in plasma volume (PV) of 15.6%, extracellular volume (ECV) of 18.8%, interstitial volume (ISV) of 19.6%, and red cell volume of 10.7%. Hemodilution (hyposmotem years) were immersed to the neck in a semireclining position for 8 h in 34.6 degree C tap water. After 8 h of immersion there were decreases (p less than 0.05) in plasma volume (PV) of 15.6%, extracellular volume (ECV) of 18.8%, interstitial volume (ISV) of 19.6%, and red cell volume of 10.7%. Hemodilution (hyposmotem years) were immersed to the neck in a semireclining position for 8 h in 34.6 degree C tap water. After 8 h of immersion there were decreases (p less than 0.05) in plasma volume (PV) of 15.6%, extracellular volume (ECV) of 18.8%, interstitial volume (ISV) of 19.6%, and red cell volume of 10.7%. Hemodilution (hyposmotem of 4 mosmol/kg H2O) and near maximal suppression of AVP (to 0.5 pg/ml) and plasma renin activity (to 0.4 ng Ang 1 .ml-1.h-1) were evident by hour 2 of immersion. The early hemodilution (2-2 h) was due to a slight increase in PV with no change in plasma Na+ or osmotic content, even though urine volume and UosmV increased significantly. The hyposmotemia and PRA suppression continued throughout immersion in spite of the progressively increasing diuresis and decreasing PV. These findings suggest the transfer of hypotonic fluid into the vascular system; this fluid does not appear to come from the intracellular volume. We conclude that hyposmotemia is an important part of the mechanism contributing to AVP suppression during water immersion.

Adult↗
PubMed1980

Extracellular hyperosmolality and body temperature during physical exercise in dogs.

The purpose of this study was to test the hypothesis that thermoregulation during exercise can be affected by extracellular fluid hyperosmolality [Osm] without changing the plasma Na+ concentration. The effects of preexercise venous infusions of hypertonic mannitol and NaCl solutions on rectal temperature (Tre) responses were compared in dogs running at moderate intensity for 60 min on a treadmill. Plasma E1Na+] was increased by 12 meq/l (P less than 0.05) after NaCl infusion, and decreased by 9 meq/l (P less than 0.05) after mannitol infusion. Both infusions increased plasma [Osm] by 15 mosmol/kg (P less than 0.05). After both infusions, Tre was essentially constant during 60 min rest. However, compared with the noninfusion exercise increase in Tre of 1.3 degrees C, Tre increased by 1.9 degrees C (delta delta Tre = 0.5 degrees C, P less than 0.05) after both postinfusion exercise experiments. It was concluded that inducing extracellular hyperosmolality, without elevating plasma [Na+], can induce excessive increases in Tre during exercise but not at rest.

Animals↗
PubMed1980

Exercise thermoregulation after 14 days of bed rest.

Rectal (Tre) and mean skin (Tsk) temperatures and sweating responses were measured during 70-min submaximal supine exercise (relative VO2 43-48%) in seven men (19-22 yr) during an ambulatory-control (AC) period and after three 2-wk bed-rest (BR) periods separated by 3-wk ambulatory recovery periods. During each of the three BR periods they performed isometric exercises (IME) or isotonic exercises (ITE) for 1 h/day or no prescribed exercise (NOE). Mean basal oral temperature decreased from 36.0 to 35.7 degrees C in the last 10 days of the control-recovery periods, but it varied between 35.7 and 35.9 degrees C during BR. In the exercise-temperature test the equilibrium level of Tre for the IME (37.92 degrees C) and NOE (37.75 degrees C) regimens were higher (P less than 0.05) than the AC level of 37.51 degrees C. Mean skin temperatures with the IME and ITE regimens increased by only 0.4 degrees C during exercise, and both equilibrium Tsk values, 31.98 degrees C and 31.87 degrees C, respectively, were lower (P less than 0.05) than the AC values of 32.71 degrees C. There were no significant differences between any of the sweat rates (range, 438-565 g/h) in the four experiments, but calculated skin heat conductances (Hsk) correlated +0.86 with equilibrium levels of Tsk. It was concluded that the excessive increase in Tre during submaximal exercise following BR deconditioning could be influenced by changes in Hsk, but inhibition of sweating may also be a factor.

Adult↗