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Biomedical subjects

G Geelen

Publications and source records attributed to G Geelen.

At least 37 records · Page 2Linked to original sources
PubMed1991

[Role of vasopressin in the modifications of renal function during aging].

In the course of aging, the renal concentrating ability is markedly reduced. This defect may result from an inappropriate synthesis of antidiuretic hormone in the central nervous system or may be due to an impaired renal response to vasopressin. The two hypotheses have been studied in vivo in rats and in vitro in mice. The results of these studies indicated that: 1) dehydration induces a comparable release of vasopressin along the hypothalamo-hypophysial axis in 10, 20 and 30 month-old rats; 2) there is no change with age of the number of nephrons, single nephron filtration rate or transport capacity of Henle's loop of cortical nephrons which could account for an impaired renal response to vasopressin; 3) the reduced concentrating ability of the kidney appears to be linked to a decreased response of the medullary thick ascending limb of Henle's loop which in part is responsible for the cortico-papillary gradient of solutes within the kidney.

Age Factors↗
PubMed1990

Involvement of vasopressin in the cardiovascular effects of quinpirole.

The effects of quinpirole, a specific dopamine D2 receptor agonist, were investigated on cardiovascular responses and plasma levels of catecholamines and vasopressin in two groups of conscious dogs: (1) control dogs and (2) dogs with diabetes insipidus (i.e. animals surgically deprived of vasopressin). In normal dogs, i.v. quinpirole (30 micrograms/kg) elicited a decrease in blood pressure associated with a rise in both plasma catecholamine and vasopressin levels. In dogs with diabetes insipidus, i.v. quinpirole induced a more marked decrease in blood pressure than in normal dogs. Quinpirole did not change plasma noradrenaline and vasopressin levels in dogs with diabetes insipidus. The present study demonstrates that the decrease in blood pressure elicited by quinpirole is associated with an increase in vasopressin release, which counteracts the hypotensive effect of the the dopamine D2 receptor agonist.

Animals↗
PubMed1990

Effects of swim training alone and in combination with clonidine and rilmenidine on blood pressure, plasma electrolytes, vasopressin, and renin activity in spontaneously hypertensive rats.

Adaptations to the effects of clonidine (CL) and rilmenidine (R) were studied during a 12-week training program (swimming) in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Systolic blood pressure (SBP) was regularly measured during this period. Body weight (BW) was determined at the beginning and at the 12th week. Plasma parameters, cardiac determinations, vasopressin (pAVP), and plasma renin activity (PRA) were measured only at the end of the experiment. Both SBP and ponderal benefit were reduced by CL, R, and training. Contrary to beta-adrenoceptor blocking agents, we found no inhibition of the beneficial effect on SBP of training in combination with CL or R. Plasma and hypothalamic vasopressin were reduced by both drugs but only CL increased plasma renin activity (PRA) although its mechanisms of action are still not clearly understood. Our results suggest that CL and R as well as swim training can be considered as an effective countermeasure in SHR. Moreover, the heterogeneity of action of CL and R on some of the parameters tested is in favor of different pharmacological properties for these drugs.

Adrenergic alpha-Agonists↗
PubMed1990

Cardiovascular effects of central injection of acetylcholine in anaesthetized dogs: a role for vasopressin release.

1. The effect of an intracisternal injection of 20 micrograms kg-1 of acetylcholine was studied on systolic and diastolic blood pressures, heart rate, and plasma levels of noradrenaline, adrenaline, vasopressin, plasma renin activity and atrial natriuretic factor in chloralose-anaesthetized dogs, 8 of which were normal and 7 with diabetes insipidus (deprived of vasopressin secretion by surgical lesion of the hypothalamoneurohypophysial system). 2. Acetylcholine significantly increased systolic and diastolic blood pressures in both groups of animals. However, the rise in blood pressure was significantly shorter lived in the dogs with diabetes insipidus. 3. Acetylcholine significantly increased plasma levels of noradrenaline but not adrenaline in control animals and in dogs with diabetes insipidus. Noradrenaline and adrenaline responses after acetylcholine were not different in the two groups of animals. 4. Acetylcholine induced a significant increase in vasopressin plasma levels only in control animals while in dogs with diabetes insipidus vasopressin remained at nearly undetectable levels. 5. Acetylcholine significantly increased atrial natriuretic factor plasma levels only in control dogs. 6. Although plasma renin activity increased in both groups of animals after the i.c. injection of acetylcholine, this change was not significant in any group. 7. These results suggest that, in the anaesthetized dog, the central injection of acetylcholine induces a rise in blood pressure through both an increase in sympathetic outflow and a release of vasopressin.

Acetylcholine↗
PubMed1990

Effect of quinpirole, a specific dopamine DA2 receptor agonist on the sympathoadrenal system in dogs.

The effects of quinpirole, a specific dopamine DA2 receptor agonist, were investigated on both cardiovascular responses in conscious dogs and catecholamine release from the adrenal medulla in anesthetized dogs. In conscious normal dogs, i.v. quinpirole (30 micrograms/kg) elicited a decrease in blood pressure and a marked increase in heart rate associated with a rise in plasma catecholamine levels. The increase in heart rate is due to both baroreflex and central mechanisms because a slight but significant positive chronotropic effect persists in sinoaortic denervated dogs (i.e., animals deprived of baroreflex pathways). The central origin of this excitatory effect was confirmed by two subsequent protocols: intracisterna magna injection of quinpirole (5 micrograms/kg) increased blood pressure, heart rate and plasma catecholamines; i.v. domperidone reversed the hypotensive effect of i.v. quinpirole into a pressor response. The rise in plasma catecholamines was associated with an increase in plasma vasopressin levels. In anesthetized dogs, i.v. quinpirole (10 micrograms/kg/min during 12 min), which also decreased blood pressure, failed to modify epinephrine (and norepinephrine) release from the adrenal medulla whatever the stimulation frequencies (1, 3 and 5 Hz) of the sectioned splanchnic nerve. Similar results were obtained with apomorphine (5 micrograms/kg/min during 12 min). These results show that two mechanisms are involved in the action of quinpirole: first, a peripheral depressor action (which elicits the decrease in blood pressure) and secondly, a central pressor component involving an increase in both sympathetic tone and vasopressin release. They also demonstrate clearly that peripheral DA2 receptors are not involved in the control of catecholamine release from the adrenal medulla under in vivo conditions.

Adrenal Medulla↗
PubMed1989

Antigravity suit inflation: kidney function and cardiovascular and hormonal responses in men.

To investigate the effects of lower body positive pressure (LBPP) on kidney function while controlling certain cardiovascular and endocrine responses, seven men [35 +/- 2 (SE) yr] underwent 30 min of sitting and then 4.5 h of 70 degrees head-up tilt. An antigravity suit was applied (60 Torr legs, 30 Torr abdomen) during the last 3 h of tilt. A similar noninflation experiment was conducted where the suited subjects were tilted for 3.5 h. To provide adequate urine flow, the subjects were hydrated during the course of both experiments. Immediately after inflation, mean arterial pressure increased by 8 +/- 3 Torr and pulse rate decreased by 16 +/- 3 beats/min. Plasma renin activity and aldosterone were maximally suppressed (P less than 0.05) after 2.5 h of inflation. Plasma vasopressin decreased by 40-50% (P less than 0.05) and plasma sodium and potassium remained unchanged during both experiments. Glomerular filtration rate was not increased significantly by inflation, whereas inflation induced marked increases (P less than 0.05) in effective renal plasma flow (ERPF), urine flow, osmolar and free water clearances, and total and fractional sodium excretion. No such changes occurred during control. Thus, LBPP induces 1) a significant increase in ERPF and 2) significant changes in kidney excretory patterns similar to those observed during water immersion or the early phase of bed rest, situations that also result in central vascular volume expansion.

Adult↗
PubMed1988

Effect of longitudinal physical training and water immersion on orthostatic tolerance in men.

To test the hypothesis that moderately intense physical training has no effect on orthostasis, orthostatic and fluid-electrolyte-endocrine responses to 60 degrees head-up tilt were compared before and after 6 h of water immersion (34.5 +/- 0.1 degrees C) up to the neck following 6 months of exercise training. During the tilt test the five male subjects (27-42 years) each wore a lower-body positive-pressure suit (MAST-111A antishock trousers). The tilt procedure consisted of a 40-min supine control period (suit deflated), followed by a maximum 90-min tilt period (suit inflated to 50 +/- 5 mm Hg for 30 min, then deflated for 60 min or until presyncope). The mean +/- S.E. pretraining cycle ergometer peak VO2 was 3.20 +/- 0.14 L.min-1 (39 +/- 2 ml.min-1.kg-1), 3.36 +/- 0.27 L.min-1 (42 +/- 4 ml.min-1.kg-1) after 3 months (N.S.), and increased by 18% to 3.78 +/- 0.36 L.min-1 (48 +/- 5 ml.min-1.kg-1, +22%, p less than 0.05) posttraining. During pretraining, water immersion tilt tolerance decreased from 74 +/- 16 min before to 34 +/- 9 min (delta = 40 min, p less than 0.05) after immersion. During posttraining, water immersion tilt tolerance decreased similarly from 74 +/- 16 min preimmersion to 44 +/- 13 min (delta = 30 min, p less than 0.05) postimmersion (74 vs. 74 min, N.S.; 34 vs. 44 min, N.S.).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Early hormonal effects of head-down tilt (-10 degrees) in humans.

The aim of this study was to determine the effects of a 5-h weightlessness simulation (using supine bed rest or head-down tilt at -10 degrees = HDT) on plasma renin activity (PRA), aldosterone (PA), and catecholamines (epinephrine-E, norepinephrine-NE, and dopamine-DA) and to compare the results with those obtained with horizontal bed rest (BR), which is often taken as a control situation for simulation studies. Ten healthy young volunteers submitted to the three following postural tests: 7 h sitting; 1 h sitting, 5 h supine, and 1 h sitting; 1 h sitting, 5 h HDT, and 1 h sitting. Our results show that a 5-h HDT or BR induced a significant progressive increase in plasma volume (14.5% for HDT and 7% for BR) and a decrease in diastolic blood pressure (18% for HDT and 17% for BR), PRA (60% for HDT and 40% for BR), PA (63% for HDT and 60% for BR), and NE (20% for HDT and 25% for BR) compared to the sitting position. E decreased only in HDT, and DA was unchanged. We concluded that the main part of the cephalad shift is achieved by bed rest as reflected by changes in hematocrit and plasma protein concentration. The decrease in diastolic blood pressure, the inhibition of the renin-angiotensin aldosterone system (in part explained by a decrease in NE) are similar in BR and HDT. We demonstrate that the use of a relevant body position as control is a major concern when investigating the hormonal effects of HDT. If recumbency is chosen as the control situation in HDT studies, it is not surprising to observe only few changes when HDT is applied.

Adrenal Medulla↗
PubMed1987

Effects of propranolol and swim-training on blood pressure, plasma electrolytes, and vasopressin in spontaneously hypertensive and normotensive rats.

The aim of this work was to study the influence of beta-adrenoreceptor blockade on the adaptation to exercise of one of the hormonal systems (arginine vasopressin) involved in the regulation of blood volume and pressure in spontaneously hypertensive rats (SHR). Systolic blood pressure (SBP) was measured in SHR and WKY rats during 11 wk of swim training. At the end of the training program we determined post-exercise values of plasma arginine-vasopressin (pAVP), osmolality (pOsm), K+ (pK+), Na+ (pNa+), hemoglobin (Hgb), and hematocrit (Hct) in SHR and WKY rats. The following groups were studied: control (C), propranolol treated (PC), swim trained (S), and propranolol-treated and swim-treated (PS). SBP was significantly reduced by swim training or propranolol, bu these beneficial effects on SBP were attenuated when propranolol and swim training were combined. pNa+ and pOsm were significantly reduced by training alone in SHR. This reduction of pNa+ and, consequently, of pOsmol without any modification of other parameters could suggest an Na+ loss. In contrast, the SHR group treated with propranolol alone showed a significant reduction in Hct, suggesting an increased plasma volume without Na+ loss. PS SHR showed a significant reduction of Hgb, Hct, proteins, pNa+, and pOsmol, probably as a consequence of the additive effects of swimming- and propranolol-induced hypervolemia with Na+ loss. The slight and nonsignificant reduction in pAVP observed with either training or propranolol treatment alone became much more pronounced and statistically significant when the 2 treatments were combined. WKY rats showed a much smaller response to exercise and beta-adrenoreceptor blockade than SHR. We conclude that the hypervolemia suggested in PS SHR could be a possible cause of attenuation of the beneficial effects of either swimming or propranolol on SBP.

Animals↗
PubMed1986

Effect of antigravity suit inflation on cardiovascular, PRA, and PVP responses in humans.

Blood pressure, pulse rate (PR), serum osmolality and electrolytes, as well as plasma vasopressin (PVP) and plasma renin activity (PRA), were measured in five men and two women [mean age 38.6 +/- 3.9 (SE) yr] before, during, and after inflation of an antigravity suit that covered the legs and abdomen. After 24 h of fluid deprivation the subjects stood quietly for 3 h: the 1st h without inflation, the 2nd with inflation to 60 Torr, and the 3rd without inflation. A similar control noninflation experiment was conducted 10 mo after the inflation experiment using five of the seven subjects except that the suit was not inflated during the 3-h period. Mean arterial pressure increased by 14 +/- 4 (SE) Torr (P less than 0.05) with inflation and decreased by 15 +/- 5 Torr (P less than 0.05) after deflation. Pulse pressure (PP) increased by 7 +/- 2 Torr (P less than 0.05) with inflation and PR decreased by 11 +/- 5 beats/min (P less than 0.05); PP and PR returned to preinflation levels after deflation. Plasma volume decreased by 6.1 +/- 1.5% and 5.3 +/- 1.6% (P less than 0.05) during hours 1 and 3, respectively, and returned to base line during inflation. Inflation decreased PVP from 6.8 +/- 1.1 to 5.6 +/- 1.4 pg/ml (P less than 0.05) and abolished the significant rise in PRA during hour 1. Both PVP and PRA increased significantly after deflation: delta = 18.0 +/- 5.1 pg/ml and 4.34 +/- 1.71 ng angiotensin I X ml-1 X h-1, respectively. Serum osmolality and Na+ and K+ concentrations were unchanged during the 3 h of standing.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Effect of hydration on plasma volume and endocrine responses to water immersion.

To determine the effect of hydration on the early osmotic and intravascular volume and endocrine responses to water immersion the hematocrit, hemoglobin, plasma renin activity (PRA), and plasma electrolyte, aldosterone (PA), and vasopressin (PVP) concentrations were measured during immersion following 24-h dehydration; these were compared with corresponding values following rapid rehydration. Six men and one woman (age 23-46 yr) underwent 45 min of standing immersion to the neck preceded by 45-min standing without immersion, first dehydrated, and then 105 min later after rehydration with water. Immersion caused an isotonic expansion of the plasma volume (P less than 0.001), which occurred independently of hydration status. Suppression of PRA (P less than 0.001) and PA (P less than 0.001) during both immersions also occurred independently of hydration status. Suppression of plasma vasopressin was observed during dehydrated immersion (P less than 0.001) but not during rehydrated immersion. It is concluded that plasma tonicity is not a factor influencing PVP suppression during water immersion.

Adult↗
PubMed1986

Effect of hydration on plasma vasopressin, renin, and aldosterone responses to head-up tilt.

If plasma vasopressin (PVP), plasma renin (PRA), and plasma aldosterone (PA) responses to change in posture are mediated only by alterations in intrathoracic baroreceptor activity, hydration status should have minimal influence on these responses. To test this hypothesis, six male subjects underwent 45 min of 70 degree head-up tilt (HUT) following 26 h dehydration, and again, 105 min later, following rehydration. Compared with preceding supine hydrated control values, PVP, PRA, and PA increased (p less than 0.001) during dehydrated HUT, but only PVP and PRA increased during rehydrated HUT (p less than 0.001). The dissociation during rehydrated HUT of PRA and PA may have been related more to the reduction (p less than 0.001) in plasma potassium concentration than to the accompanying decrease (p less than 0.001) in plasma osmolality and sodium concentration. Although increases in PVP and PRA during HUT were attenuated (p less than 0.01) following rehydration, this attenuation was associated with the absence of symptoms of overt hypotension following rehydration. However, since rehydration did not abolish the increases in PVP and PRA induced by HUT, it is concluded that the present observations support the concept of intrathoracic baroreceptor involvement in the regulation of vasopressin secretion and renin release.

Adult↗
PubMed1985

Effect of hand-arm exercise on venous blood constituents during leg exercise.

To test the hypothesis that ancillary arm and hand exercise would change the values of antecubital blood constituents during leg exercise, seven healthy men (19-27 yrs) performed static (10% of a maximal voluntary contraction) or dynamic (60 finger flexions/min) hand-arm exercise with one hand during submaximal leg exercise (50% V2 max) in the supine position. Venous blood was analyzed for serum Na+, K+, osmolality, albumin, total Ca2+, and glucose; blood hemoglobin, hematocrit, and lactic acid; and change in plasma volume. During leg exercise there were no significant differences in these blood constituents between right and left arms at rest. Only glucose and lactate were affected by additional arm exercise. Compared with resting arm values during leg exercise, glucose decreased from 4.7 to 4.5 mmol/l (delta = 4%, P less than 0.05) and lactate increased from 2.0 to 2.4 mmol/l (delta = 20%, P less than 0.05) during static arm exercise. With dynamic arm exercise, glucose decreased from a resting level of 4.8 to 4.7 mmol/l (delta = 2%, P less than 0.05). We conclude that additional static or dynamic hand-forearm exercise accompanying leg exercise could introduce significant errors in glucose (2%-4%) and lactic acid (6%-20%) concentrations measured in venous blood.

Adult↗
PubMed1985

Blood pressure and plasma renin activity as predictors of orthostatic intolerance.

Some physiological responses to head-up tilt and 3 h standing were evaluated in 13 dehydrated subjects. Seven of the subjects proved to be orthostatically intolerant (INT), exhibiting presyncopal symptoms. Before the symptoms manifest themselves the INT subjects had consistently lower (p less than 0.05) systolic blood pressures, generally lower diastolic and pulse pressures, and elevated (p less than 0.05) plasma renin activity (PRA) compared to the tolerant (TOL) subjects. Plasma vasopressin usually increased more in the INT subjects, but appeared to be related to the severity of presyncopal symptoms rather than to the upright posture per se. It is concluded that systolic and pulse pressures, with PRA, may allow discrimination between TOL, and potentially INT individuals; i.e., predict orthostatic intolerance. It is suggested that dehydration could provide a valuable physiological model for elucidating the causes of orthostatic intolerance.

Adult↗