Mechanism of Stimulation of Vasopressin Release during Beta Adrenergic Stimulation with Isoproterenol

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104

A B S T R A C T The effect of lowering the pressure of oxygen from 80 to 34 mm Hg was examined in anesthetized dogs that were undergoing a water diuresis. This degree of hypoxia was associated with an antidiuresis as urine osmolality (Uosm) increased from 107 to 316 mosmol/kg H20 (P < 0.001) and plasma arginine vasopressin increased from 0.06 to 7.5 pLU/ml, (P < 0.05).However, hypoxia was not associated with significant changes in cardiac output (CO, from 4.2 to 4.7 liters/ min), mean arterial pressure (MAP, from 143 to 149 mm Hg), glomerular filtration rate (GFR, from 46 to 42 ml/min), solute excretion rate (SV, from 302 to 297 mosmol/min), or filtration fraction (from 0.26 to 0.27, NS). Hypoxia was associated with an increase in renal vascular resistance (from 0.49 to 0.58 mm Hg/ml per min, P < 0.01). The magnitude of hypoxia-induced antidiuresis was the same in innervated kidneys and denervated kidneys. To further examine the role of vasopressin in this antidiuresis, hypoxia was induced in hypophysectomized animals. The effect of hypoxia on CO, MAP, GFR, SV, and renal blood flow in hypophysectomized animals was the same as in intact animals. In contrast to intact animals, however, hypoxia did not induce a significant antidiuresis in hypophysectomized animals (Uosm from 72 to 82 mosmol/kg H2O). To delineate the afferent pathway for hypoxiastimulated vasopressin release, hypoxia was induced in dogs with either chemo-or baroreceptor denervation. The effect of hypoxia on CO, MAP, GFR, SV, and renal blood flow in the denervated animals was the same as in nondenervated animals. Hypoxia resulted in an antidiuresis in chemoreceptor (Uosm from 113 to 357 mosmol/kg H20, P < 0.001) but not in baroreceptor (Uosm from 116 to 138 mosmol/kg H20, NS) denervated animals. To determine if hypoxia alters renal response to vasopressin, exogenous vasopressin was adminisDr.

Section: Resultscontrasting

confidence: 54%

Section: Resultsmentioning

confidence: 62%

Section: Resultsmentioning

confidence: 99%

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Mechanism of Effect of Hypoxia on Renal Water Excretion

Anderson¹,

Pluss²,

Berns³

et al. 1978

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104

“…Such hypophysectomized animals may at times have lower mean arterial blood pressures and filtration rates than intact animals, but these animals nevertheless have been adequately shown to respond to exogenous vasopressin (15). This model has therefore proved very useful in delineating the role of endogenous vasopressin in various circumstances in which renal water excretion may be altered, such as during alpha (15) and beta (17) adrenergic stimulation, bilateral cervical vagotomy (16), angiotensin (17), nicotine administration (18), or atrial tachycardia (19), In the present study, acute TIVC constriction was found to have only a slight effect on U..m (87+5 to 104+9 mosmols/kg) in animals in which the source of vasopressin had been removed. Even this modest effect was not significantly reversible.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Effect of Thoracic Inferior Vena Cava Constriction on Renal Water Excretion

Anderson¹,

Cadnapaphornchai²,

Harbottle³

et al. 1974

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A B S T R A C T Persistent secretion of vasopressin and/ or diminished distal fluid delivery have been proposed to explain the impaired water excretion associated with low-output cardiac failure. In the present investigation cardiac output (CO) was diminished in anesthetized dogs undergoing a water diuresis by constriction of the thoracic inferior vena cava (TIVC). In intact animals (group I) acute TIVC constriction decreased CO from 3.5 to 2.2 liters/min (P < 0.005) as urinary osmolality (U05m) increased from 103 to 543 mosmols/ kg (P < 0.001) and free water clearance (CH20) decreased from 2.1 to -0.6 ml/min (P < 0.001). This antidiuretic effect was disassociated from changes in renal arterial and venous pressures, glomerular filtration rate, solute excretion, and renal innervation. To examine the role of vasopressin in this antidiuresis, studies.,(group II) were performed in acutely hypophysectomized, steroid-replaced animals. In these animals TIVC constriction decreased CO to a similar degree from 3.4 to 2.1 liters/min (P <0.001). However, the effects on U03m; (87-104 mosmols/kg) and CH20 (2.1-1.6 ml/min) were significantly less than in intact dogs. In another group of hypophysectomized animals, (group III) renal arterial and venous pressures were not controlled, and the effect of TIVC constriction on Uosm was not significant (65-79 mosmols/kg) although CH20 decreased from 3.3 to 1.9 ml/min (P < 0.001). In both the group II and III studies, there were linear correlations between the changes in CH2o and the urine flow.Studies were also performed in baroreceptor-denervated animals with intact hypothalamo-neurohypophyseal tracts, and acute TIVC constriction altered neither Uosm nor CH2o when renal arterial pressure was controlled. These (TIVC) ' has been used by numerous investigators (1-4) as an experimental model of cardiac failure and is known to be associated with a diminished cardiac output (CO) (4) and increased tubular reabsorption of sodium (1-4). The effect of acute TIVC constriction on renal diluting capacity has not been previously investigated. An impairment in renal water excretion is, however, a frequent accompaniment of low-output cardiac failure (5). Although the mechanism of this defect in water excretion is unknown, it has been suggested to be mediated by either increased release of vasopressin (6) or diminished delivery of fluid to the distal diluting segment of the nephron (5). The present studies were therefore undertaken to examine the effect of acute TIVC constriction on renal water excretion and to define the mechanism of any such effect.METHODS 40 experiments were performed on 24 mongrel dogs of either sex weighing 20-30 kg. Food was withheld 18 h before the experiment and all animals had free access to water. The animals were anesthetized with i.v. pentobarbital (30 mg/kg) and intubated and ventilated with a Harvard respirator (Harvard Apparatus Co. Inc., Millis, Mass.). Nine animals underwent transbuccal hypophysectomy through the hard palate on the morning of the experiment (7). ...

“…In addition to nicotine (25), these stimuli include systemic alpha (30) and beta (31) adrenergic stimulation, acute constriction of the thoracic inferior vena cava (32), left atrial distention (33), atrial tachycardia (34), and hypoxia (35). From these results has emerged the hypothesis that the nonosmotic release of vasopressin may have evolved as an integral part of the alarm reaction (36).…”

Section: Plasma Vasopressin In Glucocorticoid Deficiencymentioning

confidence: 99%

Role of Plasma Vasopressin in Impaired Water Excretion of Glucocorticoid Deficiency

Boykin¹,

deTORRENTE²,

Erickson³

et al. 1978

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113

A B S T R A C T In the present study, the effect of selective glucocorticoid deficiency on renal water excretion was investigated in conscious, trained, adrenalectomized dogs. The animals were studied before and after a water load while on replacement therapy of desoxycorticosterone acetate, 5 mg/day, and dexamethasone, 0.8 mg/day (group I), and while off dexamethasone for 5-9 days (group II). Before the water load the weight, inulin space, cardiac output, blood pressure, glomerular filtration rate, renal blood flow, plasma osmolality, and plasma antidiuretic hormone measured by radioimmunoassay were similar in both groups I and II. However, after a 40 ml/kg water load a marked impairment in renal water excretion in the glucocorticoid deficient dogs became apparent. Maximal free water clearance was -0.046±0.16 vs. 6.51±0.72 ml/min (P < 0.001) and minimal urinary osmolality was 425±56 vs. 82±3.5 mosmol/kg H20 (P < 0.001) in group II as compared to group I. Plasma antidiuretic hormone was maximally suppressed during the water load in group I to 0.34±0.08 pg/ml but remained elevated at 9.18±1.79 pg/ml (P <0.005) in group II. This nonsuppressibility of plasma antidiuretic hormone during water loading in group II was associated with a significant tachycardia of 145±6 vs. 87±6 beats/min (P < 0.001) in group I and a significantly lower stroke volume of 27±0 vs. 59±0.5 ml/beat (P < 0.001). In conclusion, our results implicate a persistent secretion of antidiuretic hormone as an important factor in the impaired water excretion of glucocorticoid deficiency. A deleterious effect of glucocorticoid deficiency on cardiac function was observed and this hemodynamic alteration could be involved in initiating a nonosmolar, baroreceptormediated release of vasopressin.