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T Berl

Publications and source records attributed to T Berl.

100 records · Page 6Linked to original sources
PubMed1974

Mechanism of suppression of vasopressin during alpha-adrenergic stimulation with norepinephrine.

Recent studies have demonstrated that the water diuresis associated with intravenous infusion of norepinephrine is mediated primarly by suppression of antidiuretic hormone (ADH) release. To investigate whether the increase in cerebral perfusion pressure with intravenous norepinephrine (0.5 mug/kg/min) is directly responsible for suppression of ADH release, the carotid circulation of dogs was pump-perfused bilaterally to selectively increase cerebral perfusion pressure. In six experiments cerebral perfusion pressure was increased from a mean of 125 to 151 mm Hg and then returned to 120 mm Hg. This maneuver was not associated with a reversible increase in renal water excretion. The possibility was also examined that norepinephrine exerts a direct central effect to suppress ADH release. In 12 experiments norepinephrine was infused into the carotid artery in a subpressor dose (0.12 mug/kg/min) estimated to equal the amount of the catecholamine reaching the cerebral circulation with intravenous norepinephrine. The urinary osmolality (Uosm) was not significantly altered with intracarotid norepinephrine (932 to 959 mosmol/kg H(2)O. The possibility was also examined that changes in autonomic neural tone from arterial baroreceptors is responsible for suppression of ADH release with intravenous norepinephrine. In sham-operated animals intravenous norepinephrine diminished Uosm from 1,034 to 205 mosmol/kg H(2)O (P<0.001) whereas in animals with denervated arterial baroreceptors intravenous norepinephrine was not associated with a significant alteration in Uosm (1,233 to 1,232 mosmol/kg) H(2)O. These different effects on urinary osmolality occurred in the absence of differences in plasma osmolality and volume status. The results therefore indicate that norepinephrine primarily suppresses ADH release by altering autonomic baroreceptor tone rather than by a direct central or pressor effect of the catecholamine. This same mechanism may be the primary pathway for other nonosmotic influences on ADH release.

Animals↗
PubMed1974

Mechanism of stimulation of vasopressin release during beta adrenergic stimulation with isoproterenol.

Recent studies have demonstrated that the antidiuresis associated with intravenous (i.v.) infusion of the beta adrenergic agonist, isoproterenol (ISO), is mediated by release of endogenous vasopressin. To examine whether beta-adrenergic stimulation causes vasopressin release by a direct cerebral action, ISO was infused into the carotid artery in a dose estimated to equal the amount of catecholamine reaching the cerebral circulation in the i.v. studies. This intracarotid infusion did not alter renal or systemic hemodynamics, urinary osmolality (Uosm) or free-water clearance (C(H2O)). Although renal perfusion pressure was maintained constant in all experiments i.v. ISO was consistently associated with a decrease in total peripheral resistance and systemic arterial pressure as cardiac output increased. To investigate whether the decrease in cerebral perfusion pressure with i.v. ISO might be responsible for vasopressin release, the carotid arteries were bilaterally constricted both above and below the carotid sinus to lower carotid perfusion pressure by a mean of 25 mmHg, a decrement comparable to that observed during i.v. ISO. Constriction of the carotid arteries above the carotid sinus did not affect Uosm or C(H2O), while constriction below the sinus was associated with an antidiuresis as Uosm increased from 155+/-25 to 385+/-58 mosmol/kg (P < 0.001) and C(H2O) decreased from 1.20 to -0.44 ml/min (P < 0.001). This antidiuresis was not significantly different from that observed during i.v. ISO. Since these results suggested that changes in autonomic neural tone from arterial baroreceptors are responsible for vasopressin release with i.v. ISO, studies were performed in animals with denervated baroreceptors. While sham-operated animals and animals with bilateral cervical vagotomy showed a reversible antidiuresis with i.v. ISO infusion, dogs with complete denervation of arterial baroreceptors did not show a significant alteration in renal water excretion (Uosm, 187 to 182 mosmol/kg and C(H2O), 0.59 to 0.74 ml/min). The results therefore indicate that ISO stimulates vasopressin release by altering baroreceptor tone rather than by a direct central or depressor effect of the catecholamine. These same baroreceptor pathways have been recently shown to be involved in the suppression of vasopressin release with norepinephrine and may well be the common pathway whereby nonosmotic stimuli control vasopressin release.

Animals↗
PubMed1973

Mechanism of effect of prostaglandin E 1 on renal water excretion.

The present study examined the effect of prostaglandin E(1) (PGE(1)) on renal water excretion in the anesthetized dog. Renal perfusion pressure was kept constant by adjustment of a suprarenal aortic clamp. In seven experiments the intravenous administration of PGE(1) (7 mug/min) significantly increased urinary osmolality from 76 to 381 mosmol (P < 0.001) and decreased free water clearance from 2.2 to - 0.02 ml/min (P < 0.001). These effects promptly were reversed with cessation of the infusion. This antidiuretic effect occurred both in innervated and denervated kidneys and was not associated with changes in glomerular filtration rate, renal vascular resistance, or solute excretion rate. In 10 experiments in hypophysectomized dogs no effect of intravenous PGE(1) on free water clearance and urinary osmolality was observed. The intrarenal administration of PGE(1) (1 mug/min) to six water-loaded and two hypophysectomized dogs caused no systemic vascular changes and increased rather than decreased free water clearance (2.83 to 4.08 ml/min, P < 0.001). No significant change in urinary osmolality occurred. Glomerular filtration rate was not altered by the intrarenal infusion, but reversible changes in solute excretion rate and renal vascular resistance occurred. These results thus indicate that the antidiuresis associated with intravenous PGE(1) is mediated primarily by the release of vasopressin rather than alterations in renal hemodynamics or solute excretion. The diuretic effect of intrarenal PGE(1) occurs in the absence of vasopressin and is most likely mediated primarily by increased distal delivery of tubular fluid to the diluting segment of the nephron rather than changes in water permeability of the renal tubular epithelium.

Animals↗
PubMed1973

Mechanism of effect of alpha adrenergic stimulation with norepinephrine on renal water excretion.

The present study was undertaken to investigate the mechanism whereby alpha adrenergic stimulation with intravenous norepinephrine results in a water diuresis. Renal perfusion pressure was kept constant in all experiments by adjustment of a suprarenal aortic clamp. In hydropenic anesthetized dogs the intravenous infusion of norepinephrine (0.5 mug/kg per min) was associated with a mean decrease in urinary osmolality from 616 to 126 mosmol/kg (P < 0.001) which increased to 532 mosmol/kg (P < 0.001) after the infusion was discontinued. During the same period of time the mean free water clearance increased from -0.437 to 1.59 (P < 0.001) and then returned to -0.314 ml/min (P < 0.001) after cessation of the infusion. This diuretic effect occurred in both innervated and denervated kidneys and was not associated with an increase in glomerular filtration rate or solute excretion. Systemic arterial pressure increased from 121 to 142 mm Hg during the norepinephrine infusion. Studies were also performed in hypophysectomized animals receiving a constant infusion of either 80 mug/kg per min or 20-40 muU/kg per min of vasopressin. In these animals, intravenous norepinephrine was not associated with changes in either urinary osmolality or free water clearance. The intrarenal administration of norepinephrine, in doses comparable with those reaching the kidneys during the intravenous studies, also resulted in no significant change in either urinary osmolality or free water clearance in hypophysectomized animals receiving 20-30 muU/kg per min of vasopressin. These results thus indicate that the water diuresis associated with intravenous norepinephrine is mediated primarily by suppression of vasopressin release rather than by changes in renal hemodynamics, renal innervation, or an effect of norepinephrine on the water permeability of the tubular epithelium.

Animals↗
PubMed1972

Mechanism of the antidiuretic effect associated with interruption of parasympathetic pathways.

The present experiments were undertaken to investigate the mechanism whereby the parasympathetic nervous system may be involved in the renal regulation of solute-free water excretion. The effects of interruption of parasympathetic pathways by bilateral cervical vagotomy were examined in eight normal and seven hypophysectomized anesthetized dogs undergoing a water diuresis. In the normal animals cervical vagotomy decreased free-water clearance (C(H2O)) from 2.59+/-0.4 se to -0.26+/-0.1 ml/min (P < 0.001), and urinary osmolality (U(osm)) increased from 86+/-7 to 396+/-60 mOsm/kg (P < 0.001). This antidiuretic effect was not associated with changes in cardiac output, renal perfusion pressure, glomerular filtration rate, renal vascular resistance, or filtration fraction and was not affected by renal denervation. A small but significant increase in urinary sodium and potassium excretion was observed after vagotomy in these normal animals. Pharmacological blockade of parasympathetic efferent pathways with atropine, curare, or both was not associated with an alteration in either renal hemodynamics or renal diluting capacity. In contrast to the results in normal animals, cervical vagotomy was not associated with an antidiuretic effect in hypophysectomized animals. C(H2O) was 2.29+/-0.26 ml/min before and 2.41+/-0.3 ml/min after vagotomy, and U(osm) was 88+/-9.5 mOsm/kg before vagotomy and 78+/-8.6 mOsm/kg after vagotomy in the hypophysectomized animals. Changes in systemic or renal hemodynamics or electrolyte excretion were also not observed after vagotomy in these hypophysectomized animals. On the basis of these results, we conclude that the antidiuretic effect associated with cervical vagotomy is initiated by interruption of parasympathetic afferent pathways and is mediated by increased endogenous release of vasopressin. This antidiuresis was also demonstrated to occur in the absence of renal nerves and alterations in systemic and renal hemodynamics.

Animals↗
PubMedDate not supplied

Mechanism of acute hypercalcemic hypertension in the conscious rat.

Acute hypercalcemia in the conscious, unanesthetized rat, achieved by a 30-minute infusion of CaCl2 (serum calcium level, 12.8 +/- 0.6 mg/dl) resulted in significant elevation of mean arterial pressure (from 112 +/- 2 mm Hg to 129 +/- 3 mm Hg, p less than 0.001). This pressor response was associated with a significant increase in systemic vascular resistance, from 0.45 +/- 0.02 mm Hg/(ml/min)/kg body weight to 0.50 +/- 0.02 mm Hg/(ml/min)/kg body weight (p less than 0.05), but it caused no alteration in cardiac index. The pressor response to acute hypercalcemia does not appear to be mediated by vasopressor hormones or attenuated by vasodepressor hormones since inhibition of the renin-angiotensin system (nephrectomy), catecholamines (central and peripheral 6-hydroxydopamine), vasopressin (vascular antagonist), prostaglandins (indomethacin), and parathyroid hormone (parathyroidectomy) did not significantly alter the pressor response to infusion of CaCl2 in spite of similar serum calcium levels in all groups of animals. Rather, the pressor response to acute hypercalcemia seems to be mediated by a direct action of calcium ion on smooth muscle and perhaps myocardial cell contractility, since pretreatment with the calcium channel blockers verapamil or nifedipine blocked the pressor response to acute hypercalcemia.

Acute Disease↗