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Biomedical subjects

A Ungar

Publications and source records attributed to A Ungar.

At least 37 records · Page 2Linked to original sources
PubMed1985

Interactions of beta-adrenoceptor antagonists and thyroid hormones in the control of heart rate in the dog.

Propranolol, sotalol and nadolol have been infused into conscious dogs, and doses at which the three drugs are equipotent as beta-adrenoceptor antagonists determined. In euthyroid dogs, sotalol was more effective at lowering heart-rate than an equivalent dose of propranolol, while an equivalent dose of nadolol was without effect. Hyperthyroidism potentiated the lowering of heart-rate by sotalol, but inhibited that by propranolol. The effect of sotalol on heart-rate was correlated with its prolongation of the Q-T interval of the ECG. That of propranolol was correlated with its prolongation of the P-R interval. Nadolol did not affect P-R interval or Q-T interval except at relatively high dosage. We conclude that the tachycardia of hyperthyroidism is not affected by blockade of beta-adrenoceptors and therefore that it is not mediated by adrenergic mechanisms. The effectiveness of propranolol and sotalol in lowering heart-rate must be due to actions peculiar to those drugs, and not to beta-adrenoceptor antagonism.

Adrenergic beta-Antagonists↗
PubMed1984

Angiotensin sensitivity and prostaglandins in dogs with renal hypertension.

During established two-kidney one clip hypertension in dogs blood pressure is elevated despite only slightly raised plasma renin activity. Dose dependent effects of exogenous angiotensin II on systemic and renal haemodynamics were examined before and after induction of this type of hypertension in conscious dogs. There was no difference in the response of blood pressure to angiotensin II in each group, suggesting that altered pressor sensitivity to angiotensin II is not the cause of the persisting hypertension. However sodium excretion, effective renal plasma flow and glomerular filtration rate were all decreased by angiotensin II in the normotensive group, but were unchanged or increased in the hypertensive group. Renal prostaglandin E excretion was also increased in the hypertensive animals, and further increased during infusion with angiotensin II. The altered renal response to angiotensin II in the hypertensive group may reflect changes in occupancy of angiotensin II receptors and/or enhanced renal release of vasodilator prostaglandins.

Angiotensin II↗
PubMed1982

Role of prostaglandins in mediating excretion by the kidney of an intravenous infusion of sodium chloride in normal human subjects.

1. Normal male subjects were given a rapid infusion of 3 litres of sodium chloride solution (150 mmol/l) with or without pretreatment with indomethacin. 2. There was marked individual variability in the rate at which the infused sodium chloride solution was subsequently excreted which was not related to the urinary sodium excretion in the previous 24 h. 3. There was no relationship between urinary prostaglandin E excretion during the 24 h preceding the sodium chloride infusion and the rate at which different individuals subsequently excreted sodium and water. 4. Renal plasma flow was significantly higher during the sodium chloride infusion than in the post-infusion recovery period, both with and without pretreatment with indomethacin, although it was significantly lower during each period in subjects pretreated with indomethacin. 5. Urinary prostaglandin E excretion was significantly decreased after the infusion of sodium chloride solution. 6. Indomethacin slightly decreased the rate of excretion of sodium and water. 7. Prostaglandins have a role in, but are not the main determinants of, the excretion of an intravenous infusion of sodium chloride. 8. The results do not support the suggestion that prostaglandin E produced within the kidney, as indicated by urinary prostaglandin E excretion, exerts a natriuretic action.

Adult↗
PubMed1982

The role of the pituitary-adrenocortical axis in reflex responses of the adrenal medulla of the dog.

1. The release of catecholamines from the adrenal medulla, in response to carotid body hypoxia, may outlast the stimulus by more than 30 min. 2. After denervation of the adrenal gland the immediate release of catecholamines in response to carotid hypoxia is abolished, but the prolonged release remains. 3. The prolonged release of catecholamines is abolished by cycloheximide. 4. Both corticotrophin in vivo and hydrocortisone in the isolated perfused adrenal gland release adrenomedullary catecholamines. 5. It is concluded that a component of the response of the adrenal medulla to carotid body hypoxia is mediated by corticotrophin and corticosteroid release.

Adrenal Medulla↗
PubMed1981

Effects of salt and water depletion on the early phase of hypertension in Goldblatt two-kidney hypertensive dogs.

1. Hypertension was induced in dogs by partial occlusion of one renal artery, the opposite kidney remaining intact, and the changes in blood pressure, plasma renin activity, aldosterone and prostaglandin E (PGE) were monitored. 2. Two days after induction of hypertension, the retained sodium and water were removed by haemodialysis and the animals were then maintained on a low dietary intake of sodium for the following 7 days. 3. Removal of the accumulated sodium and water had no immediate effect on blood pressure, but during the ensuring 7 days there was a small decrease in blood pressure, which again increased after re-institution of a normal sodium intake. 4. Plasma renin activity and aldosterone increased during development of hypertension and remained elevated during the period of sodium restriction. 5. Sodium and water retained during the development of hypertension was not responsible for the elevated blood pressure. 6. The concentration of PGE in arterial plasma and renal venous plasma from the unclamped kidney were unchanged during the study, although we have previously shown that in the absence of sodium depletion, PGE rises. 7. PGE released from the kidney may be important in mediating the excretion of sodium and water that is retained during the development of renal hypertension.

Aldosterone↗
PubMed1981

A comparison of the effects of prostaglandins E2 and I2 on renal function and renin release in salt-loaded and salt-depleted anaesthetized dogs.

Prostaglandin E2 (PGE2) and prostaglandins I2 (PGI2) were infused into the renal artery of either sodium-loaded or sodium-depleted dogs. Systemic blood pressure was decreased and arterial plasma renin concentration increased in the sodium-loaded dogs by infusion of PGI2 (1200 ng/min). Both compounds increased renal blood flow but PGE2 had a much more potent effect than PGI2 on increasing urine flow and sodium excretion. In the sodium-depleted dogs systemic blood pressure was significantly decreased and arterial plasma renin concentration increased by infusions of PGI2 (300 and 1200 ng/min) and PGE2 (300 ng/min). Both compounds stimulated urine flow and renal blood flow but PGE2 induced a much larger increase in sodium excretion than PGI2. PGI2 exerts its actions on renal function by inducing vasodilatation whereas PGE2 also has a direct action on tubular function.

Animals↗
PubMed1981

Renal interstitial cell granularity in dogs with renal hypertension.

Hypertension was induced in dogs by the partial occlusion of one renal artery. After 12 days of hypertension the interstitial cells in the medulla of kidneys from hypertensive animals were examined by electron microscopy, and the appearance compared with interstitial cells from normal dogs. The osmiophilic granules in the cells were classified into dark and light forms, and the numbers of each counted in at least 70 cells per kidney. It was not possible to quantify the number of interstitial cells in each renal medulla. The kidneys with partially occluded renal arteries had an increased total number of granules per cell (4.93 +/- 0.51) compared with normal kidneys (0.79 +/- 0.14), and the great majority of these were dark granules (95.3% and 79.5%, respectively). In contrast the contralateral untouched kidneys had a significantly reduced number of granules per cell (0.58 +/- 0.14), and only a small proportion of the total were dark granules (31.1%). The actual number of light granules per interstitial cell was significantly increased in the untouched kidney compared with normals.

Animals↗
PubMed1980

The ventilatory responses of conscious dogs to isocapnic oxygen tests. a method of exploring the central component of respiratory drive and its dependence on O2 and CO2.

Conscious unrestrained dogs trained to breathe through a respiratory mask or, after chronic tracheostomy, through a cuffed endotracheal tube were studied in an altitude chamber operated in such a way that end-tidal PO2 was maintained at 100, 75 or 60 Torr. Each hypoxic experiment was completed within 1 h of the onset of hypoxia. At all levels of oxygenation, resting pulmonary ventilation (V), obtained from the tidal volume (VT) and ventilatory period (T), and alveolar gas tensions (PAO2, PACO2) were measured cycle-by-cycle before and during isocapnic O2-tests (IOT) at various steady levels of alveolar PCO2 ranging from 30 to 48 Torr. For this, PCO2 in the inspired gas before and during IOT was adjusted so that PACO2 remained unchanged in the course of the first few breaths which followed the switch to hyperoxia. In analysing the transient changes of V in the course IOT, it was considered that an apnoea occurred when there was no measurable deflection on the integrated pneumotachogram past a duration twice the control T from the beginning of the last recorded ventilatory cycle. (1) Control V vs. PACO2 relationships showed classic positive interaction between hypercapnia and hypoxia; (2) during IOT at PAO2 of 100, 75 or 60 Torr, an apnoea occurred, V invariably falling to zero, provided that PACO2 was below 38-35 Torr according to the level of oxygenation; (3) above that threshold PACO2 value, the residual minimum ventilation (Vres) observed during IOT was linearly related to PACO2; (4) Vres vs. PACO2 relationships showed negative interaction between hypercapnia and hypoxia. It is concluded that (a) through isocapnic O2-tests, both the peripheral and central components of the ventilatory drive can be quantitatively estimated; (b) in conscious dogs, the pulmonary ventilation appears to be entirely driven by afferent activity from the arterial chemoreceptors, even in eucapnic normoxia; (c) the lower minimum ventilation seen in the course of O2-tests from a hypoxic rather than a normoxic background is still observed at PACO2 above normal, thus cannot be due only to hypocapnia related to preceding hypoxic hyperventilation must be caused by a central respiratory inhibition directly or indirectly related to depressant effect of even moderate hypoxia.

Animals↗
PubMed1980

The reflex release of adrenaline and noradrenaline from the adrenal glands of cats and dogs.

1. We have studied the release of noradrenaline and adrenaline from the adrenal glands of dogs and cats in response to the lowering of carotid sinus pressure (baroreceptor tests) and to the perfusion of the vascularly isolated carotid bifurcations with hypoxic blood (chemoreceptor tests). 2. In cats, the resting output of catecholamines had a ratio of noradrenaline to adrenaline of 1:1. The ratio in the incremental release during baroreceptor tests rose to 3:1, and during chemoreceptor tests it fell to 1:6. 3. In dogs, the ratio of noradrenaline to adrenaline at rest was 1:4. The ratio did not change over a wide range of outputs during baroreceptor tests, chemoreceptor tests and splanchnic nerve stimulation. 4. The release of catecholamines in response to baroreceptor tests in the cat was abolished by hexamethomium bromide at doses that did not diminish the response to chemoreceptor tests.

Adrenal Glands↗
PubMed1978

Renal prostaglandins in renal hypertensive dogs.

1. Hypertension produced in two-kidney Goldblatt dogs was accompanied by a transient fluid retention, reaching a maximum 4 days after clamping. 2. Prostaglandin E and F concentrations in venous blood from the intact kidney also rose transiently, showing a maximum by the fifth day. 3. The rise in prostaglandin release from the intact kidney may be related to the fluid retention.

Animals↗
PubMed1978

Effect of cholinergic antagonists on sympathetic ganglionic transmission of vasomotor reflexes from the carotid baroreceptors and chemoreceptors of the dog.

1. In anaesthetized dogs the reflex vascular resistance changes in a perfused hind limb were studied following carotid baroreceptor or chemoreceptor stimulation. 2. The observed rises in resistance were sympathetically mediated and thus provided a means of studying the action of the cholinergic antagonists on the sympathetic ganglion transmission. 3. The reflex response to carotid baroreceptor stimulation produced by lowering the pressure in the carotid sinuses was abolished by hexamethonium bromide but not reduced by hyoscine methyl bromide. 4. The reflex response to carotid body chemoreceptor stimulation, by hypoxia, was not altered by hexamethonium bromide but was greatly reduced by the hyoscine methyl bromide. No reflex response was seen when both antagonists were present. 5. These results indicate that sympathetic ganglion synaptic transmission during the baroreceptor reflex is mediated by nicotinic receptor activation. The transmission evoked by chemoreceptor stimulation involves muscarinic receptors with a subsidiary nicotinic pathway. High doses of an antagonist were necessary to block the muscarinic component of transmission and this is discussed in relation to previous work. 6. No non-cholinergic transmission of the reflex responses was observed.

Animals↗
PubMed1977

Renal blood flow autoregulation and renal venous prostaglandins in the pump-perfused canine kidney (in situ).

1. Renal autoregulation of blood flow was re-examined in the pump-perfused canine kidney and concentrations of prostaglandins E and F in the renal venous plasma were measured by radioimmunoassay. 2. At low perfusion pressures, below the range of autoregulation, prostaglandin E and F concentrations rose and calculated prostaglandin E secretion rate fell. 3. Meclofenamate (10 mg/kg i.v.) reduced renal blood flow and prostaglandin E and F secretion rates, but did not abolish autoregulation. 4. Renal prostaglandins do not appear to mediate autoregulation in the kidney but may affect the level at which flow is controlled.

Animals↗