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Biomedical subjects

Y Gutman

Publications and source records attributed to Y Gutman.

At least 55 records · Page 3Linked to original sources
PubMed1977

Mechanism of inhibition of catecholamine release from adrenal medulla by diphenylhydantoin and by low concentration of ouabain (10(-10) M).

Catecholamine (CA) release was studied in rat adrenal incubated in vitro. Inhibition of (Na + K)-ATPase either by omission of K+ from the incubation medium or by addition of a high concentration of ouabain (10(-3) M) caused increased release of CA from the adrenal. Diphenylhydantoin (DPH) (10(-5) M) inhibited the spontaneous as well as the acetylcholine (10(-4) M)-induced release of CA. However, in K+-free medium or in the presence of 10(-3) M ouabain, DPH had no significant effect on CA release. A low concentration of ouabain (10(-10) M) caused a significant inhibition of spontaneous and of acetylcholine-induced release of CA. In a K+-free medium ouabain (10(-10) M) had no effect on CA release. DPH (10(-5) M) and a low concentration of ouabain (10(-10) M) caused a significant activation of (Na + K)-ATPase in a membrane fraction of the adrenal medulla. It is suggested that DPH and low ouabain concentrations inhibit CA release from the adrenal by activation of the sodium pump. The possible mechanism involved is discussed.

Acetylcholine↗
PubMed1977

Acetylcholine and cAMP in adrenal medulla:indirect effect.

Catecholamine release and cAMP accumulation were studied in bovine adrenal medulla slices in vitro. Acetylcholine (10(-4) M) and salbutamol (10(-6) M) caused increased release of catecholamines and accumulation of cAMP. Incubation in Ca2+ -free medium abolished the release of catecholamines and the increase of cAMP caused by acetylcholine but not that caused by salbutamol. In a membrane fraction of adrenal medulla acetylcholine (10(-4) M) had no effect on adenylate cyclase activity but salbutamol (10(-6) M) caused substantial activation of adenylate cyclase. It is suggested that acetylcholine has no direct effect on adenylate cyclase or cAMP in adrenal medulla and the accumulation of cAMP observed in slices incubated with acetylcholine is due to the effect of catecholamines, released by acetylcholine, on the medullary cells.

Acetylcholine↗
PubMed1977

Inhibition of catecholamine release by alpha-adrenergic activation: interaction with Na, K-ATPase.

In rat adrenal gland incubated in vitro, phenylephrine and naphazoline inhibited the release of catecholamines (CA) induced in a medium containing K+ (5.6mM). In K+-free medium or in the presence of ouabain (10(-3) M) phenylephrine and naphazoline had no effect on CA release. The alpha-adrenergic blockers, phentolamine and phenoxybenzamine, increased CA release in a K+-medium but had no effect on CA release from adrenal medulla in a K+-free or ouabain (10(-3) M) containing medium. PGE2 inhibited the release of CA both in the presence and in the absence of K+, as well as in the presence of ouabain (10(-3) M). Activation of alpha-adrenergic receptors in the adrenal medulla by phenylephrine and naphazoline resulted in increased Na, K-ATPase activity but no effect on Mg-ATPase. PGE2 acts through a different mechanism.

Acetylcholine↗
PubMed1977

Effect of salt loading in the rat on adenylate cyclase and phosphodiesterase activity in kidney cortex, medulla and papilla.

Adenylate cyclase (AC) and phosphodiesterase (PDE) activities were studied in the cortex, medulla and papilla of the rat kidney. Sodium loading in vivo for 14 days resulted in a decrease of AC activity in the cortex, a small increase in the medulla and a substantial increase of AC activity in the papilla. Sodium loading caused reciprocal effects on PDE activity: an increase in kidney cortex and a decrease in kidney papilla. Loading of glucose in vivo or chronic administration of antidiuretic hormone in vivo did not cause the changes in AC or PDE observed after sodium loading. The possible significance of these findings is discussed.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1977

Microsomal ATPase of kidney papilla: sensitivity to diuretics and other inhibitors.

Microsomal ATPase isolated from rat kidney papilla was compared to that from kidney medulla. Microsomal Na, K-ATPase from papilla was more sensitive to inhibition by ouabain, Cad N-ethyl-maleimide, Hg++, Thiomerin, ethacrynic acid and Furosemide than the enzyme from the medulla. Mg-ATPase of the papilla was less sensitive than the medullary enzyme to inhibition by Ca++, Cd++, N-ethyl-maleimide, Hg++, ethacrynic acid and Furosemide. Papillary Mg-ATPase was less sensitive than papillary Na, K-ATPase to all the inhibitors mentioned. Medullary Mg-ATPase was more sensitive than medullary Na, K-ATPase to inhibition by ethacrynic acid and Furosemide but less sensitive than medullary Na, K-ATPase to all the other inhibitors. Papillary Na, K-ATPase is the most sensitive to inhibition and papillary Mg-ATPase is the most resistant to inhibition by various diuretic drugs. The possible significance of these characteristics is discussed.

Adenosine Triphosphatases↗
PubMed1976

PGE2: opposite effect on catecholamine release from phaeochromocytoma and adrenal medulla.

The effect of PGE2 on catecholamine release from human adrenal medulla and phaechromocytoma was studied in slices incubated in vitro. In each of 3 normal human adrenal medullae PGE2 (10(-7) M) caused a significant inhibition of the release of catecholamines in in vitro incubation. In each of 3 phaechromocytomas studied PGE2 (10(-7) M) caused a significant increase of catecholamine release in in-vitro incubation. The possible relevance of this mechanism to the regulation of catecholamine release in phaeochromocytoma is discussed.

Adolescent↗
PubMed1976

Rat uterus renin-like activity: effect of stimuli and hormones.

1 The characteristics of renin-like activity in rat uterus were studied. The optimum temperature was 50 degrees C and optimum pH 4.0. Potassium (100 mM) enhanced this activity but sodium or calcium had no effect. 2 Uterine renin-like activity was unchanged 24 h after bilateral nephrectomy. 3 Renin-like activity in the uterus increased slowly from birth to 4 weeks of age and faster between the 4th and 8th week. 4 Ovariectomy caused a considerable fall in uterine renin-like activity. 5 The following factors, known to affect renin secretion in the kidney, i.e., hypovolaemia, sodium loading, adrenalectomy, administration of desoxycorticosterone acetate and injection of isoprenaline, had no effect on uterine renin-like activity. 6 Stilboestrol, an oestrogen, caused a significant increase of uterine renin-like activity. Progesterone and testosterone had no significant effect on this activity but blocked the increase caused by stilboestrol. 7 During pregnancy there was a small but significant fall of renin-like activity in the uterus in the first week and a continuous increase throughout the later period of pregnancy. 8 It is concluded that uterine renin-like activity is independent of kidney renin and does not respond to stimuli affecting kidney renin. Uterine renin activity is hormone-dependent and may be governed by the ratio, oestrogen : progesterone.

Adrenal Glands↗