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Biomedical subjects

G Feuerstein

Publications and source records attributed to G Feuerstein.

At least 253 records · Page 14Linked to original sources
PubMed1980

Effect of indomethacin on cardiac beta-adrenergic receptors.

Treatment of rats with indomethacin, 1.5 mg/kg per day, for one week, significantly reduced the number of beta-adrenoceptors in the heart without altering their affinity for the specific beta-adrenergic ligand. In indomethacin-treated rats there was a reduction in the cardiac response to epinephrine in vivo as indicated by a shift to the right of the epinephrine dose-heart rate response curve. These results support a possible interference by indomethacin in beta-adrenoceptor-mediated effects.

Animals↗
PubMed1980

Reversal by naloxone of hemorrhagic shock in anephric cats.

Hemorrhage, 15 ml/kg induced a rapid fall of blood pressure in intact and anephric cats, but only intact cats demonstrated significant blood pressure recovery following bleeding. Naloxone, 0.1 mg/kg x min, i.v., had a mild promoting effect on blood pressure recovery in the intact cats whereas, in the hemorrhaged anephric cats naloxone re-established an almost complete recovery of blood pressure. These results suggest that endogenous opioid substances play a significant depressor role in hemorrhagic shock, especially in anephric animals.

Animals↗
PubMed1980

The effect of indomethacin on isoprenaline-induced renin secretion in the cat.

In vivo isoprenaline infusion (0.1 micrograms/kg.min)) into the renal artery of unilaterally nephrectomized cats elicited a 5-fold increase in plasma renin concentration (PRC). This increase was suppressed by concomitant administration of propranolol (0.3 mg/kg.min). Indomethacin (250 micrograms/kg.min) intrarenally infused prior to the administration of isoprenaline, abolished the isoprenaline-induced increase in PRC. It is suggested that prostaglandins mediate beta-adrenergic-activated renin release.

Animals↗
PubMed1980

Renin-angiotensin mediation of adrenal catecholamine secretion induced by hypoglycaemia in the cat.

1 The mechanism involved in catecholamine (CA) release from the cat adrenal gland in response to insulin hypoglycaemia was studied. In intact cats, hypoglycaemia induced an 11 fold increase in adrenomedullary CA secretion. 2 Acute bilateral nephrectomy nearly abolished the increased CA release from the adrenal gland during hypoglycaemia. 3 Infusion of Sar1-Ileu8-Angiotensin II (AII), a competitive AII antagonist, suppressed the adrenomedullary response to the insulin-induced hypoglycaemia. After termination of the antagonist infusion CA secretion from the adrenal medulla increased rapidly, reaching the same level as in insulin-treated cats. 4 Infusion of rabbit anti-angiotensin I antibodies suppressed CA release from the adrenal gland of hypoglycaemic cats. This effect was more prolonged than that of Sar1-Ileu8-AII. 5 These results indicate that CA release from the adrenal medulla of the cat in response to insulin-induced hypoglycaemia, is mediated through the renal reninangiotensin system. Since hypoglycaemia causes sympathetic stimulation through a central mechanism, angiotensin may act through the central nervous system.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1980

The role of the renin-angiotensin system in mediation of adrenal catecholamine secretion in the cat induced by intrarenal beta-adrenergic stimulation.

Isoproterenol infusion (0.1 microgram/kg per min) into the renal artery of the cat induced an increase in plasma renin concentration (PRC) from 14.3 +/- 5.7 (mean +/- SE) ng angiotensin I/ml per hr to 56.8 +/- 7.7 after 70 minutes (P < 0.05) and an increase in catecholamine secretion rate from 38.7 +/- 6.0 ng/kg per 10 min to 180.0 +/- 40.0 after 70 minutes (P < 0.001). Intravenous infusion of the same dose of isoproterenol had no significant effect on adrenomedullary catecholamine secretion rate. Isoproterenol induced preferential norepinephrine release: the ratio of norepinephrine to epinephrine secretion changed from 11.5:23.7 during the control period to 130.0:40.1 70 minutes after the start of isoproterenol administration. Intrarenal infusion of propranolol (3.0 mg/kg per min) inhibited renal renin release and adrenal catecholamine secretion in response to intrarenal isoproterenol. Intravenous infusion (0.4 microgram/kg per min) of an angiotensin II antagonist [Sar1, Ileu8]angiotensin II abolished the catecholamine response to intrarenal isoproterenol infusion. It is suggested that intrarenal isoproterenol infusion stimulates renal renin release and angiotensin production which, in turn, stimulates a preferential secretion of adrenomedullary norepinephrine.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1979

Selective reduction of adrenal medulla response to angiotensin induced by suppression of renin-angiotensin.

Angiotensin II (AII) induced an increase of adrenaline (A) release from rat adrenal glands in vitro. The response of the adrenal glands was completely abolished 22--24 h after bilateral nephrectomy. Adrenal glands from DOCA-salt-treated rats did not respond to AII as well, whereas adrenal glands from rats treated with furosemide and a low salt diet retained this response. High potassium in the medium increased significantly the release of A from in vitro incubated adrenal glands of nephrectomized rats from 0.43 +/- 0.04 to 0.63 +/- 0.06 microgram/gland and salbutamol (in calcium-free medium) increased the release from 0.34 +/- 0.03 to 0.43 +/- 0.03 microgram/gland. These results indicate that the adrenal medulla develops subsensitivity to AII in vitro, following a reduction in levels of this agonist in vivo.

Adrenal Medulla↗
PubMed1979

Endogenous prostaglandins modulate adrenal catecholamine secretion.

Adrenal catecholamine secretion induced by haemorrhage in the cat was increased by administration of indomethacin to intact or to bilaterally nephrectomized animals. Infusion of PGE2 (but not of PGF2 alpha) suppressed the increased catecholamine secretion caused by indomethacin.

Adrenal Glands↗
PubMed1979

Modification by SQ 14225 of blood pressure and adrenal catecholamine response to hemorrhage.

SQ 14225 infusion to cats exposed to hemorrhage suppressed adrenomedullary catecholamine release. The immediate compensatory blood pressure response was unaffected, while the later compensatory response was of a higher magnitude in intact cats that in SQ 14225-treated animals. Adrenal gland blood flow was better preserved in SQ 14225-treated hemorrhaged cats than in cats exposed to hemorrhage only. These data emphasize the role of angiotensin II in adrenal catecholamine and blood pressure responses to hemorrhage.

Adrenal Glands↗
PubMed1979

The effect of saline loading on blood pressure and catecholamine secretion in the rat and the cat.

The effects of acute and chronic saline loading on blood pressure and catechalomine (CA) response in the rat and cat were studied. In the rat, both acute and chronic saline loading stimulated urinary CA excretion without affecting blood pressure; adrenal tyrosine hydroxylase (TH) activity was increased. Pentolinium bitartrate abolished the increase in CA excretion. Chronic saline loading reduced the plasma renin concentration (PRC) and the heart noradrenaline concentration and elevated the plasma cholesterol. Acute infusion of isotonic or hypertonic saline in the cat stimulated adrenomedullary CA secretion. This response was not significantly affected after bilateral cervical vagotomy, but was totally abolished following bilateral nephrectomy. Blood pressure was increased only during the isotonic saline infusion but not during hypertonic saline administration. It is concluded that stimulation of adrenal CA secretion by saline loading is mediated through a renal factor.

Animals↗
PubMed1978

Angiotensin II mediation of adrenal catecholamine secretion induced by intrarenal isoprenaline infusion.

Isoprenaline infusion into the renal artery of the cat induced an increase in the catecholamine (CA) secretion rate from the adrenal gland. CA release by isoprenaline was preferentially noradrenaline. Intravenous infusion of an angiotensin II (A II) antagonist abolished adrenal CA response to intrarenal isoprenaline injection. It is suggested that intrarenal isoprenaline infusion stimulates renal renin release and A II production which, in turn, stimulates adrenal CA secretion.

Adrenal Glands↗
PubMed1978

Effect of indomethacin on water intake of the rat.

Indomethacin stimulated water intake in intact rats. This effect could also be demonstrated in bilaterally ureteral ligated rats, but it was totally abolished after bilateral nephrectomy. It is suggested that the stimulatory effect of indomathacin on water consumption is mediated by a renal factor.

Animals↗