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Biomedical subjects

G Hertting

Publications and source records attributed to G Hertting.

At least 163 records · Page 9Linked to original sources
PubMed1975

Suppression of isoprenaline-induced increase in plasma renin concentration by vasoconstrictors in rats with nonfunctioning Macula densa.

The mechanism of the increase in plasma renin concentration caused by the beta-sympathomimetic agent isoprenaline has been further investigated. Rats were pretreated by occluding the left renal artery for 2 hrs, thus rendering the macula densa cells of this kidney nonfunctioning. After contralateral nephrectomy infusion of isoprenaline (1.5 mug/kg min) still caused a strong increase in plasma renin concentration. This increase was significantly suppressed by simultaneous infusion of angiotensin II (1.0 mug/kg min). The alpha-sympathomimetic amine phenylephrine (60 mug/kg min) or octapressin (10 mU/kg min). The results exclude any mediator-role of the macula densa receptors in the isoprenaline-induced release of renin. The possibility of a stimulation of renin release via the baroreceptors or a direct "secretomotoric" action of isoprenaline is discussed.

Angiotensin II↗
PubMed1974

Effect of converting enzyme blockade on isoprenaline- and angiotensin I-induced drinking.

1 Intravenous infusion of 0.072 mumol kg(-1) h(-1) (1Asp, 5-Ile) angiotensin I, 0.116 mumol kg(-1) h(-1) of (1-Asp beta-amid, 5-Val) angiotensin II or of (1-Asp, 5-Ile) angiotensin II, caused food-deprived and water-satiated rats to drink about 3.0 ml of water per animal. This indicates that angiotensin I has a 1.6 times stronger dipsogenic effect than the angiotensin II preparations when infused intravenously.2 The converting-enzyme-inhibitor SQ 20881 (Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro) (1.0 mg/kg i.v.) had no intrinsic dipsogenic effect.3 SQ 20881 given in combination with angiotensin I or angiotensin II potentiated the dipsogenic effect of angiotensin I, but not that of the two angiotensin II preparations.4 The drinking induced by isoprenaline (100 mug/kg, i.m.) was potentiated by SQ 20881 to the same extent as drinking produced by angiotensin I infusion.5 Angiotensin I plasma levels were determined after angiotensin I infusion and isoprenaline application. Both were significantly raised by SQ 20881.6 It is concluded that one of the mechanisms which mediate the dipsogenic effect of isoprenaline is stimulation of the renin-angiotensin system and that increased plasma levels of angiotensin I may play a substantial role in this type of drinking.

Angiotensin II↗
PubMed1971

Uptake kinetics and metabolism of 7-3H-dopamine in the isolated perfused rat heart.

1. The isolated, perfused rat heart accumulates dopamine by two distinct uptake mechanisms characterized by different kinetic constrants and different patterns of metabolite production (Uptake 1: Km 0.69 x 10(-6)M and Vmax (1.45 x 10(-9) mol/g)/min; Uptake 2: Km 5.9 x 10(-4)M and Vmax (0.14 x 10(-6) mol/g)/min).2. The metabolic fate of dopamine taken up by the isolated, perfused rat heart depends on the concentration of dopamine in the perfusion medium. At a very low perfusion concentration (0.047 x 10(-10) mol/ml) most of the radioactivity is stored as unchanged dopamine and the main metabolite is noradrenaline. With increasing perfusion concentrations deamination becomes the main metabolic pathway, deaminated metabolites accounting for more than 50% of the total radioactivity after perfusion with 2,614.4 x 10(-10) mol/ml for 16 minutes. The O-methylated, and the O-methylated deaminated metabolites are of minor importance at all perfusion concentrations.3. The resistance to wash out of the dopamine taken up by the isolated, perfused rat heart is dependent on the perfusion concentration used. At a concentration of 66.9 x 10(-10) mol/ml, 50% of the total activity is washed out during an 8 min wash period. Within the same time interval there is no wash out when a perfusion concentration of 0.042 x 10(-10) mol/ml is used.4. It is concluded that the metabolic fate of dopamine taken up at various perfusion concentrations reflects the distribution of dopamine within intra- and extraneuronal compartments in the hearts.

Animals↗
PubMed1971

Effect of pretreatment with 6-hydroxydopamine on the uptake and metabolism of catecholamines by the isolated perfused rat heart.

1. Isolated rat hearts from control and 6-hydroxydopamine pretreated animals were perfused with (3)H-noradrenaline or (3)H-dopamine, either at a low perfusion concentration (1.50 x 10(-10) mol/ml (3)H-dopamine; 1.18 x 10(-10) mol/ml (3)H-noradrenaline) or a high perfusion concentration (296.69 x 10(-10) mol/ml (3)H-noradrenaline, 327.45 x 10(-10) mol/ml (3)H-dopamine) for 8 minutes.2. At the low perfusion concentration, the total activity, the radioactivity in the alumina eluates (sum of (3)H-dopamine, (3)H-noradrenaline and deaminated catechol metabolites) and the concentration of (3)H-dopamine. (3)H-noradrenaline and the deaminated catechol metabolites were decreased in the hearts of the pretreated rats as compared with the controls. The O-methylated amine metabolites were increased. The deaminated O-methylated metabolites were increased in the experiments with (3)H-noradrenaline and decreased in the (3)H-dopamine experiments.3. Uptake of (3)H-dopamine and (3)H-noradrenaline by the hearts of 6-hydroxydopamine pretreated rats was decreased to a much smaller extent when perfused with the high concentration than with the low concentration.4. At the high perfusion concentration there was a significant difference between control and pretreated animals with regard to the total radioactivity and the radioactivity in the alumina eluates only. The absolute and relative amounts of metabolites were not significantly changed by pretreatment with the exception of the deaminated catechol metabolites in the (3)H-dopamine experiments.5. It is concluded that neuronal Uptake 1 is greatly impaired in the hearts from rats pretreated with 6-hydroxydopamine, but extraneuronal Uptake 2 remains intact.

Animals↗