Biomedical subjects

H Majewski

Publications and source records attributed to H Majewski.

116 records · Page 7Linked to original sources

PubMedDate not supplied

Inhibition by hydralazine of the conversion of dopamine to noradrenaline in rat atria in vitro and in vivo.

1. Hydralazine (10 to 2000 microgramol/l) produced a concentration-dependent inhibition of the conversion of (3H)-dopamine to (3H)-noradrenaline in rat isolated atria. 2. In rats treated with hydralazine (2 mg/kg, i.p.), there was an inhibition of the conversion of (3H)-dopamine to (3)-noradrenaline in the intact artia in vivo. 3. Hydralazine treatment may result in the appearance of dopamine as a significant co-transmitter in noradrenergic nerves, and this may contribute to the antihypertensive effect of hydralazine.

Animals↗

PubMedDate not supplied

Hypertension through adrenaline activation of prejunctional beta-adrenoceptors.

1. Adrenaline can enhance the stimulation-induced release of transmitter noradrenaline in sympathetically innervated tissues by activating prejunctional beta-adrenoceptors. 2. Adrenaline incorporated into sympathetic transmitter stores by neuronal uptake can be subsequently released as a co-transmitter and can then activate prejunctional beta-adrenoceptors, thus completing a facilitatory feedback loop. 3. Rats chronically treated with adrenaline develop elevated blood pressures compared to control rats. beta-Adrenoceptor blockade prevents the rise in blood pressure. 4. Activation by adrenaline of facilitatory prejunctional beta-adrenoceptors of sympathetic nerves innervating cardiovascular effector tissues may explain adrenaline-induced rises in blood pressure.

Adrenal Medulla↗

PubMedDate not supplied

Effects of isotonic saline loading on renal tubular and neurogenic dopamine release in conscious rabbits.

1. This study was designed to investigate the effects of isotonic saline loading on renal tubular and neurogenic dopamine (DA) in conscious rabbits. 2. Isotonic saline loading did not affect mean arterial pressure, heart rate or renal blood flow but markedly increased urine volume, sodium excretion and DA excretion. 3. Renal DA spillover was not affected by venous emptying, while renal noradrenaline (NA) spillover tended to decrease during saline loading. The ratio of % renal DA spillover to % renal NA spillover increased to 2.3 +/- 0.6 (P < 0.05) 3 h after saline loading. 4. Isotonic saline loading increased renal tubular DA production but had little effect on neurogenic DA release.

Analysis of Variance↗

PubMedDate not supplied

Facilitation of noradrenaline release by isoprenaline is not mediated by angiotensin II in mouse atria and rat tail artery.

The hypothesis that facilitation of noradrenaline release by prejunctional beta-adrenoceptors is linked to the local generation of angiotensin II was investigated in rat tail artery and mouse atria which were incubated with [3H]-noradrenaline. The outflow of radioactivity induced by electrical field stimulation of the tissues was taken as an index of noradrenaline release. In mouse atria, angiotensin II (0.01 microM) enhanced the stimulation-induced (S-I) noradrenaline release and this was blocked by saralasin (0.1 microM). Isoprenaline (0.01 microM) also enhanced the S-I release of noradrenaline, but this was not blocked by either saralasin (0.1 microM and 0.3 microM) or captopril (5 microM). Furthermore, the facilitatory effects of angiotensin II (0.1 microM) and isoprenaline (0.1 microM) were additive. In rat tail artery, the facilitatory effect of angiotensin II (0.01 microM) on noradrenaline release was blocked by saralasin (0.1 microM). The facilitatory effect of isoprenaline (0.1 microM) was blocked by propranolol (1 microM) but not by saralasin (0.1 microM) nor captopril (5 microM). These results indicate that beta-adrenoceptor-mediated facilitation of noradrenaline release occurs independently of angiotensin II in mouse atria and rat tail artery.

Angiotensin II↗

PubMedDate not supplied